abc revised

8/9/2019 ABC Revised

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I. Definition of Terms

1. Stress is the consequence of the failure to adapt to change. Less simply: it is

the condition that results when person-environment transactions lead the

individual to perceive a discrepancy, whether real or not, between the demands

of a situation and the resources of the person's biological, psychological or

social systems.

In medical terms, stress is the disruption of homeostasis through physical or

psychologicalstimuli. Stressful stimuli can be mental,physiological, anatomical

or physical[1] .

2. Crisis (plural: crises) may occur on a personal or societal level. It may be atraumatic or stressful change in a person's life, or an unstable and dangeroussocial situation, in political, social, economic, military affairs, or a large-scale

environmental event, especially one involving an impending abrupt change.More loosely, it is a term meaning 'a testing time' or 'emergency event'.

3. Biologic Crisis- Biology, the science of life/ Changed in persons life which could

be traumatic or stressful but not extremely serious or severe.

4. Acute Biologic Crisis- extremely serious, severe, or painful.

5. Emergency- Emergency, serious situation or occurrence that happens

unexpectedly and requires an immediate response.

6. Nursing - Nursing, in general, the process of caring for, or nurturing, another

individual. More specifically, nursing refers to the functions and duties carried

out by persons who have had formal education and training in the art

and science of nursing. Professional nurses combine many different

disciplines, including aspects of biology and psychology, to promote the

restoration and maintenance of health in their clients.

7. Care- to be interested in, or concerned about something.

8. Nursing Assessment

Nursing assessment

The nursing assessment process for any clients entering the ED is

divided into primary and secondary assessments

The purposed of the primary assessment is to immediate identify

any client problem that poses a threat , immediate or potential, to life,

limb, or vision. If any abnormalities are found during the primary

assessment immediate interventions such as cardiopulmonary

resuscitation (CPR)and Advance Life Support (ALS) must be instituted to

aid in preserving the clients life, limb or vision.

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The primary assessment uses the ABC mnemonic:

A Airway

B Breathing effectiveness

C Circulation

The secondary assessment is performed to identify any othernon life- threatening problems the client may be experiencing. Both

subjective information and objective data are obtained.

9. The purposed of this triage process is to expediently determine the

severity of a clients problem or condition. The acuity level of the

presenting problem is rated according to the predetermined categories;

the most frequently used ratings are emergent, urgent, and non-urgent.

II.Review of the Anatomy of the Heart

a. Definition

A hollow muscular organ lying between the lungsresponsible for pumping blood to the bodys circulation.

b. Description

Weight: 300 gms

Shape: Cone- shaped

Location: Mediastinum; lies on the diaphragm; the apex(tip of the cone) is at its bottom and lies left of themidline; the base is at the top where the blood from thegreat vessels enter the heart and lies posterior to thesternum.

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c. Anatomy of the Heart

Pericardium two-layered sac that encases and protects the heart

Chambers of the Heart : 2 atrium, 2 ventricles

1. Atrium : Right Atrium receives deoxygenated bloodLeft Atrium receives oxygenated blood

2. Ventricles : Right Ventricle receives blood from atriumvia

tricuspid valve, pumps it to thepulmonary circulation

Left Ventricle receives blood from atriumvia the bicuspid

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valve, pumps it to the systemiccirculation

Cardiac Valves :1. Atrioventricular Valves: Tricuspid Valve and Bicuspid (Mitral) Valve

- prevents backflow of blood from RV to RAand from LV to LA respectively

2. Semilunar Valves: Pulmonic Valve and Aortic Valve- prevents backflow of blood from PA to RV

(Pul. Semilunar)and from Aorta to Left Vent. (Aortic

Semilunar)

Cardiac Blood Supply / Coronary Arteries supply blood to the heart1. Right Coronary Artery supplies RA, RV, inferior portion of the LV, posterior

septal wall, SA and AV node.2. Left Coronary Artery3. Left Anterior Descending Artery supplies to anterior wall of LV, anterior

ventricular septum and apex of left ventricle4. Circumflex Artery supplies to left atrium, lateral and posterior surface of LV,

occasionally the posterior intraventricular septum, sometimes to the SA and AV

d. Functions of the Heart

Excitability ability of cardiac muscles to depolarize inresponse to a stimulus

Automaticity (Rhythmicity) ability of cardiacpacemaker cells to initiate an impulse simultaneouslyand repetitively without neurohormonal control.

