ftplectures cardiovascular system lecture notes cardiology · 2015-05-23 · ftplectures...

Ftplectures Cardiovascular system Lecture Notes

CARDIOLOGY

Medicine made simple

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Title: Abdominal Aortic Aneurysm Objectives for learning: Define AAA, risk factors, causes, pathogensis, diagnosis and treatment. Definition: Aneurysms are enlarged blood vessels. Aortic aneurysm are mostly infrarenal. Causes/ Risk factors: High incidence in males, Age > 50 years, (65-‐70 years) -‐ Smoking increases risk of developing AAA-‐ due deposition of atherosclerosis – deposition of fatty plaques inside the wall of the abdominal aorta. This causes the wall to weaken, and that weakening causes that to balloon out. Atherosclerosis pathogenesis is due to deposit LDL which the macrophages are getting caught, eat it up, and become forming macrophages. They are going to cause the proliferation of the smooth muscle cells, they are going to form a plaque which is going to form in the walls of this aorta. And that plus smoking, hyperlipidemia, which means high LDL and low HDL, basically is going to predispose you to develop the aneurysm.

-‐ Hypertension, -‐ Vasculitis – inflammation of small blood vessels in aorta leading to ischemia

and weakening of aortic walls. -‐ Syphilis -‐ Marfan syndrome -‐ Fibrillin deficiency or any connective tissue disorder

Pathophysiology Clinical symptoms and signs

-‐ patients are asymptomatic except when aorta ruptures -‐ palpable, pulsating abdominal mass -‐ ruptured AAA is a life threatening emergency with a mortality of 90%. The

pumping heart pumps all the cardiac output into the abdominal cavity leading to sever hemorrhagic shock.

Symptoms -‐ severe abdominal or lower back pain,-‐ patient complain of sudden onset of

abdominal pain. -‐ Physical Exam may show grey tunre sign-‐ flank ecchymosis -‐ Cullens sign-‐ Periumbilical ecchymosis-‐ sign of blood in abdominal cavity

Sigs: Triad of AAA-‐ hypotension, abdominal pain, and pulsatile abdominal mass. Possible syncope if sever hypotension from hemorrhagic shock and inadequate perfusion to brain. -‐ nausea, vomiting. Diagnosis Ultrasound-‐ 100% sensitive CT scan only for stable patient with no hemodynamic instability-‐ normal blood pressure Treatment Surgery with synthetic graft Treat risk factors-‐ Hyperlipidemia with statins, hypertension with beta-‐blockers, thiazides, or ACE inhibitors Advice patient to stop smoking because it increases risk of developing another AAA


Title: Acute Coronary Syndrome Objectives for learning: Understanding the basic facts about acute coronary syndromes including unstable angina, NSTEMI and STEMI. Definitions: Acute coronary syndrome encompasses unstable angina (USA), non-‐ST elevation (NSTEMI), and myocardial infarction (STEMI). Causes/ Risk factors:

• Stable angina • Smoking • Diabetes • Obesity

Pathophysiology: Atherosclerotic plaques in coronary arteries cause the initial pathology. The plaque can rupture which leads to increased tendency to increased thrombosis. Thrombosis can lower the blood flow through the affected coronary artery, thus causing ischemia to the regions distal from the occlusion.

• Unstable angina appears on the basis of previously developed stable angina. Due to seriously decreased diameter of coronary blood vessels caused by atherosclerotic plaque progression, these patients have increased frequency of chest pain occurring even during the rest.

• Non-‐STEMI is the type of myocardial infarction which is not big enough to cause ST-‐elevation.

Clinical symptoms and signs

• Increased frequency of chest pain even during the rest • Prolonged duration of chest pain (>10 minutes)

Diagnosis

• EKG can be normal in the case of unstable angina and NSTEMI, but it can also show ST-‐depression and T wave inversion due to the ischemia. ST-‐depression has to be greater than 0.5 mm and T inversion greater than 2 mm in order to be significant.

• In order to distinguish unstable angina and NSTEMI, cardiac enzymes are used (CK-‐MB, Troponin I/T)

Treatment

• Morphine • Oxygen • Nitrates • Aspirin (COX-‐inhibitor which decreases tromboxan A2 and platelet

aggregation) • Beta-‐blockers (decreasing heart frequency and blood pressure) • Glycoprotein IIb / IIIa inhibitors • Exonoparin (low-‐molecular heparin) • Coronary catheterization is performed if the patient is not feeling better after

medicamentous treatment. Lifestyle modifications:

• Diet • Exercise • Glucose control • Statins • Stop smoking • Lose weight


Title: Acute Myocardial Infarction (MI) Objectives for learning: Learning the pathophysiological and clinical features of acute myocardial infarction, as well as treatment options. Definitions: Acute myocardial infarction is necrosis of myocardium due to massive ischemia caused by coronary artery occlusion. It is the most common cause of the death in the United States (30% mortality). Causes/ Risk factors: Acronym: FLASH – MD

• Family history • Low HDL • Age (men>45, women>55) • Smoking • Hypertension • Male gender • Diabetes

Pathophysiology: Acute myocardial infarction represents the necrosis of some parts of heart muscle which happens due to the massive ischemia caused by complete occlusion of the coronary artery responsible for supplying that region. Clinical symptoms and signs

• Chest pain (crushing; radiation to the neck, jaw, and left arm) • Nausea • Vomiting • Diaphoresis • Shortness of breath • Weakness, fatigue

Symptoms last more than 30 minutes. Atypical clinical picture in:

• Diabetics • Elderly • Women • St. post surgery

Diagnosis • EKG changes (ST-‐elevation, Q-‐waves (at least 0.04s and 25% of R wave), T-‐

waves inversion o I, aVL, V5, V6 – lateral wall o V1, V2, V3 – anterior wall o II, III, aVF – inferior wall o V1, V2 – Septal wall

• Cardiac enzyme o CK-‐MB (increases during the first 4-‐8 hours; returns to normal values

after 48-‐72 hours) o Troponin I/T (increases in the first 3-‐5 hours; returns to normal

values after 5-‐14 days) * CK-‐MB is an important marker for reinfarction

Complications

• Ventricular fibrillation • Reinfarction

Treatment

• Morphine • Oxygen • Nitrates • Aspirin – antiplatelet (aspirin decreases mortality) • Beta-‐blockers (reduce mortality) • ACE inhibitors • Statins • Anticoagulant -‐ Low molecular weight heparine • Revascularization


Title: Acute Pericarditis Objectives for learning: Learning clinical signs, diagnostic techniques, and treatment options for acute pericarditis. Definitions: Pericarditis is an inflammation of pericardium. Causes/ Risk factors:

• Idiopathic • Viruses (Coxsackie B, HIV, Echoviruses) • Radiation • Uremia • Acute myocardial infarction (Dressler’s syndrome) • Lupus • Amyloidosis • Rheumatoid arthritis • Sarcoidosis • Procainamide, hydralazine, izoniazide (drug induced pericarditis)


• Retrosternal chest pain (pleuritic pain which radiates to trapezius or scapula)

o Leaning forward lowers the pain. o Swallowing, cough, and lying down increase the pain.

• Fever • Pericardial rub

Diagnosis

• EKG o Diffuse S-‐T elevation o P-‐R depression (the most specific for pericarditis) o T wave inversion

• Echocardiogram

Complications • Pericardial effusion

• Pericardial tamponade Treatment

• Aspirin • Steroids are given if the patient does not respond well to aspirin


Title: Aortic Dissection Objectives for learning: Understanding pathophysiology, causes, and clinical features of aortic dissection, learn how to diagnose it fast and what type of treatment to apply. Definitions: Severe hypertensive emergency where the blood flow damages tunica intima and accumulates in the space between tunica intima and tunica media. Causes/ Risk factors:

• Hypertension • Trauma • CTD – Connective Tissue Diseases (Ehlers-‐Danlos syndrome, Marfan

syndrome)

Pathophysiology: There are two types of aortic dissection – type A and type B. In type A, proximal part of ascending aorta is dissected, so there is a risk of coronary ischemia because the dissection can reach coronary arteries. In type B, aortic arch is dissected, and the dissection can prolong distally, down to renal arteries causing renal ischemia. Clinical symptoms and signs

• Ripping chest pain (anterior in proximal dissection and interscapular in distal dissection)

• Diaphoresis • Aortic regurgitation signs and symptoms • Hemiplegia or hemiparesis (due to ischemic stroke)

Diagnosis

• Transesophageal echocardiogram (TEE) • CAT scan (aorta with two lumens) • AP chest X-‐ray (widened mediastinum)

Complications

• Coronary ischemia • Stroke

• Renal ischemia Treatment

• Beta-‐blockers • i.v. Sodium nitroprusside (decrease systolic pressure below 120 mmHg) • Surgical treatment is necessary in type A aortic dissection

Title: Aortic Stenosis

Objectives for learning: Definition, Pathophysiology, Causes/ Risk factors, Clinical symptoms and signs, Diagnosis and Treatment.

Definition:

Pathophysiology

Stenotic aortic wall causes left ventricular outflow obstruction. Valve being stenotic becomes unable to push blood to left ventricle. Decrease LV outflow leads to left ventricular hypertrophy due to excessive amount of force heart has to put to pump the blood. Over a passage of time LV dilatation and then mitral regurgitation develops. Cardiac output becomes decrease.

Causes/ Risk factors:

Calcification of the bicuspid valve (olderly patients most develop calcification of the valve due to deposition of calcium)

History of rheumatic fever

Clinical symptoms and signs:

Symptoms:

• Asymptomatic for years • With the worsening of obstruction • Syncope • Angina • Dyspnea due to CHF

Signs:

• Murmur • Crescendo-‐decrescendo murmur. Can be heard at second intercostal space and carotid

artery • S4 sound • Parvus et tardus a decreased or delayed carotid stroke

Diagnosis

• Chest-‐x-‐ray • Echocardiogram (LV and LA enlargement) • Cardiac catherization: It is a definite diagnostic test and gradient and valve area less

than 0.8 is considered normal.

Quiz

1. A 57 year old patient presents with complaints of Syncope, chest pain on physical exertion and malaise. On examination a murmur is present over second intercostal space. S4 sound is also heard. He has a previous history of rheumatic fever. What is the likely diagnosis? A. Aortic stenosis B. Aortic regurgitation C. Mitral stenosis D. Mitral regurgitation

The correct answer is: A

The history, clinical picture and physical examination all point towards the development of aortic stenosis in this patient. The murmur of aortic stenosis is usually heard at second intercostal space. S4 sound is prominent here. Rheumatic fever is the most common cause of aortic stenosis in the adult patient.

In case of aortic regurgitation S3 sound is heard whereas the murmur of aortic regurgitation is heard at third left intercostal space.

Mitral stenosis is characterized by the loud first heart sound and tapping apex beat. The murmur of mitral stenosis is heard at the apical region and is low-‐pitched.

The murmur of mitral regurgitation is best heard at the apex of the heart. Here first heart sound is soft. The most common cause of mitral regurgitation is mitral valve prolapsed.

2. Which of the given option is related to the aortic stenosis? A. Diastolic murmur B. Atrial fibrillation C. Right heart failure D. Systolic ejection murmur

The correct answer is: D

Systolic ejection murmur is related to the aortic stenosis. This murmur is the due to turbulent flow of blood forward across the right ventricular outflow tract, aortic valve, or via the aorta. It is also related to pulmonary stenosis.

Diastolic murmur has no relation to the aortic stenosis. Diastolic murmurs begin at or after S2 heart sound and remains till at or before S1.

Aortic stenosis does not lead to atrial fibrillation but mitral stenosis can cause the development of atrial fibrillation.

Right heart failure may result with aortic stenosis but when disease is quite old so best option is D.

3. A 43-‐year-‐old patient presents with confirm diagnosis of aortic stenosis. He has a history of fever and joint pains. What would be the most likely cause here? A. Bacterial endocarditis B. Congenital bicuspid valve C. Rheumatic fever D. Marfan’s syndrome

The correct answer is: C

Aortic stenosis in an adult is usually the result of rheumatic fever. Rheumatic fever is an inflammatory condition that precedes an infection by the Streptococcus pyogenes. It can involve the skin, heart, brain and joints.

A congenital bicuspid valve is basically a congenital disease vulnerable to endocarditis and ultimately develops calcification as well as symptomatic stenosis.

Aortic stenosis is usually seen after the bacterial endocarditis. There must be a history of development of bacterial endocarditis.

