OS 210LEC 0X: TITLE

OS 210LEC 0X: TITLE

OS 213: Circulation and RespirationLEC 36: CVS COURSE SUMMARYExam # 3 | Dr. Antonio Dans | October 10, 2012

TransersUPCM 2016: XVI, Walang Kapantay!3 of 3

\\Leandro Baldemor, Anne Curtis, Kristina AquinoUPCM 2016: XVI, Walang Kapantay!6 of 6

OUTLINEI. Anatomic Categories of Cardiovascular DiseaseA. Prototypes of DiseasesB. Risk FactorsII. Disorders of Conduction SystemA. Early BeatsB. TachycardiasC. PausesD. BradycardiasE. DysrhythmiasIII. Congenital Heart DiseaesA. Atrial Septal DefectB. Ventricular Septal DefectC. Patent Ductus ArteriosusD. Transposition of the Great ArteriesE. Tetralogy of FallotIV. Peripheral Vascular Diseases

I summarized all your lectures into 4 tables. Dr. Dans

I. ANATOMIC CATEGORIES OF CV DISEASE

A. PROTOTYPES OF DISEASES

Note: Sir tackled the anatomical diseases by layers, emphasizing prototype diseases to facilitate better understanding and easier recall.

Table 1: Anatomic Categories of CV DiseasesEndocardial DiseaseMyocardial DiseasePericardial Disease

PrototypeRHD (when chronic) because it affects the valves.Other variation: IE (when acute)

IHD (most common; rare: myocardial cardiomyopathies due to alcoholism and pregnancy) *others: IDC, RCMConstrictive Pericarditis (CP)(rare: pericardial malignancy to pericardium, tamponade)

Early SymptomsEasy Fatigue;SOBOE (shortness of breath on exertion) (MS)Angina

Pleuritic Chest Pain

Late SymptomsWorsening SOBOE->RVF (edema/ anasarca)

Acute MI or Unstable Angina Pectoris CHFEdema (failure to fill), RVF, usually no SOBOE unless lesion is exclusive at the RV

Main RxVasodilate or decrease HR (MS); repair or replace valve (AS)

Rx (need statins even if cholesterol is normal; ACE-I even if BP is normal) PTC Angiogram, CABGSurgery (removal of the pericardium which is a dispensable layer)

PreventionRheumatic Fever prophylaxis (penicillin injections, esp for high risk); IE Prophylaxis (undergo surgery with high possibility of bacteremia)Risk factor control (HPN, DM, smoking, high cholesterol, obesity, lack of exercise, unhealthy diet, stress)

TB Control

Review for differentiating etiologies of edema: Cardiac ascending; Renal descending; Hepatic stomach (centrifugal)-> ascending then descending.

ENDOCARDIAL DIASEASE: RHEUMATIC HEART DISEASE

Patient: G.G., 24/F, consulted for dyspnea Shortness of breath on exertion (SOBOE) Ascending edema 3-pillow orthopnea Paroxysmal nocturnal dyspnea (PND) Cardiac cachexia Social and financial costs

Notes:Symptoms initially stopped her from sports, later from climbing stairs, later from even going to school Highly intelligent. Quit school at 2nd year, although she really wants to study. Wants to become a nurse one day so she can help her sibs through school Deathly afraid of dying, so she doesnt work Cant afford surgery (400 thou), and she cant afford PTMC (350 thou) - even as a charity patient Lost weight in the past year, partly from the disease, partly from depression She is literally dying before our eyes

Plain Radiography

Fig.1. Normal heart. Heart shows no signs of enlargement and observable abnormalities in the aorta and the pulmonary artery; with unremarkable pulmonary vascular markings

Fig. 2. Pathologic heart common in mitral stenosis (MS). There is enlargement of the heart, straightening of the left border of the cardiac silhouette and a rounded apex. Apex forms right angle with diaphragm, which is indicative of RVH. (Note: A cardiophrenic angle >90 forming a rounded apical edge indicates RVH while an angle >90 indicates LVH). Increased vascular markings are also observable. The LA is enlarged while the LV is underloaded.

Electrocardiogram

Fig.3. ECG tracings of a normal heart. Normal sinus rhythm; neither hypertrophy nor axis deviation may be observed; no ischemia nor infarction.

Fig. 4. ECG Tracings of the RHD patient. There is normal sinus rhythm and rate. There is an observable increase in the height of the P-wave indicating the presence of RA overload. There is no axis deviation however the tall R waves in lead V1 indicate RV hypertrophy.

2-D Echocardiography Main Finding: Mitral valve stenosis (most common lesion in RHD) The anterior leaflet elbows out before diastolic filling (manifests as the diastolic Opening Snap upon auscultation) Observable blood sludging. Latrine of blood may be visible which is about to form a thrombus, blood swirls in the LA causing LAE.