Contractility muscle contraction of the heart Refractoriness hearts inability to respond to a new

stimulus while still in a state of depolarization from anearlier stimulus.

Conductivity ability of heart muscle fibers topropagate electrical impulses along and across cellmembranes.

** ** Conduction System:

1. Sinoatrial (SA) Node initiates electrical impulses

2. AV Node - receives elec. Impulses from the SA node3. Bundle of His and Bundle Branches4. Purkinje Fibers

** The bundles give rise to thin filaments known as Purkinje fibers.

These fibers distribute the impulse to the ventricular muscle.

Collectively, the bundle branches and purkinje networkcomprises

the ventricular conduction system. It takes about 0.03-0.04s for the

impulse to travel from the bundle of His to the ventricular muscle

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Right Ventricle Mitral Valve

Pulmonary Valve Left Ventricle

f. Heart Rate

Normal - Adult 60-100 ; Children 80-120 ;Newborn 120-160

Tachycardia

Bradycardia

g. Arterial Pressure

Blood Pressure/ Arterial Pressure pressure of blood

against arterial walls. Systolic Pressure maximum pressure of blood against

the arterial walls when the heart contracts ( normally100-140mmHg)

Diastolic Pressure force of blood exerted against theartery walls during the hearts relaxation (or filling)phase (normally 60-90mmHg)

II. Risk Factors of Coronary Heart Disease

A. Two ( 2) Categories of CHD Risk Factors

a. Non- modifiable Factorsb. Modifiable Risk Factors

Non-Modifiable Risk Factors Modifiable risk Factors

Heredity, including race Cigarette Smoking/Habits

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AgeGender

HypertensionElevated Serum CholesterolDiabetes MellitusPhysical InactivityObesity

B. Contributing Risk Factors include:

a. Response to Stressb. Homocysteine Levelsc. Inflammatory Responsesd. Menopause

III.Coronary Artery Diseases (CAD) / Coronary Heart Diseases (CHD)

Arteriosclerosis

Atherosclerosis

Angina Pectoris

Myocardial Infarction

Transient Ischemic AttackARTERIOSCLEROSIS:

When the arteries become obstructed with plaque andcholesterol, they harden and constrict, and the circulation ofblood through the vessels becomes difficult, forcing the bloodthrough narrower passageways. As a result, blood pressurebecomes elevated.

Arteriosclerosis occurs when lipids in the blood, includingcholesterol, accumulate inside the walls of blood vessels andreduce the size of the veins or arteries through which bloodflows.

ATHEROSCLEROSIS:

A degenerative condition of the arteries characterized bythickening due to localized accumulation of fats, mainlycholesterol. The term atherosclerosis refers to a condition inwhich fatty deposits build up in and on the artery walls,interfering with the normal flow of blood and oxygenthroughout the body. When this happens, the heart has to work

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harder to pump blood through the narrowed blood vessels, anda heart attack or a stroke may result.

Predisposing factors:

cigarette smoking high fat levels in the blood high cholesterol high blood pressure obesitySigns and symptoms:

The symptoms of atherosclerosis depend on the part of the body

where the condition is taking place. Sometimes there aren't any

noticeable symptoms until the condition has advanced to a very

serious stage. When the arteries of the heart are affected, one of

the first symptoms is chest pain, often called angina. A person

with clogged arteries of the heart may also have occasional

difficulty in breathing and may experience unusual fatigue after

short periods of exertion.