Marfan’s syndrome can cause aortic stenosis but that adult must have the features of Marfan’s syndrome.

4. Crescendo-‐decrescendo is the murmur found in aortic stenosis. What is its exact location? A. Fifth intercostal space

B. Second intercostal space and carotid artery C. In the fourth intercostal space medial to mid-‐clavicular line. D. At the apex of the heart

The correct answer is: B

Since Crescendo-‐decrescendo murmur occurs due to stenosis of aorta, so its location would be where aorta is present. The correct answer therefore is second intercostal space and carotid artery. All other options are not correct.

5. Syphilis is the infection which can cause heart disease. What is the most common valve of the heart involved by it? A. Mitral valve B. Pulmonary valve C. Aortic valve D. Tricuspid valve


In the later stages of disease, syphilis involves the heart and remains confined to the base of the aorta. When it involves the wall of the aorta, syphilis leads to loss of the elastic properties of the aorta and even the formation of aortic aneurysms.

Mitral valve, pulmonary valve and tricuspid valve are not affected by the syphilis.

Title: Atrial Septal Defect (ASD) Objectives for learning: Definition, Pathophysiology, Clinical symptoms and signs, Physical Exam, Diagnosis, Complications, and Treatment. Definition: The defect between the two atria is called atrial septal defect. There are two types: Ostium primum: The little hole at the top between the right and the left atrium is called ostium primum. 80% septal defects are ostium primum. Septum primum: It is the defect at the lower side between the right and the left atrium. Causes/ Risk factors: Pathophysiology Deoxygenated blood normally comes from the head and the lower side of the body into the superior vena cava (SVC) and inferior vena cava (IVC) respectively. From here it enters into the right atrium. Right atrium now has deoxygenated blood which enters into the right ventricle. Right ventricle contracts during systole and pumps blood into the pulmonary arteries which now enters into the lung. The pulmonary arteries become smaller pulmonary capillaries which take oxygen, exchange with carbon dioxide. Now oxygenated blood is taken up by the pulmonary veins into the left atrium. The left atrium always has oxygenated blood. In case of atrial septal defect the left atrium cannot pump blood into the left ventricle. The oxygenated blood is not transferred to the whole of the body through aorta. Thus, oxygen is not transmitted to the body. The pressure from the IVC and SVC coming into the right atrium is always at low side. The pressure in the RV is 25/10 mmHg, in the left atrium is 12 mmHg and in the left ventricle is 130/80 mmHg. Clinical symptoms and signs The patients are normally asymptomatic. But as the patients reach to 40 years of age, they develop: • Dyspnea at exertion • Exercise intolerance • Anemia • Fatigue Physical Exam • Mid-‐systolic ejection murmur is heard at pulmonary area.

• Wide fixed split S2 sound • Diastolic rumble in the tricuspid region • Irregularly irregular heart rate • No p waves on EKG • Atrial fibrillation Diagnosis • Transesophageal Echocardiogram (TEE) • Chest x-‐ray • Electrocardiography (EKG) Complications • Pulmonary hypertension • Right ventricular failure • Eisenmenger's disease • Paradoxical emboli • Stroke Treatment Surgical repair – close up the valve

Title: Blood Pressure Regulation I: Baroreceptor Pathway

Objectives For Learning: Mean arterial blood pressure, Normal blood pressure, Pathways and Neural Pathways.

Mean Arterial Blood Pressure

• Mean arterial blood pressure: 2 (diastolic blood pressure) + systolic blood pressure / 3. • Normal blood pressure is less than 120/80 mmHg i.e. systolic blood pressure over diastolic

blood pressure.

Pathways

There are two pathways

• Neural pathways à fast à sympathetic • Hormonal pathways à slow à Renin-‐angiotensin, aldosterone pathway

Neural Pathways

When someone is bleeding, it causes decrease in intravascular volume. The blood pressure also decreases. Normally, the aortic arch and baroreceptors feel the stretch in the walls of the carotid sinus. They also sense the decrease in blood pressure. Glossopharyngeal nerve of the hering’s nerve in the carotid sinus after sensing this sends signals to the brainstem. Automatically, the decrease in parasympathetic tone is achieved while increase of sympathetic tone occurs to compensate the decrease in blood pressure. Sympathetic nervous system acts on the SA nodes and causes:

• Increase in the heart rate • Increase in the contractility of cardiac muscles • Increase in stroke volume

All this eventually increases the cardiac output and finally the BP. The sympathetic system also activates the alpha and beta receptors in the vasculature leading to vasoconstriction and increase in total peripheral resistance (TPR). Increase in TPR leads to increase in BP.


Title: Cardiac Tamponade Objectives for learning: Understanding the basics of cardiac tamponade pathophysiology, clinical features, diagnosis, and treatment. Definition: Cardiac tamponade is impaired ventricular filling due to excessive pericardial effusion. Causes/ Risk factors:

• Penetration of the chest • Iatrogenic damage to the atrial or ventricular wall during central venous

catheter placement or pericardiocentesis • Pericarditis • Myocardial infarction

Pathophysiology:

• The rate of effusion is important for the development of cardiac tamponade. If more than 300 mL of fluid are rapidly going into the pericardial space, it will cause tamponade. On the other hand, in cases of slow filling, the pericardium has time to stretch so there can be 1.5 L of fluid in pericardial space before developing a tamponade.

• Impaired ventricular function leads to decreased preload, which then leads to low cardiac output. Consequently, the blood pressure is going to be low.

• The pressures in all four cardiac cavities is going to be equal. Clinical symptoms and signs

• Beck’s triad: o JVD o Hypotension o Muffled heart sounds

• Narrowed pulse pressure (due to low stroke volume) • Pulsus paradoxus (blood pressure decrease for >10mmHg during

inspiration) • Tachycardia

Diagnosis • Echo • Chest X-‐ray

o Increased cardiac silhouette o Clear lung fields

• EKG o Electrical alternans

• Cardiac catheterization o Increased intrathoracic pressure o RA pressure is decreased with the loss of Y descent

Treatment

o If the patient is stable and there is no blood – just watch o If the patient is unstable – pericardiocentesis o Surgery if the vasculature walls are damaged

Title: Cardiac Tumors: Myxomas Objectives for learning: Types Of Cardiac Tumor, Most Common Primary Liver Cancer, Most Common Liver Cancer, Most Common Brain Cancer Types of Cardiac Tumor 1. Myxomas 2. Rhabdomyomas The most common primary cardiac tumor of adults is atrial myxomas. Patients present with syncope because this atrial myxoma causes ball valve effect in the left atrium. Due to the tumor blood cannot get into the left ventricle because this tumor seals up the mitral valve, causing a decrease in the left ventricular and diastolic volume. The cardiac output also decreases, perfusion also decreases and the brain gets affected, therefore leads to syncope. ü In children the most common primary tumor of heart is Rhabdomyomas. Tuberous sclerosis

is the most common disease associated with this tumor. ü The most common primary liver cancer is the hepatocellular carcinoma from liver cirrhosis. ü The most common liver cancer is the metastasis usually from melanoma or lymphoma. ü The most common brain cancer is the metastasis usually from melanoma or lymphoma.

Title: Cardiogenic Shock Objectives for learning: Definition, Causes, Clinical symptoms and signs, Diagnosis, Treatment, Intra aortic balloon pump (IABP).

Definition: Cardiogenic shock is the decrease in cardiac output that leads to decrease in tissue perfusion. This is due to insufficient circulation of blood owing to failure of the ventricles of the heart to work effectively. We know that Mean arterial pressure = CO x TPR CO= cardiac output TPR= Total peripheral resistance With decrease in cardiac output, mean arterial pressure also decreases. Cardiogenic shock is a medical emergency.

Causes/ Risk factors • Acute myocardial infarction (most common cause) • Cardiac temponade • Tension pneumothorax • Arrhythmias (ventricular tachycardia) • Massive pulmonary embolism

Pathophysiology

Clinical symptoms and signs Symptoms: • Hypotension –Blood pressure can fall up to 80/60 • Oliguria • Tachycardia • Altered mental status Signs: • Skin appears pale and cold. • Jugular venous distension is found • Pulmonary congestion or edema is present.

Diagnosis EKG: To see the presence of elevated ST segments, indicating myocardial infarction (MI) Echo to check cardiac temponade

Chest X-‐ray to detect the presence of tension pneumothorax Hemodynamic monitoring: Swan-‐Ganz catheter is used to monitor blood flow and heart's function. It measures left atrial pressure by measuring capillary pulmonary wedge pressure.

Treatment The initial management is maintaining of Airway Breathing Circulation Afterwards following treatment is started depending upon the cause. • In case of myocardial infarction the following treatment is given.

− Oxygen − Beta blocker − Morphine − Ace inhibitors − Nitroglycerin − NG intubation − Statin − Tissue plasminogen activator (TPA) − CABG − Angioplasty

• For cardiac temponade pericariocenthesis is performed. • Thoracotomy is carried out for tension pneumothorax • The drug such as amiodarone is given for cardiac arrhythmias. • Low molecular weight heparin is given to manage pulmonary embolism. Vasopressors are also given in cardiogenic shock. They tend to increase after and preload and thus increase the reduced blood pressure. These are: − Dopamine: It increases the renal flow and renal perfusion − Dobutamine: It increases the cardiac output − Norepinephrine or phenolepinephrine: It is used when both dopamine and dubutamine do

not help to raise the BP. Norepinephrine increases contractility, cardiac output and eventually the blood pressure.

Don’t give IV (intravenous) fluids here since they are harmful for the patient with cardiogenic shock. Left ventricular pressure is already elevated so IV fluid should be avoided.

Intra aortic balloon pump (IABP) Intra aortic balloon pump (IABP) is sometimes used to boost myocardial oxygen perfusion. Balloon is placed in aorta. During systole this balloon deflates while during diastole it inflates. By doing so it increases afterload and cardiac output and consequently the perfusion and oxygen to the coronary artery also increases and myocardiac oxygen demand decreases.

Quizzes 1. A patient presents with chest pain, difficult breathing and confusion after long trip in an

airplane. His BP was 80/40mmHg. His skin is cold. Jugular vein is distended. Based on the findings and history what is the likely complication of pulmonary embolism in this patient? A. Hypovolemic shock B. Cardiogenic shock C. Anaphylactic shock D. Neurogenic shock

The correct answer is B. The most likely complication pulmonary embolism in this patient is cardiogenic shock. This is because massive pulmonary embolism leads to the development of cardiogenic shock. It is also apparent from the condition of the patient. He has developed hypotension, skin is cold and his jugular vein is also distended, pointing toward cardiogenic shock. Hypovolemic shock may present wit hypotension, cold skin but there is no chest pain unless there is a trauma there. Also, in this shock hemorrhage or bleeding occurs. Jugular vein is not distended. The most important is that pulmonary embolism does not lead to hypovolemic shock as no blood loss occurs here. Anaphylactic shock is the characteristic of severe allergic reaction. There may be a number of signs and symptoms such as itch, swelling, rash, low BP, reduce heart rate, dyspnea, etc. it is not the complication of pulmonary embolism. Neurogenic shock is again not the complication of pulmonary embolism. It occurs after spinal cord injury. 2. In a patient with diagnosis of myocardial infarction and cardiogenic shock, what will be the

most important treatment of choice?

A. Intra aortic balloon pump (IABP) B. Angioplasty C. CABG

D. Pericariocenthesis The correct answer is A. Intra aortic balloon pump (IABP) is the most effective and important treatment of choice in patient with myocardial infarction and cardiogenic shock. This is because it increases the perfusion to the myocardium by increasing the coronary blood flow as well as simultaneously decreases the myocardium oxygen demand, which is important to prevent re-‐infarct and tissue death. Angioplasty can be used but it is merely used to open up the obstructed vessels. Coronary artery bypass grafting (CABG) is basically a surgical procedure that is performed to improve the blood flow. It is performed when there is severe coronary heart disease (CHD). 3. Pericariocenthesis is not performed here and is mainly done in case of cardiac temponade. A patient presents with cardiogenic shock and myocardial infraction. After resuscitation all of the following should be administered based except?