Table 2. Murmurs of Prototype Lesions of Endocardial DiseasesSTENOSIS Failure to OpenINSUFFICIENCY Failure to close

MITRAL VALVE

Location Apex Apex

Timing Diastolic Systolic

Quality LUB-DUB-Brrr (Diastolic rumble); opening snap because of elbowing of MV ZHHHHH-DUB (Holosystolic murmur) *S2 disappears in severe cases

Effect Exertional dyspnea (Hinihingal kapag napagod) Caused by the LVs inability to fill, leading to pulmonary congestionEasy fatigability (Latang-lata)Caused by poor forward flow, due to regurgitation

Treatment Reduce HR to prolong diastolic filling time Beta-blocker; digitalis (fibrillation) Vasodilators

AORTIC VALVE

Location Base Base

Timing Systolic Diastolic

Quality ssSSHHhh-DUB(Systolic Ejection) Diamond-shaped murmur

LUB-dhuu (Diastolic blow-softest murmur) High pitch

Effect Easy fatigabilityCaused by poor forward flow. If severe/long-standing, may cause syncope.Easy fatigabilityCaused by poor forward flow

Treatment No medical treatment (worst lesion)Surgery if severe Vasodilators are contraindicated; will cause hypotension.DONT inc HR, Px might faintVasodilators (Ca Blockers; ACE inhibitors)

*Main determinants: location and timing (phase of murmur)

Clinical Pearl: In the end, as the disease progresses, they all present with dyspnea, so its important to find out the order the symptoms came about.

MYOCARDIAL DIASEASE: ISCHEMIC HEART DISEASE

Patient: E.H., 70/M consulted for chest discomfort Chest discomfort upon exertion, relieved by rest; tighten rather than pain Quit work because of illness Recent widower, lives alone, worries about his health Walk-through phenomenon slowing down makes the chest pain go away Just came back recently because he couldnt afford med Stopped follow-up and his meds Came back with acute MI Developed heart failure and no needs more meds

Clinical Pearl: It is important to probe if pain is really felt during exertion. Px could misunderstand and report pain upon exertion although pain was felt in the afternoon at rest after a particularly taxing day at work.

Plain Radiography

Fig.5. Left Ventricular Enlargement. Cardiac apex is infero-laterally displaced. Edge of cardiac border meets diaphragm in an acute angle, indicative of LVE. Ration of cardiac shadow to thoracic diameter >0.5

Electrocardiogram

Fig.6. ECG tracings of myocardial infarction. Note ST-depressions in the lateral wall (V4-V6)-ischemia; ST-elevations in (V1-V3)-MI

2-D Echocardiography Findings: A heart contracting more weakly than a normal heart. LV is seen to be larger than normal (LV enlargement is actually an adaptive Modification). Given the same % Ejection Fraction, a larger ventricular volume results to more blood pumped.

Review of IHD Pathogenesis 1. Normal2. Early Streak (early 20s)3. Asymptomatic Plaque (30-40s)4. Significant Obstruction (with pain) - angina5. Acute thrombus formation (partial or complete obstruction)6. Reorganization7. Chronic Obstruction syndrome (heart failure symptoms, myocardial weakness)

Fig.7. IHD Pathogenesis

Notes: In significant obstruction, there is stable angina (pain during exertion)In acute thrombus formation, acute MI may occur In reorganization, there is unstable angina In chronic obstruction, symptoms manifest

Table 3. Comparison of Common (Prototype) Syndromes: Angina, Acute MI and CHFCommon SxConfirmationSurgical Intervention (e.g. bypass) if:

Angina Chronic recurrent mild chest pain Clinical (stress test to confirm if mild or severe) -Sx are severe -Stress test (with triple vessel disease)-Angiogram -Patients who dont respond to medical treatment

Acute MI Acute severe chest pain Enzymes (T, CKMB), ECG, pain Residual Sx Stress test

CHF SOBOE, orthopnea PND, RVF 2-D Echo Check for angina

Table 4. Medications for Angina, Acute MI and CHFMedicationsSxRecurMR

Angina Beta blockers>Nitrates>Calcium channel blockersASAStatinsACE/ARB+

----

+++-

+++

Acute MI PCI> FibrinolyticLMWH (low molecular weight heparin) AS+Clopidogrel Statins*BBACE/ARBNitrates (control acute pain)+---+-+++++++-+-++++-

CHF ASA Statins BB ACEDigitalisDiuretics--++++++++-+++++--

Heading: Sx (symptoms), recurrence of events, MR (mortality)*BB-use with caution. Studies show they may reduce mortality by allowing receptors to regenerate. Relieve pain, prevent re-infarction, lower mortality rateEx. ASA(aspirin) cannot relieve the symptoms of agina but is used to prevent recurrence of events and mortality

PERICARDIAL DIASEASE: CONSTRICTIVE PERICARDITIS

2D-Echocardiography LVH; echo free space has constant diameter, indicating that it is thickened pericardium (vs. non-constant diameter if it contains fluid)

B. RISK FACTORS

Sir did not discuss this.