Medical & Surgical Interventions for Athero and

Arteriosclerosis:

a. Lifestyle Modification ; Reduce Risk Factorsb. Coronary Artery Bypass Graft (CABGc. Percutaneous Transluminal Coronary Angioplasty (PTCA)d. Directional Coronary Atherectomy (DCA)

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e. Intracoronary Stents

Nursing Intervention:

a. Health Teachingb. Reduce Risk Factors

c. Restore Blood Supplyd. Pre & Post-op Care for Surgical Patients

ANGINA PECTORIS: - insufficient coronary blood flow, thus inadequate O2 causes

intermittent chest pain.

-the result of myocardial ischemia caused by an imbalance

between myocardial blood supply and oxygen demand. Angina

is a common presenting symptom (typically, chest pain)

among patients with coronary artery disease. It is caused bychemical and mechanical stimulation of sensory afferent nerve

endings in the coronary vessels and myocardium.

- Angina pectoris can be relieved with rest. It lasts only for 1-5

minutes and taking up of nitroglycerine will be beneficial for

the client.

Signs and symptoms:

Patient experiences retrosternal chest discomfort ratherthan flank pain. Usually described as pressure, heaviness,squeezing, burning and choking sensation.

It localize primarily in the epigastrium, back neck jaw or inthe shoulders. The typical location for radiation of pain is in thearms, shoulders and the neck.

Precipitating factor:

over exertion

eating

exposure to cold

emotional stress

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The New York Heart Association classification is used to quantifythe functional limitation imposed by patients symptoms asfollows: (Killips)

Class I no limitations of physical activity (ordinary physical

activity does not cause symptoms).

Class II slight limitation of physical activity (ordinary physicalactivity does cause symptoms).

Class III moderate limitation of activity (patient is comfortable

at rest, but less than ordinary activity can cause symptoms).

Class IV unable to perform any physical activity without

discomfort, therefore severe limitations (patient may be

symptomatic even at rest).

Nursing Interventions:

a. Assess pain location, character, ECG (ST elevation),precipitatingfactors

b. Help client to adjust lifestyle to prevemt anginaattack avoid excessive activity in cold weather,avoid overeating, avoid constipation, rest aftermeals, exercise

c. Teach patient how to cope with angina attack

nitroglycerin every 5 mins upto 3x, if still not relievedgo to the hospital

Diagnostic Assessment:

a. ECGb. Stress Testc. Radioisotope Imagingd. Coronary Angiography

Medical Management:

a. Opiate Analgesic MoSo4b. Vasidilators Nitroglygcerin, Isosorbide

Mononitrate/Dinitratec. Calcium Channel Blockers Dlitiazem, Nifedipined. Beta Blocking Agents Propanolol

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===============================================================================

MYOCARDIAL INFARCTION- process by which myocardial tissue is destroyed due toreduced coronary blood flow.

- Myocardial infarction (MI) is the rapid development ofmyocardial necrosis caused by a critical imbalance betweenthe oxygen supply and demand of the myocardium.

- This usually results from plaque rupture with thrombusformation in a coronary vessel, resulting in an acute reductionof blood supply to a portion of the myocardium.

Causes:

1. Atherosclerotic heart2. Coronary Artery Embolism

Pathophysiology:

- The most common cause of MI is narrowing of the epicardial

blood vessels due to atheromatous plaques. . This can result in

partial or complete occlusion of the vessel and subsequent

myocardial ischemia. . Total occlusion of the vessel for more

than 4-6 hours results in irreversible myocardial necrosis, but

reperfusion within this period can salvage the myocardium andreduce morbidity and mortality.

- MI is a leading cause of morbidity and mortality in the United

States.

- Male predilection exists in persons aged 40-70 years. Evidence

exists that women more often have MIs without atypical

symptoms. The atypical presentation in women might explain

the sometimes delayed diagnosis of MIs in women.

- MI occurs most frequently in persons older than 45 years. Apositive family history includes any first-degree male relative

aged 45 years or younger.

Signs and symptoms :

1. chest pain heavy (viselike, crushing, squeezing)

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usually across the anterior pericardium typically isdescribed as tightness, pressure, or squeezing.