A. Beta blocker B. IV fluids C. Tissue plasminogen activator (TPA) D. Morphine

The correct answer is B. IV fluids should not be administered in the patient with cardiogenic shock. This is because they are harmful for the patient with cardiogenic shock. They can raise the volume and eventually left ventricular pressure which is already elevated so IV fluid should be avoided. Beta blockers are useful in patient with cardiogenic shock and myocardial infarction because they reduce the size of infarct as well as early mortality when administered early. Beta blockers also decrease the incidence of development of recurrent ischemia, ventricular arrhythmias, or reinfarction. Tissue plasminogen activator (TPA) can be given in patient with cardiogenic shock and myocardial infarction. It helps to breakdown the thrombosis. Morphine is also used in myocardial infarction as it reduces the pain. 4. A 18-‐year-‐old patient is admitted to the hospital because he presents with confusion, chest

pain, and confusion and shortness of breath after a blunt injury in the chest. On examination he is pale with cold clammy skin. His BP is 80/60 mmHg. His jugular vein is distended and urinary output noted is 17ml/hour. A diagnosis of cardiogenic shock is made. What is the likely cause of cardiogenic shock in this patient?

A. Acute myocardial infarction B. Arrhythmias C. Tension pneumothorax D. Massive pulmonary embolism

The correct answer is C. History of blunt trauma with chest pain and shortness of breath is the typical symptoms of tension pneumothorax. It is the result of penetrating injury of the lung causing development of one-‐way valve. Tension pneumothorax can further cause the development of cardiogenic shock, thus it is the most likely cause here. Acute myocardial infarction does not occur after trauma. Also, its symptoms are different such as here a person develops chest pain that radiates towards neck and left arm, sweating, palpitation, etc. Arrhythmias are the condition in which heart beat is irregular. It is either too fast or too slow. It is presented with shortness of breath and also does not develop after trauma. Massive pulmonary embolism cannot be the likely cause of cardiogenic shock here because it does not develop following a trauma. For it to develop, there should be a history of prolong bed rest, deep venous thrombosis, a long trip in a car or aero plane, etc.

Title: Coarctation Of Aorta Objectives for learning: Definition, Classification of Coarctation of Aorta, Clinical Symptoms and Signs Definition: It is the stenosis or narrowing of the aorta. Classification of Coarctation Of Aorta • Pre-‐ductual • Post ductual The most important duct is the ductus arteriosum. It is a little pipe that connects the aorta and the pulmonary artery during intrauterine life. The ductus arteriosum later becomes ligamentum arteriosum. If something happens before, it is called preductual coarctation. If something happens after, post Preductal coarctation only occurs in infants. The adult type is the post ductual coarctation. By definition this is a stenosis of the aorta past the ligamentum arteriosum or stenosis distal to the ductus arteriosus is known as post ductual coarctation. Coarctation of aorta is associated with Turner syndrome. Aortic regurgitation eventually develops. The murmur of coarctation of aorta is the blowing high pitched diastolic murmur. Causes/ Risk factors: Pathophysiology Clinical symptoms and signs • Low blood pressure in lower extremities (hypotension) • High blood pressure in upper extremities (hypertension) • Notching of the ribs and pleural effusion on chest X-‐rays may be present. • Poor growth Diagnosis Treatment


Title: Complications of Acute Myocardial Infarction Objectives for learning: Identifying acute and chronic complications of acute myocardial infarction. 1. Chronic Heart Failure

• The main symptom is shortness of breath • Therapy:

o ACE inhibitor to decrease blood pressure o Diuretics (furosemide) to eliminate fluid

• It can progress to cardiogenic shock 2. Arrhythmias

• Premature Ventricular Complexes (PVCs) • Atrial Fibrilation • Ventricular tachycardia

o Therapy: § Amjodaron § Electrical cardioversion (if hemodynamically unstable)

• Ventricular fibrillation o Therapy

§ Unsynchronized defibrillation • Paroxysmal Supraventricular Tachycardia (PSVT) • Sinus tachycardia • Sinus bradycardia (atropine if they are dynamically unstable) • Asystole • AV block (pacemaker is needed if there is IIb or III degree AV block)

3. Reinfarction

• New ST elevation o Check CK-‐MB level

4. Rupture

• Occurs due to scar tissue forming 10 days after myocardial infarction • Types:

o Free wall rupture (cardiac tamponade) – pericardiocentesis is needed o Interventricular wall rupture – surgery is needed

o Papillary muscles rupture (mitral regurgitation) – mitral valve replacement is needed

o Ventricular aneurysm 5. Pericarditis

• Inflammation of pericardium • Dressler’s syndrome can develop weeks to months after myocardial

infarction • Treatment:

o Aspirin 6. Ventricular embolism

• Can cause stroke

Title: Congenital Heart Diseases

Objectives for learning: Right To Left Shunt, Left To Right Shunt and Pathophysiology.

Definition:

1) Right to left shunt – it means early cyanosis, blue babies 2) Left to right shunt – late onset cyanosis also known as blue kids

Right to left shunt occurs in

• Tetralogy of Fallot (TOF) • Transposition of great vessels • Persistent truncus arteriosus • Tricuspid atresia • Total anomalous pulmonary venous return

Left to right shunt

− Ventricular septal defect (VSD)—the most common congenital cardiac defect. − Atrial septal defect (ASD) − Patent ductus arteriosus (PDA)

Pathophysiology

The normal pressure inside the right atrium (RA) is less than 5 mmHg

The normal pressure of the right ventricle (RV) is 25/5mmHg, in the left atrium (LA) is less than 12 mmHg, in the LV is 130/10 and in the aorta is 130/90 mmHg.

The pressure in the RA is less than 5mmHg because this allows blood to go into the heart during preload because pressure in the veins has to overcome the pressure in the atrium. The pressure in the RV is 25 mmHg, so to receive blood; pressure in it would be equal or less than the pressure in the RA during diastole so that blood can easily flow into the right ventricle. It means when heart contracts the pressure the systole pressure which ejects blood into the pulmonary artery has to be as high as 25mmHg so that it can get blood into the pulmonary artery. Also, blood from pulmonary artery enters into the left atrium. The systolic pressure inside the pulmonary artery is 25 and in the left atrium is less than 12; mean high pressure to low pressure.

The systolic ejection pressure of 130/10 in the LV pushes out the blood into the aorta.

Initially, blood moves from higher pressure to lower pressure, i.e. it shunts from LV to RV. But there is still a blood to enter into the systemic circulation. Over time, the wall of the RV gets thick and thicker the wall the higher the diastolic pressure. Overtime, pressure in the RV overcomes the pressure in the LV, now we get deoxygenated blood into the RV. That’s why it takes time and children are called blue kids and a patient is said to develop late onset cyanosis. Similar happens when blood shunts from LA to RA and patient develops late onset cyanosis.

Same is with the PDA, an open space between the aorta and the pulmonary artery.

Clinical symptoms and signs Diagnosis Treatment


Title: Congestive Heart Failure Objectives for learning: Understanding the pathophysiology of different types of heart failure, as well as risk factors, clinical features, diagnostics, and treatment options. Definition: Heart failure is a syndrome which appears when heart is not able to maintain circulation and to provide adequate perfusion to the rest of the body. Causes/ Risk factors:

− Hypertension − Excess salt in intake

Pathophysiology: − Normally, heart receives the blood from the venous side of the body, through the

superior and inferior vena cava (preload). After the blood enters the right atrium and then right ventricle, the heart muscle stretches, which is the stimulus for the contraction. That way, the blood is being pushed from the ventricles, which is called stroke volume. Frank – Starling relationship says that if the preload is increased, the contractility increases too, thus causing increased stroke volume and consequently increased cardiac output.

− Decreased cardiac output causes the activation of compensatory mechanisms, including carotid sinus baroreceptors, which in turn increases sympathetic activity (increased heart rate, contractility, increased preload and afterload). Another, slower compensatory mechanism includes rennin-‐angiotensin-‐aldosterone system (water and sodium retention).

− The cause of heart failure can be either systolic or diastolic dysfunction. o Systolic dysfunction is caused by lowered contractility of some parts of

heart muscle due to myocardial infarction, dilated cardiomyopathy, myocarditis.

o Diastolic dysfunction appears due to impaired relaxation of heart muscle. The common causes are hypertrophic ventricular failure (due to hypertension, aortic stenosis, aortic regurgitation, and mitral stenosis) and restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis).


− Shortness of breath – Dyspnea (because of pulmonary congestion) − Orthopnea – breathing difficulties when lying on the back − Paroxysmal nocturnal dyspnea − Nocturnal cough − Diaphoresis − Cold extremities

Specific signs of left-‐sided heart failure include: − Cardiomegaly − S3 gallop − S4 − Crackles (rales) in the lungs − Dullness to percussion of the lungs

Specific signs of right-‐sided heart failure include: − Jugular venous distension (JVD) − Liver congestion and hepatomegaly − Ascites − Peripheral edema − Right ventricular heaves − Nocturia

Diagnosis − Chest X-‐Ray – cardiomegaly, Kerley B-‐lines, interstitial markings, pleural

effusion (blunting of the costophrenic angle) − Echocardiogram is the most important examination to make, because it

shows whether the systolic ejection fraction is lowered. − ECG findings are not specific.

Treatment 1. Diet restriction (less than 4g of salt/day) 2. Diuretics

o Furosemide – first line treatment o Thiazide – second line treatment o Spironolactone (can cause hyperkalemia!)

3. ACE inhibitors decrease mortality in patients with heart failure by decreasing preload and afterload. Side effects of ACE inhibitors are: angioedema, cough, and elevated potassium levels. ACE inhibitors can be replaced with sartans (angiotensin receptor blockers) in patients with serious cough.

4. Beta blockers (Carvedilol) are shown to slow the progression of heart failure and decrease mortality.

5. Group IV patients (the terminal stadium of heart failure) should receive Digitalis in order to improve cardiac output. Hydralazine and isosorbid nitrate can also be used to regulate the blood pressure in these patients.


Title: Coronary Circulation Objectives for learning: Define coronary arteries and their topography, and explain coronary circulation as well as physiology of coronary blood supply. Definition: Coronary circulation is composed of coronary arteries, the most proximal branches of aorta. Their purpose is blood supply to the heart muscle. Anatomy: Left coronary artery (LCA) and right coronary artery (RCA) come off the ascending aorta as its first branches. LCA splits into two arteries: the circumflex artery (CFX), which wraps around the left lateral side of the heart and finishes on the posterior side, and left anterior descending artery (LAD) which travels down the interventricular septum and finishes at the apex of the heart. RCA travels downwards giving its branch – acute marginal artery (AMA). RCA then curves around the back of the heart forming posterior descending artery (PDA). Blood supply: CFX – posterior left ventricle LAD – anterior septum and apex AMA – right ventricle PDA – posterior septum Physiology: -‐ At rest, myocardium uses 70% of oxygen contained in the blood that comes from coronary blood vessels, while during exercise, it extracts 90% of oxygen from the blood. -‐ Coronary arteries receive blood only during the diastolic phase of cardiac cycle.


Title: Deep Venous Thrombosis Objectives for learning: Understanding the causes, risk factors, pathophysiology, diagnosis, complications, and treatment of deep venous thrombosis. Definition: Deep venous thrombosis is the presence of clots in deep veins of legs. Causes/ Risk factors:

• Virchow's triad o Endothelial damage o Hypercoagulability o Stasis

Risk factors: • Congestive heart failure (CHF) • Immobilization • Obesity • Estrogen (use of birth control pills or pregnancy) • Family history of DVT • Varicose veins

Pathophysiology: Unlike arterial blood vessels, blood flow in veins depends only on muscle contraction. One way valves enable bringing the blood up towards the heart. Endothelial damage can be caused by:

• surgery • stasis (prolonged rest or travel) • malignancies • age.

Some hereditary diseases can cause hypercoagulability. • Factor V Leiden deficiency – leads to increased clotting • Protein C and S deficiency • Antithrombin III deficiency

DVT most often comes from iliac and femoral veins. Clinical symptoms and signs Signs and symptoms are very variable from patient to patient. Classic findings include:

• Lower extremity pain and swelling (especially while walking) – non-‐specific, non-‐sensitive

• Homan’s sign – calf pain with dorsiflexion • Fever

Diagnosis

• Order Doppler ultrasound of the lower extremities to determine compressibility of the veins. It is highly specific and highly sensitive for the detection of blood clots in proximal parts of extremities, but not in the calf.

• The most accurate test is venography. • D – Dimer (very specific but only about 50% sensitive)

Complications

• Pulmonary embolism -‐ detached clots from deep veins of lower extremities travel through the inferior vena cava to the heart and are then towards the lungs. The result is pulmonary embolism.