THE BIG 9 (now 10) RISK FACTORS FOR CVD ND CAD (with RR) 1. Smoking 4.79 6. Fruits and vegetables 0.70 2. Dyslipidemia 2.90 7. Alcohol 0.793. Hypertension 2.608. Exercise 0.72 4. Diabetes 2.409. Stress-free 0.77 5. Obesity 2.30 10. Education attainment & Socioeconomic class (protective)

Table 5. Risk Factors and Relative Risks for CV DiseasesRisk FactorsRR for Stroke RR for CAD Deaths in 2004

DM= 4.6% 4.0 2.4 4,148

Chol= 8.5% 1.8 2.9 5,730

Obes= 12/55 % - 2.3 8,046

HPN 4.4 2.6 14,015

Smoking=35% 4.8 4.7 28,694

Smoking is most common RF in men and most common overall Obesity is most common RF in women (55% F vs. 12% M) Waist-Hip Ratio: better indicator of obesity than BMI because it is the ratio of adiposity to bone and not of weight to height Waist-between lowest rib and hip; measure of central adiposity, hardly any muscle and bone Hip-level of ASIS; bone density Normal values: F Pulmonary congestion/hypertension -> RV Overload -> RVH -> Eisenmengerization complex Absence of murmur due to low interatrial pressure differences Pulmonary congestion and increased pulmonary flow results in (1) systolic ejection murmur and (2) delayed and loud P2 (fixed splitting) Shunting occurs in diastole

B. VENTRICULAR SEPTAL DEFECT

Initial RL shunt All shunted blood goes back to LV, resulting in LVH Loud holosystolic murmur (the smaller the VSD, the more turbulent the movement, the louder the murmur) Predisposes patient to atherosclerosis and pulmonary HPN Shunting occurs in systole

C. PATENT DUCTUS ARTERIOSUS

Initial LR shunt Shunting occurs first in diastole then systole Continuous machinery-like murmur, due to gradient present in both systole and diastole LV overload Classic pulmonary hypertension presentation May present with cyanosis, usually in legs

If shunt is before the subclavian artery -> diffused cyanosisIf after subclavian artery > differential cyanosis, only on the toes

D. TRANSPOSITION OF THE GREAT ARTERIES

Fatal unless septal defect is present to provide the necessary mixing of oxygenated and deoxygenated blood

E. TETRALOGY OF FALLOT

Comprised of VSD, Aortic Overriding, PS and RVH RL shunt Aorta sits on top of the defect and automatically collects blood from the R chamber

IV. PERIPHERAL VASCULAR DISEASES

Table 5. Summary for Peripheral Vascular DiseasesACUTECHRONIC

ARTERIALArterial EmbolismChronic Arterial Occlusion

Cardio-embolismAtherosclerosis

Acute PainChronic Pain*

Heparin then warfarin**Aspirin, clopidogrel

VENOUSDeep Vein ThrombosisChronic Venous Insufficiency

In-Situ embolismVaricose Veins

Acute SwellingChronic Swelling

Heparin then warfarin**Compression Stockings

* A.K.A Intermittent Claudication; ** Taken for 6mo if uncomplicatedIf taking acute PVD meds, check for prothrombin time (PT) monthly

SAMPLE CASES

Case 163/M with bilateral leg edema 5 years PTA;excellent exercise capacity;(-) exertional dyspnea or chronic cough;(+) edema and hyperpigmentation of legsDx: Chronic venous insufficiencyTx: Compression stockings

Case 258/F with painful toe 3 hours PTA;(+) occasional palpitations, no other Sx;(+) irregularly irregular HR(+) gangrenous toeDx: Acute arterial embolismTx: Anticoagulants

Case 353/F with severe back pain after avehicular accident 1 week PTA;Underwent spinal surgery 3 days agowas doing well until today;Developed sudden right lower extremity pain and swellingDx: Deep vein thrombosisTx: Anticoagulants

Case 453/F with calf pain during her morning walks since almost a year ago;pain used to occur after 30 minutes of walking and whould be relieved by rest; in the past month, pain has been bothering the patient after just 10 minutes; pain has been occurring more frequentlyDx: Chronic artertial occlusion -> intermittent claudicationTx: Antiplatelets

THE MOST IMPORTANT TABLE AMONG TABLESCLASSROOM LEARNINGCLINICAL LEARNING

Books, Read, Memorize, Few Years, IQ, BoringPeoples Lives, Empathize, Remember, Lifelong, EQ, Fun

END OF TRANSCRIPTION

TransersUPCM 2016: XVI, Walang Kapantay!8 of 8

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ACUTE THROM.

LIPID STREAK

ASXIC PLAQUE

NORMAL

SIGNIF. OBST.

REORGANIZ.

CHRON. OBST.14Lets look at 4 (CSAP), 5 (AMI) and 7 (CHF)