Pain may radiate to the jaw, neck, arms, back, andepigastrium. The left arm is affected more frequently;however, a patient may experience pain in both arms.

2. Dyspnea, Orthopnea sense of suffocation

3. Nausea and/or abdominal pain- gas pains around theheart4. Anxiety5. Light headedness with or without syncope6. Cough7. Nausea with or without vomiting8. Cold diaphoresis, gray facial color,9. Wheezing10.Weakness and altered mental status common in

elderly patients.11.Rales may be present in congestive heart failure.12.Neck vein distention represents right pump failure.

13.Dysrythmias - an irregular heart beat or pulse, usuallytachycardic.14. Oliguria urine less than 30 ml/hr15. Apprehension

Risk factors:

Age , Male gender, Smoking, DM, Family history, Sedentarylifestyle, obesity, diet, stress, hypertension, Type A personality

DIAGNOSTICS:

Lab studies:

Troponin - is a contractile protein that normally is notfound in serum. It is released only when myocardial necrosisoccurs.

- have the greatest sensitivity and specificity in

detecting MI. The test result is both diagnostic as well as

prognostic of outcome.

Creatine kinaseMB (CK-MB)

Myoglobin - a low-molecular-weight heme protein found incardiac and skeletal muscle, is released more rapidly frominfarcted myocardium.CBC is indicated if anemia is suspected as a precipitant.

Transfusion with PRBC may beindicated.

Potassium and magnesium level should be monitoredand corrected.

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Creatinine level

C Reactive protein (CRP) - is a marker of acuteinflammation.

Erythrocyte sedimentation rate (ESR)

Serum lactate dehydrogenase (LDH)

Imaging studies:

Chest radiography or chest x-ray reveals pulmonaryedema secondary to heart failure.

CT scan

Radionuclide Imaging

Positron Emission Imaging

Transesophagial Echocardiography

Magnetic resonance imaging (MRI) - can identify wallthinning, scar, delayed enhancement (infarction), and wallmotion abnormalities (ischemia).

Electrocardiogram (ECG) - ST-segment elevation greaterthan 1 mm.

- the presence of new Qwaves.

- intermediate probability of MI are ST-segmentdepression, T-wave inversion, and other

nonspecific ST-T wave abnormalities.

Immediate emergency intervention:

IV access thrombolytic agents e.g. heparin

supplemental oxygen

pulse oximetry maintain oxygen saturation at >90%

Immediate administration of aspirin en route

Nitroglycerin for active chest pain, given sublingually or byspray

ECG

Treatment is aimed at:

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1) Restoration of the balance between the oxygen supply anddemand to prevent further ischemia.

2) Pain relief3) Prevention and treatment of complications.

Drug of choice for patient with MI:

Antithrombotic agents -These agents prevent the formation of thrombusassociated with myocardial infarction and inhibit platelet function. (aspirin,-heparin)

Vasodilators - Opposes coronary artery spasm, which augments coronaryblood flow and reduces cardiac work by decreasing preload and afterload. It iseffective in the management of symptoms in AMI.

- can be administered sublingually by tablet or spray,topically, or IV.

-nitroglycerine

Beta-adrenergic blockers - reduce blood pressure, which decreasesmyocardial oxygen demand. (-metoprolol)

Platelet aggregation inhibitors inhibits platelet aggregation.-clopidogrel(plavix)

Analgesics reduce pain which decreases sympathetic stress.-morphine sulfate

Angiotensin converting enzyme (ACE) inhibitors prevents conversion ofangiotensin I to ngiotensin II, a potent vasoconstrictor. -captopril(capoten)

Complications of MI:

DysrhytmiasCardiogenic ShockHeart FailurePulmonary EdemaPulmonary EmbolismRecurrent MIComplications due to Necrosis VSD, rupture of the heart,

ruptured papillary musclesPericarditis

Recommendations:

- All MI patients should be admitted in the ICU.- Patient should remain on complete bed rest during his stayin the hospital and avoid straining activities.