− Big saddle emboli that obstruct pulmonary artery cause right ventricular failure and arrhythmia and hypoxia.

• Postthrombotic syndrome appears due to insufficiency of venous valve system and the increase in hydrostatic pressure in venous capillaries.

• Phlegma cerulea dolens – severe leg edema resulting in ischemia which causes loss of sensitive and motor neural function.

Treatment

• Anticoagulant treatment is the most important − Heparin (prolongs PTT) − Varfarin (inhibits vitamin K) − TPA (Tissue Plasminogen Activator)

INR should be maintained between 2 and 3 for 3-‐6 months. • Greenfield filter is used to prevent pulmonary embolism • Surgery post-‐management (leg elevation, compression stockings, early

ambulation, pneumatic compression boots.

Title: Einsenmengers Disease

Objectives for learning:

Before studying Einsenmengers Disease, first discuss the diseases that cause right to left shunt.

• Ventricular septal defect (VSD) • Atrial septal defects (ASD) • Patent ductus Arteriosus (PDA)

These are the leading cause of development of Einsenmengers Disease. A patient may have either of these diseases for very long duration and if not corrected, they can lead to the development of Einsenmengers Disease.

Definition:


Pathophysiology

Usually an uncorrected VSD, ASD and PDA lead to compensatory pulmonary hypertrophy which further results in progressive pulmonary hypertension which increases pulmonary vascular resistance. This causes reversing of shunt from left to right to right to left. This causes late cyanosis, clubbing and polycythemia.

The RA pumps blood into the RV and from there to PA to the lungs. But when there is a space i.e. ventricular septal defect the pressure in the LV overcomes pressure in the RV. This patient starts pump blood into the RV. But with the passage of time RV hypertrophy develops. Blood does not pump into the lungs and causes the patient to become cyanosed.

In case of ASD, lots of blood goes into the pulmonary artery. This causes development of pulmonary hypertension due to increase blood flow into the lungs. The blood again comes to RV, causing RV hypertrophy.

In case of PDA, there is an open space between the aorta and the pulmonary artery. This patient shunts deoxygenated blood into the PA into the lungs. Overtime, vasoconstriction develops, causing pulmonary hypertension. If it is not corrected the blood come backs into the aorta, causing cyanosis, polycythemia and clubbing to develops.

Polycythemia

Poly means many

Cythemia means cell

When body senses that it is not getting oxygen, it stimulates the production of erythropoietin to further stimulate the production of more red blood cells, thus causing polycythemia.

Clinical Symptoms And Signs

• Cyanosis • Clubbing

Diagnosis

Treatment

Title: Atrial Fibrillation Objectives for learning: Definition, Causes, Pathophysiology, Clinical symptoms and signs, Diagnosis and Treatment. Definition: It is the fibrillation or quickering of the atrium. Causes/ Risk factors: • Pulmonary embolism, COPD • Iatrogenic • Rheumatic heart disease / Mitral regurgitation • Arthrosclerosis • Thyroid (Hyperthyroidism, thyrotoxicosis) • Endocarditis • Sick sinus syndrome Pathophysiology Normally, SA nodes fires and causes depolarization of the muscles. When atrium depolarizes an atrial contraction occurs. Atrium also squeezes at the same time, causing blood to enter into the ventricles. But in case of atrial fibrillation, multiple different ectopic nodes start firing. Not only atrium contracts, but blood stasis also occurs. Clinical symptoms and signs • Lightheadedness • Syncope • Fast heart beat • Hypertension Diagnosis On EKG having atrial fibrillation, check • Rate • Regular or irregular QRS complex • P waves • P:QRS ratio • PR interval • QRS width

In atrial fibrillation, there are no P waves present. The patient heart rate is very variable. The heart beat is irregularly irregular. No P: QRS ratio since no P waves are present. The normal PR interval is less than 0.02 seconds but in atrial fibrillation, no P waves are present so PR interval cannot be determined. QRS complex is usually of 120 milliseconds. In atrial fibrillation QRS width is less than 120 milliseconds or normal. Treatment Patients are given: • Anticoagulants such as warfarin (because of blood stasis and if anticoagulants are not given

patients with AF can develop stroke, mesenteric ischemia, claudication, myocardial infractions, etc.)

• Beta blockers such as methoprolol: These help to decrease the heart rate. • Calcium channel blockers e.g. nefidipine: They slow down the heart rate. • Digoxin: It has a parasympathetic effect, stimulating the vagal nerves which slow down the

firing from SA and AV node and thus allows decreasing the heart rate.

Title: Fetal Red Cell Production Objectives for learning: Types of Hemoglobin and Organ responsible for Blood formation during intrauterine life. Fetal hemoglobin α2γ2 Adult hemoglobin α2β2 Weeks • First three to ten weeks: Yolk sac is responsible for making blood. • 6 weeks: Liver is responsible for erythropoises. • 15 and 30 weeks: Spleen takes on this responsibility. • 22 weeks to adult: Bones becomes responsible. Quiz 1. Which organ is responsible for formation of blood during 6 week of intrauterine life?

A. Spleen B. Bones C. Yolk sac D. Liver

The correct answer is D. Liver is responsible for erythropoises during 6 week of intrauterine life. Yolk sac is responsible for making blood during first 3 to 10th week of intrauterine life. Spleen becomes responsible for erythropoises during 15 and 30 weeks of life. Bones becomes responsible from 22 weeks to onward in adult life. Which organ is responsible for formation of blood during 25 week of intrauterine life?


The correct answer is A. Spleen becomes responsible for erythropoises during 15 and 30 weeks of life. Liver is responsible for erythropoises during 6 week of intrauterine life. Yolk sac is responsible for making blood during first 3 to 10th week of intrauterine life. Bones becomes responsible from 22 weeks to onward in adult life. During which stage does the yolk sac take part in erythropoises?

A. Does not take part B. 4th week C. 22 week D. 15th week

The correct answer is B. Yolk sac is responsible for making blood during first 3 to 10th week of intrauterine life. So, correct option is 4th week here. Yolk sac does take part in the formation of blood during intrauterine life. During 15 and 30 weeks of life spleen becomes responsible for erythropoises. Bones becomes responsible from 22 weeks to onward in adult life. 4. What is the difference between Fetal hemoglobin and Adult hemoglobin with regard to their structure?

A. Fetal hemoglobin has two alpha and two beta chains. B. Adult hemoglobin has two alpha and two gamma chains. C. Fetal hemoglobin has two alpha and two gamma chains. D. Both are same and have no difference.

The correct answer is C. Fetal hemoglobin has two alpha and two gamma chains while adult has two alpha and two beta chains. Fetal hemoglobin has not two alpha and two beta chains but has two alpha and two gamma chains. Adult hemoglobin does not have two alpha and two gamma chains but have has two alpha and two gamma chains. Fetal and adult hemoglobins are not same but differ structurally as well as with respect to their life. 5. Which organ is responsible for formation of blood during adult life


The correct answer is B. Bones are responsible for formation of blood from 22 weeks to onward in adult life. Spleen becomes responsible for erythropoises during 15 and 30 weeks of life. Yolk sac is responsible for making blood during first 3 to 10th week of intrauterine life. Liver is responsible for erythropoises during 6 week of intrauterine life.

Title: Heart Blocks

Objectives For Learning: Atrio ventricular nodal block, Types, First degree AV block, Second degree AV block, and Third degree heart block.

Atrio Ventricular Nodal Block

In AV nodal block there is an impairment of the conduction between the atria and ventricles of the heart. SA node fires but this discharge does not go beyond the atria to the ventricles.

Types

There are three types of blocks.

1. First degree AV block:

It is always prolonged in case of first degree AV block. Normally, it is less than 200 mili seconds. But in first degree AV block, the PR interval is greater than 200 mili seconds (greater than 5 boxes). This is because there is a block causing a delay in the conduction between the AV node down into the ventricle. It is a begin condition and requires no treatment.

2. Second degree AV block

It is of two types

Mobitz type 1: It is also known as Wenckebach. A prolonged PR interval until a p wave fails to conduct is known as mobitz type 1. It is again a begin condition and requires no treatment.

Mobitz type 2: P waves here fail to conduct but the PR interval is constant. Here AV node is conducting and the block is actually in the bundle of His. For this reason, constant PR interval appears. Patients may have palpitations. They need pace maker implantation. This type of condition can progress into complete heart block.

3. Third degree heart block

It is the absence of conduction of atrial impulses to the ventricles which means there is no correspondence between P waves and QRS complexes. The atrial conduction is doing everything independently. There is a complete AV block. There is dissociation between atrial impulses and ventricular conduction. Complete heart block leads to asystole. Patients suffer from presyncope episodes. They develop lightheadedness or dizziness. They also develop ventricular tachycardia and atrial fibrillation. In EKG, atrio-‐ventricular rates are different from each other. P waves are present. P: QRS ratio is variable. QRS width is normal. A pace maker is needed to treat third degree AV block.

Title: Heart Sounds Basics

There are four heart valves

• Aortic valve (right upper sternal border) • Pulmonary valve • Tricuspid valve (left lower sternal border) • Mitral valve

The apex is in the 5th and 6th intercostal space.

The normal heart sound is S1 and S2

S1 is the sound heard when the mitral and the tricuspid valve close as the blood flow from atrium to the ventricle and ventricle starts to squeeze.

S2 heart sound is due to closure of aortic and pulmonary valve and is heard as the ventricular systole ends and the ventricular diastole begins.

S3 sound is present in case of pregnancy or in congested heart failure. It can be heard in the apex and in the tricuspid area.

S4 sound is due to the atrium contracting against a non-‐compliant ventricle.


Title: Hypertensive Emergency Objectives for learning: Understanding the basics of hypertensive urgency and emergency, and learn to diagnose them and apply fast and effective treatment. Definitions:

• Hypertension is a medical condition in which blood pressure is higher than 140/90 mmHg in two separate occasions.

• Hypertensive urgency – blood pressure of 220/120 mmHg or higher without any end organ damage.

• Hypertensive emergency – blood pressure of 220/120 mmHg or higher with end organ damage.

• Hypertensive encephalopathy – blood pressure of 240/140 mmHg or higher with neurologic symptoms.

• Preeclampsia – Hypertensive episodes during pregnancy (140/90mmHg or higher) with proteinuria and edema of lower extremities.

Causes/ Risk factors: Risk factors:

• Hypertension is the most prevalent in African Americans • Men are more often affected than women

Causes: • Noncompliance to medications • Sympathomimetic drugs • Cushing’s syndrome • Eclampsia • Pheochromocytoma • Hyperaldosteronism

Pathophysiology: − Patient using can develop hypertensive urgency due to bad compliance to

antihypertensive medication they normally use. − Cocaine, LSD, and phenylephrine users can experience hypertensive urgency

due to sympathomimetic effects of these drugs. Increased blood pressure damages the endothelium of blood vessels. That causes the deposition of proteins in the walls of the blood vessels, thus causing basement

membrane thickening. That thickening narrows the walls of blood vessels causing ischemia by decreasing blood flow through the blood vessels. Clinical symptoms and signs

• Head o Headaches o Blurry vision (due to papiloedema) o Altered mental status o Weakness in arms or legs, numbness, tingling, etc. o Retinal hemorrhages

• Chest o Chest pain o Shortness of breath o Pulmonary crackles/rales o Jugular venous distension o S3

• Kidneys o Anuria o Hematuria o Increased creatinine

• Legs o Edema

Diagnosis

− It is necessary to take good history. − Physical exam:

o If there is altered mental status, rule out the other possible causes in order to blame hypertension.

o Full neurological exam o Fundoscopic exam

− Laboratory techniques: o ECG o Electrolytes o Creatinine o BUN o WBC count o LFTs o Proteins and blood in urine

− Iamging: o CT scan of the head o Chest X-‐Ray

Treatment The aim is to decrease the blood pressure by 25% in first 1 – 2 hours. *If patient’s blood pressure is 240/140 mmHg, the pressure after 1 – 2 hours should be 180/90 mm Hg. Medication:

• Beta blockers (contraindicated if the patient used drugs) • Sodium nitroprusside • Fenoldopam • Hydralazine • Nitroglycerin

Title: Hypovolemic Shock Objectives for learning: Definition, Causes, Pathophysiology, Signs and Symptoms Stages of hypovolemic shock, Diagnosis and Treatment

Definition: Low blood volume leads to decrease cardiac output.