Nursing interventions for MI

1. Earlya. Treat arrythmias promptly lidocaine

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b. Give analgesic- morphinec. Provide physical restd. Administer O2 via cannulae. Frequent VSf. Nifedipineg. Propanolo HCLh. Emotional Support

2. Latera. Give stool softenerb. Provide low fat, low cholesterol, low sodium diet, soft foodc. Commoded. Self-caree. Plan for rehabilitation

Exercise program

Stress management

Teach risk factors

f. Psychological supportg. Long-term drug therapy

Antiarryhtmics- quinidine, lidocaine

Anticoagualnt heparin, aspirin

Antihypertensives propanolol, chlorathiazide

3. TRANSIENT ISCHEMIC ATTACK (TIA)

- temporary episode of neurological dysfunction lasting only a fewminutes or seconds (in a day/ 24hrs) due to decreased blood flowto the brain.

- A warning sign of stroke especially in first 4 weeks after TIACauses:

1. Atherosclerosis2. Microemboli from atherosclerotic plaque

Manifestations:

1. Sudden loss of visual function2. Sudden loss of sensory function

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3. Sudden loss of mmotor function

Management: - Surgical Carotid Endarterectomy (bypass)

1. Post-op focus assess neurologic deficits; avoid flexingneck

Inability to swallow, move tongue, raise arm, smile may

indicate

problem in the specific cranial nerve.

2. Anticoagulant therapy: aspirin, etc.

4. Arrythmias

a. Review of Conduction System

Heart Conduction System

The sinoatrial node (SAN), located within the wall of the right atrium (RA), normally

generates electrical impulses that are carried by special conducting tissue to the

atrioventricular node (AVN).

Upon reaching the AVN, located between the atria and ventricles, the electrical impulse

is relayed down conducting tissue (Bundle of HIS) that branches into pathways that

supply the right and left ventricles. These paths are called the right bundle branch

(RBBB) and left bundle branch (LBBB) respectively. The left bundle branch further

divides into two sub branches (called fascicles).

Electrical impulses generated in the SAN cause the right and left atria to contract first.

Depolarization (heart muscle contraction caused by electrical stimulation) occurs nearly

simultaneously in the right and left ventricles 1-2 tenths of a second after atrial

depolarization. The entire sequence of depolarization, from beginning to end (for one

heart beat), takes 2-3 tenths of a second.

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All heart cells, muscle and conducting tissue, are capable of generating electrical

impulses that can trigger the heart to beat. Under normal circumstances all parts of the

heart conducting system can conduct over 140-200 signals (and corresponding heart

beats) per minute.

The SAN is known as the "heart's pacemaker" because electrical impulses are normally

generated here. At rest the SAN usually produces 60-70 signals a minute. It is the SAN

that increases its' rate due to stimuli such as exercise, stimulant drugs, or fever.

Should the SAN fail to produce impulses the AVN can take over. The resting rate of the

AVN is slower, generating 40-60 beats a minute. The AVN and remaining parts of the

conducting system are less capable of increasing heart rate due to stimuli previously

mentioned than the SAN.

The Bundle of HIS can generate 30-40 signals a minute. Ventricular muscle cells may

generate 20-30 signals a minute.

Heart rates below 35-40 beats a minute for a prolonged period usually cause problems

due to not enough blood flow to vital organs.

Problems with signal conduction, due to disease or abnormalities of the conducting

system, can occur anyplace along the heart's conduction pathway.

Abnormally conducted signals , resulting in alterations of

the heart's normal beating, are called arrhythmias or

dysrrythmia.

By analyzing an EKG a doctor is often able to tell if there

are problems with specific parts of the conducting system

or if certain areas of heart muscle may be injured.

b. Basic ECG Interpretation

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Electrocardiogram (ECG):

-An electrocardiogram (ECG) is a test that records the electrical

activity of the heart.

-is used to measure the rate and regularity of heartbeats as well as

the size and position of the chambers, the presence of any damage tothe heart, and the effects of drugs or devices used to regulate the

heart.