Causes/ Risk factors: 1. Hemorrhagic

• Trauma • GI Bleed • Retroperitoneal bleed

2. Non hemorrhagic

• Burns • Vomiting • Massive watery diarrhea • Third space-‐-‐ Ascites in massive liver cirrhosis • Low albumin (hypoalbuminemia)

Pathophysiology Low blood volume causes low cardiac output. The parameters of hypovolemic shock include decreased cardiac output, increased total peripheral resistance (TPR) and decreased pulmonary wedge pressure.

Clinical Symptoms And Signs • Hypotension • Cold, clammy skin

Diagnosis • CVP (central venous pressure) • Pulmonary capillary wedge pressure is low. • Systemic vascular resistance is high.

Stages Of Hypovolemic Shock Stage 1: It is characterized by 10 to 15% (<75ml) loss of blood. The normal cardiac output is equal to 5L (5000ml) so all the parameters such as pulse, systemic blood pressure, respiration, capillary refill, CNS dysfunction and urine output are not affected but normal.

Stage 2: Here 20 to 30 % (75 to 1500ml) blood is lost. Here systemic BP is normal, but pulse is increased and heart rate is high, while all other parameters are decreased. Stage 3: Here 30 to 40% (1500 to 3000 ml) blood loss occurs. Here blood pressure decreases severely, heart rate increases (due to reflex tachycardia), pulse pressure and capillary refill both decrease. Lactic acidosis ensues. A patient is confused and his urinary output becomes less than 20ml/hour (patient develops severe oliguria and almost going to develop anuria). Stage 4: Here greater than 40% blood loss occurs (i.e. > 2000ml). The affect person is lethargic.

Treatment • Maintain airways, breathing and circulation. For maintaining airways incubate the patient. • Manual pressure over bleeding is important to stop bleeding. • Pass NG tube to avoid development of aspiration pneumonia • IV fluids Normal saline.

Quizzes 1. A patient presents with confusion and lethargy. He sustains a trauma on his abdomen. On

examination his BP is 80/50. His skin is cold and clammy. The jugular venous pressure is normal. What is the most likely diagnosis? A. Hypovolemic shock B. Cardiogenic shock C. Aortic aneurysms D. Neurogenic shock

The correct answer is A

The most likely diagnosis is hypovolemic shock. This is because patient suffers from a trauma on his abdomen so it may have cause retroperitoneal bleed. For this reason, his BP has fallen and his skin is cold.

Since there is no complaint of chest pain, so the cardiogenic shock is unlikely here. The jugular venous pressure must be elevated in case of cardiogenic shock.

Aortic aneurysm is a condition in which aorta is dilated to greater than 1.5 times than its normal size. The symptoms of this problem appear when aneurysm is ruptured. There may be abdominal and back pain. Aortic aneurysm rupture is a serious medical condition.

Neurogenic shock results when there is injury to the spinal cord, affecting the sympathetic system. Skin here is warm. Bradycardia is also present.

2. A patient is admitted in the hospital after a diagnosis of hypovolemic shock is made. What is the most common cause of this shock? A. Burns B. Injury to spinal cord C. Fluid shift D. Blood loss

The correct answer is D.

The most common cause of hypovolemic shock is blood loss. Loss of blood leads to immediate volume depletion. This depletion further affects cardiac output which becomes reduced.

Burns may lead to development of hypovolemic shock but is not as common as blood loss is.

Injury to spinal cord is the most common cause of neurogenic shock.

Fluid shift can also cause hypovolemic shock since it leads to decrease in blood pressure to severe extent but it occurs rarely.

3. A patient is presents with severe bleeding and confusion after a trauma. His BP is 80/40mmHg. His heart rate is 120beats/min. He is admitted in the hospital and necessary resuscitation is given. It is however found that his urinary output is 15ml/ hour. What is the most likely stage of hypovolemic shock in this patient? A. Stage 1 B. Stage 2 C. Stage 3 D. Stage 4

The correct answer is C.

The most likely stage of hypovolemic shock in this patient based on his clinical presentation is stage 3. In this stage 30 to 40% blood loss occurs, leading to severely dropping of blood pressure and urinary output. Heart rate however is increased. A person develops lactic acidosis

and consequently altered mental status and confusion. In this patient urine output is markedly reduced.

In case of Stage 1 person does not have above mentioned symptoms. He may be asymptomatic because here only 10 to 15% blood loss has occurred.

Stage 2 is characterized by 20 to 30 % loss of blood. Here systemic BP is normal, but heart rate is high.

Stage 4 is a severe form of hypovolemic shock characterized by greater than 40% blood loss. A person may be unconscious and anuric.

Title: Infective Endocarditis Objectives for learning: Definition, Causes, Classification, Complications Of Infective Endocarditis, Clinical symptoms and signs, Diagnosis and Treatment Definition: Infection of the heart valve is called infective endocarditis. Causes/ Risk factors: Bacteria Classification 1. Acute Endocarditis (less than 6 weeks): The culprit is staphylococcus aureus (more common

in IV drug abusers) 2. Subacute Endocarditis is caused by:

• Streptococcus viridians, most prone to dentistry procedures • Enterococcus (bacteria arise from GI tract)

3. Native Valve Endocarditis

• Streptococcus viridans • Haemophilus • Actinobacillus • Cardiobacterium • Ekenella • Kingella

4. Prosthetic Endocarditis The bacteria responsible here are:

• Staphylococcus epidermidis (60 days of surgery) • If more than 60 days then staphylococcus aureus is responsible

In blood cultures if streptococci bovi appears positive then it may probably be due to colon cancer Complications Of Infective Endocarditis

• Cardiac failure • Glomerulonephritis • Mycotic abscess

Pathophysiology Clinical Symptoms And Signs

• Fever • Roth spots (retinal lesions due to vasculitis) • Osler’s nodes (painful nodes in the pads of the finger or the toes due to vasculitis) • Murmur • Jane way lesions (lesions on the palm and the soles due to emboli) • Anemia • Nail bed hemorrhages/ Splinter hemorrhages • Emboli

Diagnosis

• Blood culture • Transesophageal echocardiogram

Treatment Empiric Treatment: Start with vancomycin and gentamycin and give intravenously before the results of blood culture come. Once the blood cultures come positive for particular organism, such as for streptococcus viridians then give penicillin. But if a person is allergic to penicillin then switch to ceftriaxone and gentamycin. If person is IV drug abuser, then given antibiotic against staphlococcus aureus. Nafcilin for 4 weeks is given plus gentamycin for 5 days In case of Methicillin-resistant Staphylococcus aureus (MRSA) give vancomycin for 6 weeks. And if blood culture comes positive for enterococcal bacteria give penicillin/ampicillin (for 4 to 6 weeks) If a person is allergic to penicillin then administer vancomycin + gentamycin (for 4 to 6 weeks).

Quiz 1. A 15-year-old patient presents with fever and joints pain for 3 day. A patient also complains

of night sweat. On examination she is pallor. Splinter hemorrhage and painful nodules on the fingers’ pad are found. What is the most likely diagnosis? A. Polymyalgia Rheumatica B. Atrial Myxoma C. Reactive Arthritis D. Infective endocarditis


The most likely diagnosis is infective endocarditis. It is characterized by low grade fever, Osler’s nodules, anemia and splinter hemorrhage. In addition, Jane way lesions and Roth’s spots are also present. It is a condition of the inflammation of the valves of the heart.

Polymyalgia rheumatica (PMR) is basically a syndrome of unidentified etiology. It usually occurs in adults and is characterized by muscle pain frequently of the shoulder girdles and the hip. A patient usually complains of morning stiffness that lasts for more than one hour.

Atrial Myxoma is a tumor of the heart. It is a benign tumor. Fever, joint pain, shortness of breath and weight loss occur. Painful nodules are not found here, so it is not a correct diagnosis.

Reactive arthritis is an autoimmune condition which is the result of an infection. It is characterized by conjunctivitis, urethritis and arthritis. This is not correct as patient has no such complaints.

2. Which of The following is not the cutaneous involvement of infective endocarditis? A. Janeway's lesions B. Skin petechiae C. Roth's spots D. Osler's Nodules


Roth's spots are not the cutaneous involvement of infective endocarditis. These are basically the retinal lesions due to vasculitis.

Skin petechiae are usually found in patient with infective endocarditis.

Janeway's lesions are one of the cutaneous involvements of infective endocarditis. These are lesions on the palm and the soles and are due to emboli.

Osler's Nodules are again the cutaneous manifestation of this condition i.e. infective endocarditis. These are painful nodes present in the pads of the finger or the toes due to vasculitis.

3. A person with infective endocarditis has a history of using drugs for pleasure. Which antibiotic is best for this patient? A. Nafcilin B. Vancomycin C. Amoxacillin D. Rifampicin

The correct answer is A.

Nafcilin is the drug of choice for the person who is a drug abuser and also suffered from infective endocarditis.

Vancomycin is usually preferred for those who are allergic to penicillin.

Amoxacillin has no such role in case of infective endocarditis.

Likewise, rifampicin is not the drug used for patients with infective endocarditis.

4. Which of the following statements concerning infective endocarditis is not right? A. Empiric treatment of infective endocarditis includes vancomycin and gentamycin B. Splenomegaly is found to occur commonly in acute infective endocarditis than the sub

acute one. C. Glomerulonephritis is one of the complications of infective endocarditis D. Infective endocarditis takes place within 2 weeks of bacteremia

The correct answer is B.

The incorrect option regarding infective endocarditis is A. Splenomegaly is not commonly found in case of acute infective endocarditis. It is rather present in sub acute infective endocarditis.

Empiric treatment of infective endocarditis includes vancomycin and gentamycin. This treatment is generally started before the report of blood cultures come.

Clinical manifestations of this condition usually take place within 2 weeks of the provocative bacteremia in approximately 80% of cases.

Glomerulonephritis is one of the complications of infective endocarditis.

5. All of the following are responsible for native valve endocarditis except

A. Streptococcus viridans B. Streptococcus viridians C. Haemophilus D. Ekenella


Streptococcus viridians do not cause native valve endocarditis instead infection by these bacteria occurs following a dentistry procedure. Streptococcus viridians are responsible for native valve endocarditis. 55-65% cases of all native valve endocarditis are caused by viridans streptococci. Haemophilus and Ekenella both are the cause behind native valve endocarditis.


Title: Introduction to hypertension Objectives for learning: Causes, risk factors and pathophysiology and complications of hypertension. Definition: Hypertension is high blood pressure (>140/90). Essential hypertension is high blood pressure without identified cause (95% of all patients). Secondary hypertension has known causes (5% of patients). Causes/ Risk factors: Risk factors:

• Age • Gender (men have higher risk than women) • Race (African Americans have higher risk of hypertension) • Obesity • Sedentary lifestyle • Increased sodium intake (>4g/day) • Alcohol

Causes:

• Secondary hypertension o Renal causes

§ Renal artery stenosis § Chronic renal failure § Polycystic kidney disease

o Endocrine system § Hyperthyroidism § Hyperaldosteronism § Hyperparathyroidism § Cushing syndrome § Pheochromocytoma

o Medications § Oral contraceptives § Decongestives § NSAIDs § TCAs

o Coarctation of the aorta o Illegal drugs

§ Cocaine o Sleep apnea o Birth control pills

Pathophysiology:

• Decreased perfusion through the renal artery stimulates rennin-‐angiotensin-‐aldosterone system, thus increasing peripheral vascular resistance and blood pressure.

• Hyperthyroidism increases metabolic rate and consequently the blood pressure.

• Hyperaldosteronism increases sodium reabsorption and causes hypernatremia, thus increasing intravascular volume and blood pressure.

• Patients with Cushing syndrome have excess amount of cortisol which activates adrenal medulla to produce more norepinephrine and epinephrine, thus increasing blood pressure.

• In pheochromocytoma, high amounts of norepinephrine and epinephrine are produced due to tumor of adrenal medulla.

• Decongestives are intended to make a local vasoconstriction, but also have impact on systemic blood pressure increase.

• NSAIDs block COX2, thus blocking the synthesis of vasodilatatory prostaglandins.

• Cocaine inhibits the reuptake of norepinephrine, thus increasing its blood concentration and blood pressure.

• Sleep apnea causes respiratory acidosis which provokes hypoxia. Hypoxia leads to hypoxic vasoconstriction in the lungs which leads to pulmonary hypertension and eventually high blood pressure.