The ECG Waves:

P wave - represents the wave of depolarization that spreads from the

SA node throughout the atria, and is usually 0.08 to 0.1 seconds (80-

100 ms) in duration.

P R interval - the period of time from the onset of the P wave to

the beginning of the QRS complex, which normally ranges from 0.12

to 0.20 seconds in duration. This interval represents the time

between the onset of atrial depolarization and the onset of ventricular

depolarization.

QRS complex - represents ventricular depolarization. The duration

of the QRS complex is normally 0.06 to 0.1 seconds.

ST segment - following the QRS is the time at which the entire

ventricle is depolarized and roughly corresponds to the plateau phase

of the ventricular action potential. The ST segment is important in

the diagnosis of ventricular ischemia or hypoxia because under those

conditions, the ST segment can become either depressed or elevated.

T wave - represents ventricular repolarization and is longer in

duration than depolarization.

Q T interval - represents the time for both ventricular

depolarization and repolarization to occur, and therefore roughly

estimates the duration of an average ventricular action potential.

This interval can range from 0.2 to 0.4 seconds depending upon heart

rate.

Abnormal ECG results may indicate the following:

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V1: Fourth intercostal space to the right

of the sternum.

V2: Fourth intercostal space to the Left of

the sternum.

V3: Directly between leads V2 and V4.

V4: Fifth intercostal space at

midclavicular line.

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Myocardial (cardiac muscle) defect Past heart attacksEnlargement of the heart Present orimpending heart attackCongenital defects Inflammation ofthe heart (myocarditis)Heart valve diseaseArrhythmias (abnormal rhythms)

Tachycardia (heart rate too fast) or bradycardia (too slow)Coronary artery

How to perform ECG Using Disposable Electrodes.

Skin Preparation:

Clean with alcohol or usual skin prep, if necessary. If the patients are very hairy shave

the electrode areas.

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Trouble Shooting.

When no signal or a poor signal is observed the following should be considered:

1. Have the cables been correctly connected?2. Is the equipment functioning correctly?

3. Could external electrical equipment interference be a problem?

4. Was skin preparation adequate?

5. Could the electrodes suffer from

a) gel dry out?

b) Poor adhesion?

========================================================================

12 Lead (10 Electrode) Placement Guide:

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Normal adult 12-lead ECG

The diagnosis through electrocardiogram is made by excluding any recognised

abnormality. It's description is therefore quite lengthy.

normal sinus rhythmo each P wave is followed by a QRS

o P waves normal for the subject

o P wave rate 60 - 100 bpm with 10% = sinus

arrhythmia normal QRS axis

normal P waveso height < 2.5 mm in lead IIo width < 0.11 s in lead II

for abnormal P waves see right atrial hypertrophy, left atrialhypertrophy, atrial premature beat, hyperkalaemia

normal PR interval

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o 0.12 to 0.20 s (3 - 5 small squares) for short PR segment consider Wolff-Parkinson-White

syndrome or Lown-Ganong-Levine syndrome (other causes- Duchenne muscular dystrophy, type II glycogen storagedisease (Pompe's), HOCM)

for long PR interval see first degree heart block normal QRS complex

o < 0.12 s duration (3 small squares)

for abnormally wide QRS consider right or left bundlebranch block, ventricular rhythm, hyperkalaemia, etc.

o no pathological Q waveso no evidence ofleft or right ventricular hypertrophy

normal QT intervalo Calculate the corrected QT interval (QTc) by dividing the QT

interval by the square root of the preceeding R - R interval.Normal = 0.42 s.

o Causes oflong QT interval myocardial infarction, myocarditis, diffuse myocardial

disease hypocalcaemia, hypothyrodism subarachnoid haemorrhage, intracerebral haemorrhage drugs (e.g. sotalol, amiodarone) hereditary

Romano Ward syndrome (autosomal dominant)