Increased systemic vascular resistance increases the afterload, so the heart has to work much harder, which leads to left ventricular hypertrophy. Over time, heart function becomes weaker leading towards dilation of the heart and heart failure. High blood pressure accelerates arteriosclerosis by damaging endothelium of blood vessels. Complications

• Cardiac complications o Coronary artery disease (myocardial infarction) o Left ventricular hypertrophy and heart failure o Stroke (hemorrhagic), TIAs, ischemic stroke o Aortic dissection o Peripheral arterial disease

• Eye changes o Papilloedema o Retinal hemorrhages

• Kidneys o Nephrosclerosis o Renal failure

Title: Kawasaki’s Disease

Objectives for learning: Clinical Features, Complications, and Treatment Definition Causes/ Risk factors: Pathophysiology Clinical Features

• Conjunctivitis • Rash all over the body (desquamating rash) • Adenopathy (cervical lyphmadenopathy) • Strawberry tongue • Hands and foot (swelling, erythema and peeling) • Burn • Uncontrolled fever for more than 5 days

Complications

• Predisposed to coronary artery aneurysm • Myocardial infraction

Diagnosis

Treatment

• Intravenous immunoglobulins (IVIG) + aspirin

Title: MITRAL REGURGITATION

Objectives for learning: Definition, Causes/ Risk factors, Pathophysiology, Symptoms, Diagnosis and Treatment. Definition: Blood returns into left side of the heart into the left atrium from the pulmonary vein right back into left ventricle into the aorta to the rest of the body. When mitral valve closes it gives S1. The blood flows out through the aorta during systole and during diastole mitral valve opens up to allow blood to return back to the heart but at the same time aortic valve and pulmonary valve both close and it gives S2. During systole both tricuspid and mitral valve close to give S1 sound. During systole mitral valve blow up and so blood goes back to the left atrium, increasing the pressure inside it, causing decrease in cardiac output, hypertension and cardiogenic shock. Causes/ Risk factors: Acute causes: Endocarditis, S.aureus infection, Myocardial infarction (rupture of papillary muscles) Chronic Causes: Rheumatic heart disease, Marfan syndrome, and cardiomyopathy. Pathophysiology LA pressure increases here. The size of left atrium is normal but blood now backs up, back to the pulmonary vein, pulmonary capillaries, pulmonary edema, congestion and eventually pulmonary hypertension. Clinical symptoms and signs

− Dyspnea − Palpitations − Proximal nocturnal dyspnea − Pulmonary edema

PE: Holosystolic murmur Diagnosis

− Chest x-‐ray shows dilated left ventricle and pulmonary edema − Echo show presence of MR, dilated left ventricle and decreased left ventricular function

Treatment Medical therapy: It is started with afterload reduction medications such as ACE inhibitors (such as lisinopril)

Decrease salt intake

Digoxin

For arrhythmias give CCB (calcium channel blocker) to treat atrial fibrillation (AF)

Anticoagulation therapy (patient may have AF)

Surgical Treatment: Patient needs a mitral valve replacement or mitral valve repair.

Quiz

1. A patient presents with complain of attacks of severe shortness of breath and coughing at night. The first heart sound appears soft while the apex beat is laterally displaced. There is a murmur appeared following first heart sound and is of high-‐pitched. Chest x ray shows enlargement of the left atrium and the left ventricle. What is the most probable diagnosis? A. Mitral regurgitation B. Mitral stenosis C. Tricuspid regurgitation D. Tricuspid stenosis


The most probable diagnosis is Mitral regurgitation. This is characterized by the post nocturnal dyspnea, orthopnea and palpitations. Holosystolic murmur appears following first heart sound and is of high-‐pitched. Chest x ray shows enlargement of the left atrium and the left ventricle.

Mitral stenosis is a condition characterized by the narrowing of the mitral valve orifice. It is presented with the same symptoms as that of mitral regurgitation. Tapping apex beat is present with very loud first heart sound. Chest X ray shows left atrial enlargement.

Tricuspid regurgitation is the consequence of problem within the tricuspid valve. The symptoms include those of right-‐sided heart failure, such as edema, ascites, jugular venous distension and hepatomegaly. Jugular venous pressure is found to be elevated. Echo shows the presence of enlargement of right ventricle and right atrium.

Tricuspid valve stenosis is a disease of the valves of the heart which results due to narrowing of the tricuspid valve orifice. An abnormal pulse is felt in the jugular vein within the neck during a physical examination.

2. When does the mitral regurgitation take place?

A. During systole B. During diastole C. During both systole and diastole


The mitral regurgitation takes place during systole. During systole mitral valve being abnormal could not propel blood to the left ventricle and so blood goes back to the left atrium, increasing the pressure inside it with subsequent consequences.

The option B and C are not correct since during diastole pressure exerted on the walls of the arteries are not enough to proper blood from left atrium to left ventricle.

3. A 46 year old man with severe mitral regurgitation has no symptoms. His left ventricular ejection fraction is approximately 45% while an end-‐systolic diameter index is about 2.9 cm/m2. What would be the most suitable treatment in this patient?

A. No treatment B. Mitral valve replacement or repair C. ACE inhibitor therapy D. Diuretic therapy and digoxin

The correct answer is:B

A zurgical treatment is recommended in case of severe mitral regurgitation even if the patient is asymptomatic. This is because when the left ventricular ejection fraction falls down below 60% it may cause a progressive dysfunction of left ventricle.

If no treatment is given patient may develop cardiac failure and even death of the person ensues.

ACE inhibitor therapy is of no value in case of asymptomatic patient. It is however used when patient with mitral regurgitation develops hypertension.

Diuretic therapy and digoxin are indicated when there is presence of hypertension and arrhythmias respectively. Since this patient is asymptomatic therefore both drugs are not used here.

4. What is the type of murmur found in mitral regurgitation (MR)? A. Pansystolic murmur B. Presystolic murmur

C. Holosystolic murmur D. Holodiastolic murmur

The correct answer is: C.

In mitral regurgitation Holosystolic murmur is present. It is a high-‐pitched murmur found at the apex. It starts from the end of S1 and remains till the beginning of S2.

Pansystolic murmur is although found in MR but it is also present in other conditions of the heart. It starts from the beginning of S1 and remains till the end of S2.

Presystolic murmur is present in case of mitral stenosis and appears between the A sound and S1.

Holodiastolic murmur begins from the end of S2 and remains till the beginning of S1 and is not present in MR.

5. A 55 years old patient presents with difficulty in breathing for one month. He also suffers from apprehension. He gave a history of severe fever and formation of lesions on the hand and fingers. A diagnosis of mitral regurgitation was made based on the clinical examination and radiological results. What is the likely cause of mitral regurgitation in this patient? A. Infective endocarditis B. Myocardial infarction C. Rheumatic heart disease D. Marfan syndrome

The correct answer is: A.

Although all the options can cause mitral regurgitation but if we see that this patient gives history of fever as well as lesions on hands and finger (might be Roth's spots or Osler's nodes), it is then infective endocarditis.

Myocardial infarction is a serious condition presents with chest pain, dyspnea, sweating and palpitation. Therefore, this is not correct with regard to this patient’s scenario.

Rheumatic heart disease is usually more common in children. It not only affects the heart, but also the joints and the central nervous system. It is the result of rheumatic fever caused by a preceding infection by group A streptococcal.

Marfan syndrome is basically a genetic disorder which is diagnosed earlier. This syndrome tends to affect the skeletal system. People with this disorder are abnormally tall and have long limbs and fingers.

Title: Neurogenic Shock Objectives for learning: Definition, Causes, Pathophysiology, Parameters of Neurogenic Shock, Clinical symptoms and signs and Treatment.

Definition: Neurogenic Shock is defined as the absence of sympathetic tone leading to systemic vasodilatation. However, there is an unopposed vagal nerve activity.

Causes/ Risk factors: Spinal cord Injury (It causes loss of sympathetic tone and unopposed vagal activity vagal nerve tone leads to hypotension).

Pathophysiology Systemic vasodilatation causes decrease in systemic vascular resistance and hypotension (80/40). The end result is bradycardia with heart rate of 20beats/minute.

Parameters of Neurogenic Shock Decreased cardiac output, decreased total peripheral resistance (TPR) and decreased pulmonary capillary wedge pressure.

Clinical symptoms and signs • Hypotensive • Bradycardia as sympathetic system is loss • Warm skin • Urine output might be low or normal

Diagnosis

Treatment • Maintain Airway, breathing and circulation (ABC) • Mobilize spine (cover on neck) • IV fluids is the mainstay of therapy • Also start domapine since it improves cardiac contractility and thus the perfusion is

enhanced. • Administer dobutamine to increase cardiac output. • For braydcardia give atropine • For neurodeficit give methylprednisolone • Try to maintaining their body temperature

• Call neurosurgery department, orthopaedics and trauma surgeons

Quiz

A patient sustains an injury in the back. Now he is presented in the night with decrease urinary output and lethargy. He tells that he has urinated once in the morning up till now. He has been urinating twice a day only for 2 days. On examination his temperature is 99⁰F. BP is 90/60mmHg. His heart rate is 50 beats/min. What is the mainstay of therapy?

A. IV fluids B. Dobutamine C. Spine mobilization D. Antibiotics

The correct answer is A.

This patient is basically suffering from neurogenic shock, so here IV fluids are the mainstay of therapy.

Dobutamine is no doubt very important but it only works to enhance the cardiac output whereas IV fluids increase blood volume and also correct dehydration.

Spine mobilization is important too to prevent further trauma but it alone won’t work.

Antibiotics are beneficial and mainstay of therapy when there is a septic shock. In this case, antibiotics will be given only when there is a suspicion of infection.

A 36-‐year-‐old injured male is presented in emergency with warm extremities, increased respiratory rate, oliguria and rapid pulse. On examination his B.P. is 70/40mmHg, pulse is 140/min and there is bluish discoloration of tip of nails and tongue. Which kind of shock is developed in this patient? Hemorrhagic Shock

A. Septic shock B. Neurologic shock C. Anaphylactic shock D. Hypovolemic shock


The clinical findings go with the condition of neurogenic shock. Since patient is injured, it is possible he has got an injury to his spinal cord. This causes loss of sympathetic tone and systemic vasodilation due to unopposed vagal activity.

Septic shock occurs when there is a history of infection. In this condition peripheries are usually cold.

Anaphylactic shock is due to severe allergic reaction and is manifested with a rash, itching, swelling, low BP and shortness of breath.

Hypovolemic shock is the result of bleeding or hemorrhage anywhere from the body. Although, this patient is injured, injury can cause internal bleeding but his peripheries are warm instead of being cold.

A patient has devolved neurogenic Shock shortly after getting an injury to the spinal cord. How will he be presented clinically?

A. Cold & clammy peripheries B. Increased heart Rate C. Increased total peripheral resistance (TPR) D. None of these


The correct option is D. The periphery is usually warm because of systemic vasodilatation. Heart rate is decreased due to loss of sympathetic activity and also total peripheral resistance (TPR) is decreased.

Title: Patent Ductus Arteriosus Objectives for learning: Definition, Pathophysiology, Murmur of PDA, Clinical Symptoms and Signs, Treatment. Definition: Patents means opened Duct means artery During fetal development, there is an open space between the pulmonary artery (PA) and the aorta. It is known as PDA. Blood actually gets shunted from PA into the aorta because lungs are not developed. Causes/ Risk factors: Pathophysiology Normally blood goes to the right atrium to right ventricle and that blood shunts through pulmonary artery. The pulmonary artery shunts blood to the lungs which comes back to left atrium to aorta to rest of the body. When the baby borns, and takes deep breathe, the resistance inside the lungs decreases and they expand and opened up. Afterward, there is no need of ductus to shunt blood. It becomes ligamentum arteriosum. The problem arises when aorta starts to work and pumps blood into the circulations and the lungs expand as the baby borns, the resistance inside the lungs decreases, the blood starts to shunt from left aorta into the pulmonary circulation because pressure in aorta is very high i.e. blood now shunts from left to right (aorta to pulmonary artery). Now the right ventricle has to pump blood against higher pressure. Thus, a patient with patent ductus arteriosus develops right ventricular hypertrophy because the pressure gradients of the right ventricle are higher so to pump blood against the higher pressure of PA. As the blood enters into the lungs, they develop vasoconstrictions inside the lungs and therefore increasing the pulmonary pressures. Overtime the pulmonary vascular hypertension causes pulmonary vascular sclerosis inside the pulmonary vasculature. When the pressure inside the RV is high enough, the patients will now be able to reverse this flow and starts to shunt this deoxygenated blood from right side to left side. The deoxygenated blood mixes with oxygenated, causing the patient to become cyanosed and exhausted.