Jervill + Lange Nielson syndrome (autosomalrecessive) associated with sensorineural deafness

normal ST segmento no elevation or depression

causes of elevation include acute MI (e.g. anterior, inferior),left bundle branch block, normal variants (e.g. athleticheart, Edeiken pattern, high-take off), acute pericarditis

causes of depression include myocardial ischaemia, digoxineffect, ventricular hypertrophy, acute posterior MI,pulmonary embolus, left bundle branch block

normal T wave causes of tall T waves include hyperkalaemia, hyperacute

myocardial infarction and left bundle branch block

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causes of small, flattened or inverted T waves arenumerous and include ischaemia, age, race,hyperventilation, anxiety, drinking iced water, LVH, drugs(e.g. digoxin), pericarditis, PE, intraventricular conductiondelay (e.g. RBBB)and electrolyte disturbance.

normal U wave1. Different kinds of Arrythmias

a. Atrial tachycardia sudden onset of atrial rates 140 250 per minute.

rhythm: regular

P waves: present before QRS complex.

PR interval: usually not measurable.

QRS complex: normal in shape (0.06 0.10 secs.)

T wave: distorted in appearance.

b. Atrial flutter atrial stretching or enlargement, MI, CHF. rate 250 400 beats per minute

rhythm: regular or irregular

P wave: not present; replaced by a saw toothed pattern (F waves).

PR intervals: not measurable.

QRS complex: normal shape and time.

T wave: present but may be obscured by flutter waves.

ECG TRACING OF AN ATRIAL FLUTTER

c. Ventricular tachycardia life threatening dysrythmias thatoriginates from an irritable focus within the ventricle.

o metabolic acidosis (lactic acidosis)o electrolyte imbalanceo digitalis toxicity

rate: 140 220 bpm.

rhythm: usually regular but may be irregular

P wave: not present.

PR interval: immeasurable. .

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T wave: usually deflected opposite to the QRS complex.

d.Atrial fibrillation rapid and chaotic firing of atrial impulses.a. fibrotic changes associated with aging process.

b. AMIc. valvular diseased. digitalis

rate: immeasurable because fibrillatory waves replace P waves;ventricular rate may vary from brady to tachycardia.

Rhythm: irregular

P wave: replaced by fibrillatory waves (little f waves)

PR interval: immeasurable

QRS complex: normal

T wave: normal

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e.Ventricular fibrillation random and chaotic discharging ofimpulses within the ventricles at rates that exceeds 300 bpm.

a. produces clinical death and must be reversedimmediately.b. AMIc.Acidosisd.Electrolyte disturbance

rate: immeasurable because of absence of well formed QRS complex.

rhythm: chaotic

P wave: not present

PR interval: not present

QRS complex: bizarre, chaotic, no definite contour

T wave: not apparent

ECG TRACING OF A VENTRICULAR FIBRILLATION

a. Premature atrial contraction ectopic beat that originates inthe atria and is discharged at a rate faster than that of the SAnode

the atrial beat occurs sooner than the next normalbeat and is said to be early or premature.

Occurs in healthy or diseased heart (ischemia) Precursor of more serious dysrhytmias

rate: slow or fast

rhythm: irregular because of the early occurrence of the PAC

P wave: present for each normal QRS complex; the P wave of thepremature contraction

will be distorted in shape.

PR interval: may be normal or shortened depending on where in theatria the impulses originated; the closer the site of atrial impulse formation tothe AV node, the shorter the PR interval will be.

QRS and T wave: normal

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g.Premature ventricular contraction ectopic beat originating in theventricle and is being

discharged at a rate faster than that of the nextnormally occurring beat.

most common dysrythmias in the hospital

AMI

All other forms of heart disease Pulmonary disease

Electrolyte disturbances

Metabolic instability

Drug abuse

rate: slow or fast

rhythm: irregular because of the premature firing of the ventricularectopic focus.

P wave: absent since the impulse originates in the ventricle, bypassingthe atria and the AV

node.

PR interval: immeasurable QRS complex: QRS of the PVC will be widened (>0.12 sec.), bizarre in

appearance whencompared to normal QRS complex.