Murmur of PDA The murmur of PDA is machinery murmur.

ü Prostaglandins (PGE) keep PDA open. Clinical Symptoms And Signs Symptoms of cyanosis in the lower extremities Diagnosis Treatment It is important to close this PDA. Indomathacin helps to close this PDA.


Title: Peripheral Vascular Disease -‐ Atherosclerosis Objectives for learning: Learning the process of atherosclerotic plaque formation and its consequences. Definition: Atherosclerosis is a peripheral vascular disease which manifests with creation of atherosclerotic plaques inside the walls of blood vessels. Causes/ Risk factors:

• Hyperlipidemia • Bad eating habits

Pathophysiology: Damage of the endothelial wall causes the migration of macrophages. Macrophages then accumulate LDL and form so called “foam cells”. That way, fatty streak is formed in the wall of the blood vessel. Platelets send signals to fibrous cells and smooth muscle cells to migrate from tunica media to tunica intima producing a fibrous plaque, which then progresses to atheroma. Narrowed blood vessels than cause organ ischemia. Abdominal aorta is the most common place for artheroma formation. Clinical symptoms and signs

• Pain due to ischemia • Claudications

Complications:

• Thrombosis • Myocardial infarction • Stroke


Title: Prinzmetal’s Angina Objectives for learning: Understanding Prinzmetal’s angina clinical features and treatment options. Definitions: Transient coronary vasospasms of coronary arteries. Pathophysiology: Coronary arteries affected by Prinzmetal’s angina usually already have thrombosis occluding up to 75% of their lumen. Transmural ischemia is present. Clinical symptoms and signs

• Chest pain Diagnosis

• Transient ST-‐elevation • Coronary angiography

Treatment

• Calcium channel blockers • Nitrates

Title: Rheumatic Heart Disease Objectives for learning: Definition, Causes, Pathophysiology, Clinical symptoms and signs,and Diagnosis Definition: Rheumatic Heart Disease is the consequence of the pharyngeal infection. Causes/ Risk factors:

• Group A beta hemolytic Streptococcus Pathophysiology This is a type II immune mediated hypersensitivity. Patients with this disease develop a murmur. They have vegetation and fibrosis. The most affected valve is the mitral valve. In case of acute disease the antibodies of the M protein of the organism destroy the valve. The antibodies come and bind to M protein of the organism. They then both attack and destroy the valve causing an inflammation. In case of acute inflammatory response on mitral valve, the patient suffers from mitral regurgitation. These protein attack the glycoproteins of the antigen present on the valve. In case of chronic disease, fibrosis of the mitral valve occurs causing stenosis of the mitral valve. Not only mitral valve gets affected but also aortic valve can be affected. Likewise, tricuspid valve can also get affected. However, mitral and the aortic valve get affected more as compared to others. Patients with rheumatic heart disease also develop myocarditis. Clinical symptoms and signs • Fever (101.2 ⁰F) • Erythema marginatum (a red margin rash) • Valvular damage (patients develop murmur due to vegetation of the valves. The most

affected valve which is affected is the mitral valve) • Erythrocyte sedimentation rate is very high • Red hot joints (joints pain—migratory polyarthritis) • Sub-‐cutaneous nodules (Ashoff bodies: These are the granuloma with histocytes with giant

cells) • Saint vitus dance or Sydenham's chorea

Sydenham's chorea is due to the CNS pathology. The patient has an immune reaction. The antibodies bind the neurons in the brain and thus affect the caudate nucleus and subthalamic nuclei. Caudate nucleus is important in the body movement. Diagnosis ASO: antistreptolysin O titers Treatment

Title: SEPTIC SHOCK Objectives for learning: Definition, Causes/ Risk factors, Pathophysiology, Complications, Symptoms, Diagnosis and Treatment of septic shock. Definition: The sepsis pathway Systemic inflammatory response syndrome (SSRI) (i.e. inflammation and source) à sepsis (one organ failure)à severe sepsis (sepsis plus end organ damage)à septic shock >2 àMODS • Systemic inflammatory response syndrome is defined as fever of more than 38⁰C and higher

heart rate. • Sepsis is the systemic inflammatory response syndrome and the presence of a known

infection. • Septic shock is persistent hypotension despite giving IV fluids or vasopressors. It is the most

common cause of death in ICU. Causes/ Risk factors: • Bacterial infection by bacteria such as

− E.Coli − Klebsialla − Staph aureus − Pseudomonas

Pathophysiology As the bacteria enter the blood, it leads to activation of neutrophils, monocytes, interleukin and cytokines. They rush the blood stream to attach the bacteria. Bacteria possess different endotoxins. These toxins damage the endothelial cells walls and also activate the macrophages, interleukins, cytokines, and neutrophils leading to systemic vasodilation. This systemic vasodilation further causes hypotension and underperfusion of the tissues causing lactic acidosis. Coagulopathy occurs as the endothelium of the blood vessels gets damaged by the toxins. Eventually body organs begin to damage or organ failure ensues. Bacterial infection and sepsis lead to decrease systemic vascular resistance and cardiac output increases to compensate this. Sepsis parameters include: decreased systemic vascular resistance, increased cardiac output and decreased capillary pulmonary wedge pressure. 1. SIRS IN this condition following important findings are present: • Fever > 38⁰C or <36⁰C • HR and pulse > 90 beats/min

• Tachypnea (develops due to lactic acidosis and so to blow out excess CO2 it leads to hyperventiliation) Respiratory Rate is greater than 20 whole PCO2 is less than 32 mmHg.

• WBC > 12,000 cells/ml or <4000 cells/ml or 10% band (if person is immunocompromise). There may therefore be leukocytosis or leukopenia.

2. Sepsis It is defined as SIRS (fever and increased heart rate) plus infection source. It can be understood by following: Fever and neck rigidity— it means person is suffering from meningitis Fever and productive cough— signify pneumonia Fever and flank pain-‐-‐-‐ define to be pyelonephritis Fever and redness – give hint for cellulitis Fever and right upper quadrant pain – it means person is suffering from ascending cholangitis. 3. Severe Sepsis Severe sepsis is explained as: • Lactate levels > 4mm/dl • Oliguria <0.5 ml/kg/hour • Change in mental status such as confusion or lethargic • Molted skin • Thrombocytopenic < 100,000 leading to coagulopathy • ARDS injury Complications • Acute respiratory distress syndrome (ARDS) • Disseminated intravascular coagulation (DIC) • Acute tubular necrosis (ATN) • Multi organ dysfunction syndrome (MODS) • Death Clinical symptoms and signs • Hypotension • Oliguria • Altered mental status • Warm skin • fever Diagnosis • Sepsis is diagnosed on the basis of Clinical picture i.e. based on symptoms & • Blood cultures Treatment • Intravenously broad spectrum antibiotics are given at maximum dose.

• If there is abscess then surgical drainage is used. • IV fluids administration is must and important. Normal saline is usually given intravenously. • Vasopressors are also administered to support perfusion and heart. These include

dopamine, Dubutamine or norepinephrine. Dopamine is given to increase renal perfusion

Quiz

1. A previously healthy 33 year old man presents to emergency with septic shock secondary to cellulitis of the arm. He is slightly confused and his peripheries are cold. His heart rate is 125/min, BP 70/30 mmHg, and respiratory rate 25/min. What should be the most suitable first line management in this case? A. Steroids B. Analgesics C. Broad spectrum antibiotics D. Antipyretics


In this case the most suitable first line management is the broad spectrum antibiotics. The rationale behind is that this patient has a previous history of cellulitis and due to which he has now developed a shock. So to combat the infection, antibiotics are essential.

Steroids are usually not given or given only when there is a presence of inflammation.

Analgesics are not used here as patient has not complained of any kind of pain.

Antipyretics are given to treat fever but these are not the first line of management of septic shock.

2. A febrile patient was diagnosed with E. coli sepsis. Shorty, he develops septic shock. Which of the given option is responsible for this reaction? A. Bacterial surface antigens causing stimulation of a humoral immune response B. A cell-‐mediated immune response to E.coli C. Cytokines secretion by monocytes as a result of stimulation by endotoxin D. Granule contents released by basophils and mast cells E. Bacterial superantigen toxin causing activation of TH cells

The correct answer is: C.

The correct option is C. cytokines are responsible for the occurrence of septic shock. Cytokines are secreted by the monocytes owing to the stimulation by the bacterial endotoxins. Cytokines are basically immunomodulating agents.

Bacterial surface antigens causing stimulation of a humoral immune response does not lead to this picture but the toxin produced by E.coli is responsible for septic shock.

A cell-‐mediated immune response also takes place to E.coli but again it does not give rise to septic shock. Cell mediated immunity in fact offers protection against majority of intracellular bacterial pathogens.

Granule contents released by basophils and mast cells do not lead to septic shock. Instead anaphylactic shock may occur if there is severe allergic reaction taken place.

Bacterial superantigen toxin causing activation of TH cells leads to release of cytokine but can produce the picture of Toxic Shock Syndrome not the septic shock.

3. A patient with septic shock develops hypotension. What is the cause behind hypotension? A. Increased capillary permeability and massive vasodilation B. Decreased systemic vascular resistance and vasoconstriction C. Decreased capillary permeability D. Massive vasoconstriction


Increased capillary permeability and massive vasodilation are both held responsible for producing hypotension in septic shock. The increase in capillary permeability as well as vasdilation occurs as a result of inflammatory mediators affecting the capillaries. The systemic immune response to microbial infection brings about venous blood pooling and arterial vasodilation.

Vasoconstriction does not occur here instead vasodilation takes place. The peripheral vascular resistance is however decreased here.

Capillary permeability is not decreased but it is increased due to systemic immune response to endotoxins.

Massive vasoconstriction is not possible so this option is not correct.

4. A patient presents with confusion. He has a history of fever and vomiting for 5 days. On examination his skin is warm, neck is rigid, pulse is 120/minute and BP is 90/70mmHg. What is the most probable diagnosis? A. Meningitis B. Sepsis and meningitis C. Sepsis D. Neurogenic shock


The clinical picture goes with the diagnosis of sepsis and meningitis. Fever, vomiting and neck rigidity show increased intracranial pressure. This is most likely due to meningitis while confusion, decreased BP, hot flushed skin and increased heart rate show the occurrence of sepsis (i.e. fever and source of infection).

Although meningitis is present but there is an element of sepsis as well so alone meningitis is not a correct option.

Likewise, sepsis alone is not correct since there is a clear picture of meningitis.

Neurogenic shock may present with decreased BP, but history of fever is unlikely. However, there is a history of trauma to back or spinal cord. Additionally, skin of the patient is usually cold here due to hypotension.

5. A patient presents with molted skin, oliguria, hypotension, confusion, elevated lactate and purpura all over the skin. What would be complication of sepsis causing these problems? A. Acute respiratory distress syndrome (ARDS) B. Metabolic acidosis C. Systemic inflammatory response syndrome (SIRS) D. Multi organ dysfunction syndrome (MODS)

The correct answer is: D

Molted skin, oliguria, hypotension, confusion, elevated lactate and purpura all over the skin demonstrate the occurrence of multi organ dysfunction syndrome (MODS). It is one of the most common complication that affect different organs of the body.

If an acute respiratory distress syndrome (ARDS) occurs, then patient complains of shortness of breath or difficult breath.

Metabolic acidosis does not produce these symptoms. It may present with headache, pain in chest, palpitations, weakness, etc.

Systemic inflammatory response syndrome (SIRS) is an inflammatory condition affecting the whole body, and is mainly a response of the body’s immune system to infection. Temperature is either high or low; there is tachypnea and increased heart rate. Oliguria, hypotension, confusion, elevated lactate and purpura are not present here.


Title: Stable Angina Objectives for learning: Learning pathophysiological and clinical features of stable angina; understanding the importance of correct diagnosis and treatment. Definitions: Stable angina is an imbalance between blood flow through the coronary arteries and oxygen demand. Causes/ Risk factors: Acronym: FLASH – MD

• Family history of coronary disease • Low HDL (<40) • Age (men>45, women>55) • Smoking • Hypertension • Male gender • Diabetes

Pathophysiology: Due to atherosclerotic plaques that occlude the lumen of coronary arteries, there is a higher demand for oxygen than it could be delivered through the occluded arteries. Decreased perfusion to the heart muscle causes ischemia of the myocardium presented with chest pain, especially during the exercise. Clinical symptoms and signs

• Chest pain • Exertion • Symptoms can last for 10 – 15 min, but usually 1-‐5 min. • Symptoms are relieved by rest and sublingual nitroglycerin

Diagnosis • EKG (normal findings) • Cardiac enzyme (no elevation) • Stress test

o Exercise (treadmill) – until the maximum heart rate is reached (220 – age)

§ Chest pain § Hypotension

§ ST-‐depression § Arrhythmia

o Stress echo • Cardiac catheterization – if stress test is positive. • Pharmacologic stress test (for patients that are not able to perform exercise)

o IV adenosine (causes coronary vasodilatation) o Dipyridamol (causes coronary vasodilatation) o Dobutamine (increases myocardial oxygen demand; increases heart

rate, contractility, and blood pressure) Complications Progression of stable angina leads to acute coronary syndrome (unstable angina, non-‐STEMI, and STEMI) Treatment

• Risk factor modification o Diet (<7% saturated fat; <200 mg/day cholesterol) o Exercise o Lose weight o Strict blood glucose control o Statins o Blood pressure control o Stop smoking

• Medication o Aspirin o Beta-‐blockers o Nitrates

• Revascularization o PTCA (percutaneous transluminal coronary angioplasty) – stent

implantation o Coronary bypass

Title: Tricuspid Regurgitation

Objectives for learning: Definition, Causes/ Risk factors, Clinical symptoms and signs and v Definition: It is the inability of three valves (tricuspid valves) to close completely during systole. Causes/ Risk factors: • The most common cause is right ventricular dilation. Other causes include: • Left ventricular failure • Right ventricular infraction • Cor pulomonale (pulmonary hypertension) • Staph aureus infection • Ebstein anomaly (congenital heart disease) • Carcinoid syndrome Pathophysiology: Clinical symptoms and signs: • Ascites: Jugular Venous Distention, heptomegaly • Pulsatile liver • Blowing holo-systolic murmur: When patient is asked to deep breath, the murmur is heard

louder. • Atrial fibrillation Diagnosis: Treatment: • Treat the underlying cause • Surgery involve valve repairmen or valvuloplasty

Quiz

1. A patient came with leg edema and swollen abdomen. On examination jugular vein was found to be distended, ascites were present and liver was enlarged and pulsatile. What is the most likely diagnosis? A. Aortic stenosis B. Pulmonary stenosis C. Tricuspid regurgitation D. Mitral regurgitation

The most likely diagnosis based on the clinical symptoms and signs is the tricuspid regurgitation. In this condition tricuspid valve fails to close during systole, causing the blood to passes with

each heart beat from the right ventricle to the right atrium, i.e. in the direction opposite to that of the normal one. Symptoms of right-sided heart failure often develop. Jugular vein is usually distended. The important finding of tricuspid regurgitation is the pulsatile liver. It is not present in the other conditions mentioned in the options.

Aortic stenosis is the condition of narrowing of the aortic valve. It may present with pedal, exertional dyspnea, paroxysmal nocturnal dyspnea, but liver is not pulsatile here.

Pulmonary stenosis is the condition of obstruction of blood flow from the right ventricle to the pulmonary artery. Due to this right ventricular hypertrophy develops. There may be complaint of chest pain, palpitations, dysnpea but liver is not pulsatile.

Mitral regurgitation is characterized by the symptoms of decompensated congestive heart failure. Liver here is not pulsatile but normal.

2. Which of the given option is associated with pansystolic murmur?

A. Aortic stenosis ejection systolic B. Pulmonary stenosis C. Tricuspid regurgitation D. Pulmonary regurgitation decrescendo diastolic murmur

Tricuspid regurgitation is associated with pansystolic murmur. This type of murmur is of low frequency and shows tendency to increase with inspiration. Aortic stenosis is associated with ejection systolic murmur. The murmur of pulmonary stenosis is systolic murmur.

Pulmonary regurgitation is associated with decrescendo diastolic murmur.

3. Identify the condition in which pulsatile liver is found?

A. Tricuspid regurgitation B. Mitral regurgitation C. Pulmonary hypertension D. Mitral stenosis

Liver becomes pulsatile in case of tricuspid regurgitation. This condition is responsible for liver dysfunction. Mitral regurgitation, pulmonary hypertension and mitral stenosis do not lead to the liver to become pulsatile. Liver usually remains normal.

4. What is the surgical management of tricuspid regurgitation?

A. Removal of valves B. There is no surgical treatment of tricuspid regurgitation C. Only repair of the valve D. Valve repair (valvuloplasty) or replacement

The surgical management of tricuspid regurgitation is Valve repair (valvuloplasty) or replacement. The valves are repaired surgically to make them functional. Valves cannot be removed but can be replaced for the normal functioning of the heart. The surgical treatment of tricuspid regurgitation is present and is successful. Valve can be repaired or can be replaced depending upon the condition. 5. A 9-year-old boy is found to have tricuspid regurgitation. What would be most common

cause behind this? A. Atrial septal defect B. Ventricular septal defect C. Ebstein anomaly D. Carcinoid syndrome

The most common cause in the 9-year-boy is Ebstein anomaly. Ebstein anomaly is a basically a congenital cardiac defect characterized by the displacement of septal leaflet of the tricuspid valve towards the right ventricular apex. Atrial septal defect is not presented with the tricuspid regurgitation. It is basically a defect between the two atria, right and left, causing the oxygenated blood to mix with the deoxygenated blood. Ventricular septal defect as the name implies is the congenital anomaly characterized by the presence of defect ventricular septum. This condition is not presented with tricuspid regurgitation. If defect is small, it remains asymptomatic or disease usually becomes apparent a few weeks after birth. Carcinoid syndrome is the complex of different symptoms such as diarrhea, dysnpea, flushing, palpitations etc. this syndrome is due to carcinoid tumor. Although tricuspid regurgitation occurs in carcinoid syndrome but in this patient, no such history is there regarding the symptoms of carcinoid syndrome. Also, this syndrome is more common in adults. Thus, it is not considered a correct option here.

Title: Understanding The Basics Of Shock

Objectives for learning: Definition, Types, Complications, Symptoms, Diagnosis and Treatment of shock.

Definition: Shock is the under perfusion of the tissues. Blood flow is important for the normal functioning of the brain, heart, kidney, liver, muscles and different other body tissues. Blood delivers oxygen, nutrients and glucose needed for metabolism. It is a serious medical emergency and therefore requires an immediate medical intervention otherwise it will prove fatal if irreversible organ damage occurs.

Parameters going to be affected • Cardiac output • Systemic resistance • Pulmonary capillary wedge pressure


Pathophysiology

Clinical symptoms and signs • Hypotension (low BP) • Oliguria • Tachycardia • Altered mental status

Complications of Shocks • Lactic acidosis (anaerobic respiration) • Oliguria (decreased urine output) • CNS dysfunction (altered mental status)

Types of Shock • Neurogenic shock • Cardiogenic shock • Anaphylactic shock • Septic shock • Hypvolemic shock

Diagnosis/ Approach to shock History: If there is history of fever and low BP, it shows infection (it may be a septic shock). If there is history of trauma, GI bleed, vomiting, or diarrhea, it means volume depletion has occurs so hypovolemic shock is possible. If there is complaint of chest pain and low BP and cardiac output is decreased, a person may be having acute myocardial infarction (MI), then it will be a cardiogenic shock. In case of neurologic shock there will be neurologic deficit. IV infusions is important and given with 2 large bored IV lines. A fluid of about 500 to 1000 ml should be given for organ perfusion. Labs include: blood sampling for CBC, PT/APTT, RFTs (BUN/Creatinine) and BMP EKG: To check the presence of ST elevation, depression or other possible findings Chest X-‐ray: It will help in identifying the chronic heart failure (CHF), cardiomegaly, tension pneumothorax Pulse oximetry: It should be 100% Vasopressors are given such as dopamine, dubutamine and norepinephrine.

Treatment The basic and most important early treatment of shock involves: ABC i.e.

• Maintain airways • Breathing • Circulation

Other treatment varies depending on the type of shock and its causes.

Quiz 1. A 14-‐year-‐patient presents with fever, confusion and weakness. On examination he is pale

with weak thread pulse. His temperature is 102⁰F. His attendant tells that patient has been suffering from flank pain for 4 days before. His BP is 80/60mmHg. What is the most likely diagnosis?

A. Acute Kidney Injury B. Shock C. Adrenal Crisis D. Toxic Shock Syndrome


This patient is a typical case of shock, most probably the septic shock. This is because there is a history of flank pain and fever. His temperature is also raised. Low BP and altered mental status indicate that he has developed a shock.

Acute kidney injury is not presented with low BP. It is presented mostly with high BP and there is generalized edema. Patient complains of headache and vomiting.

Adrenal Crisis is characterized by severe adrenal insufficiency due to inadequate levels of cortisol in the body. There is although symptoms of confusion, fever, and low BP but there is a wide range of metabolic abnormalities such as hyperkalemia, hypercalcemia, hypoglycemia and hyponatremia.

Toxic shock syndrome (TSS) is a acute life-‐threatening condition mediated by bacterial toxin usually by either Staphylococcus aureus or Streptococcus. It is characterized by rash, high fever, desquamation hypotension, and multi-‐organ failure. It is presented with severe myalgia, headache, diarrhea, vomiting, and non-‐focal neurologic deficit.

2. In a patient with reduced cardiac output and low BP with the diagnosis of shock, what would be the best treatment option to boost cardiac output? A. IV Fluids B. Beta Blockers C. Antibiotics D. Vasopressors


The best treatment option to enhance the cardiac output and low BP in patient with shock is the vasopressors. These drugs work by increasing the BP, contractility of the heart as well as the renal perfusion.

IV fluids are although must here but sometimes they fail to increase the BP and cardiac output.

Beta Blockers have no role in increasing the heart rate or blood pressure; in fact they reduce blood pressure and tachycardia.

Antibiotics are usually prescribed when there is any evidence of infection. They have no role in increasing the cardiac output and BP.

3. Which of the given feature helps to differentiate the hypovolemic shock from septic shock? A. Blood pressure B. Cardiac Output C. Temperature D. Heart rate


Body temperature is the differentiating feature in case of the hypovolemic shock and septic shock. In hypvolemic shock temperature is reduced so patient’s skin is cold while in septic shock due to infection temperature is raised so skin is warm.

Blood pressure and cardiac output both are reduced in both hypvolemic and septic shock. So these parameters cannot help in differentiating.

Likewise, heart rate is also increased in both shock therefore, it won’t help in confirming whether a patient is suffering from hypovolemic and septic shock.

4. A patient presents with the progressive stage of shock. What will happen with the metabolism of patients if the shock is not treated and hypoxia of the tissue occurs? A. Compensatory mechanisms B. Lactic acidosis C. Arteriolar constriction due to vasomotor reflex D. Metabolism will be unaffected


A patient with the progressive stage of shock, if not treated and developed hypoxia of the tissue, most likely enters into anaerobic metabolism and therefore develops lactic acidosis.

Compensatory mechanisms are already working well before the person enters into progressive shock, so this option is not correct.

Arteriolar constriction due to vasomotor reflex is again already working here to compensate.

Metabolism will be affected here when oxygen delivery and nutrients are not sufficient so to compensate aerobic metabolism shifts to anaerobic.

5. A patient presents with confusion after severe bleeding in the vomiting. He has developed tachycardia while his pulse is weak. Which kind of shock is associated with low levels of blood?

A. Hypovolemic shock B. Anaphylactic shock C. Cardiogenic shock D. Septic shock

The correct answer is A

Hypovolemic shock is associated with low levels of blood and is characterized by bleeding or hemorrhage.

Anaphylactic shock is associated with allergic reaction to drug, chemical, etc and is the serious sort of allergic reaction.

Cardiogenic shock is characterized by different conditions affecting the heart causing the heart difficult to pump the blood as the body requires.

Septic shock occurs after the infection/bacteria enter into the blood stream and is an extreme response by the immune system.

ftplectures cardiovascular system lecture notes cardiology · 2015-05-23 · ftplectures...

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