T wave: usually deflected opposite to the QRS.

ECG TRACING OF A PREMATURE VENTRICULAR CONTRACTION

4. Heart Block

a. transmission of the wave of impulse from the SA node through thenormal conduction

pathway is altered at the level of AV node.

b. the altered state does not allow the impulse to be conducted ontime or at all.

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TYPES:

a. First degree AV block the impulse is transmitted normally

but, but is delayed longer at the level of the AV node.

c. may be a sign of CAD, acute rhuematic carditis,electrolyte imbalance.

rate: usually normal but may be slow.

Rhythm: regular

P wave: present for each QRS complex and isidentical.

PR interval: >20 sec.

QRS complex: normal (0.06 0.10 sec.)

T wave: normal

b. Second degree AV block the AV node becomes selective aboutwhich impulses are conducted to the ventricles.

c. Third degree AV block complete heart block.d. no relationship between the atrial and ventricular activity

Acute Inferior Myocardial Infarction

ST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads

Acute Anterior Myocardial Infarction

ST elevation in the anterior leads V1 - 6, I and aVL

reciprocal ST depression in the inferior leads

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Acute Posterior Myocardial Infarction

(hyperacute) the mirror image of acute injury in leads V1 - 3

(fully evolved) tall R wave, tall upright T wave in leads V1 -3

usually associated with inferior and/or lateral wall MI

Old Inferior Myocardial Infarction

a Q wave in lead III wider than 1 mm (1 small square) and a Q wave in lead aVF wider than 0.5 mm and a Q wave of any size in lead II

Acute myocardial infarction in the presence of left bundle branch block

Features suggesting acute MI

ST changes in the same direction as the QRS (as shown here)

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ST elevation more than you'd expect from LBBB alone (e.g. > 5 mm inleads V1 - 3)

Q waves in two consecutive lateral leads (indicating anteroseptal MI)

5. Difference between Angina Pectoris, Myocardial Infarction, TransientIschemic Attack

Angina Pectoris MyocardialInfarction

TIA

Definition - insufficient

coronary bloodflow, thusinadequate O2causesintermittentchest pain.

-can be relievedwith rest andnitroglycerine

- process by

which myocardialtissue isdestroyed due toreduced coronaryblood flow.

- not relieved withrest andnitroglycerine

- needs immediatemedicalintervention

- temp

orary episode ofneurologicaldysfunctionlasting only a fewminutes orseconds (in aday/ 24hrs) dueto decreasedblood flow to thebrain.

- A warning signof stroke

especially infirst 4 weeksafter TIA

Signs andSypmtomsChest pain

pressure,heaviness,

squeezing, burningand chokingsensation

localized primarilyin the epigastrium,back neck jaw or inthe shoulders.

The typical location

viselike, crushing,squeezing

Pain may radiateto the jaw, neck,arms, back, andepigastrium.

The left arm isaffected morefrequently;

Sudden loss ofvisual function

Sudden loss ofsensoryfunction

Sudden loss ofmotor function

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for radiation of painis in the arms,shoulders and theneck

however, apatient mayexperience painin both arms.

=====================================================

6. Acute Respiratory Failure

Pulmonary edema

- often occurs when the left side of the heart is distended and fails topump adequately

Clinical Manifestation

Constant irritating cough, dyspnea, crackles, cyanosis

Pathophysiology

Fluid accumulation in the alveolar sacs due to hypovolemia, fluid

congestions in the lungs, alveoli are congested

Diagnostic Tests

CXR

Medical Surgical MgtDiuretics, low sodium diet, I&O

Nursing Mgt

1. promote effective airway clearance, breathing patterns andventilation

2. Monitor VS3. Psychological support4. Administer medications

------------------------------------------------------------------------------------------------

-------------------7. Acute Respiratory Failure

Pneumonia

- inflammtory process of lung parenchyma assoc. w/ marked increase inalveolar and interstitial fluid

Risk factors:

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1. Smoking, air pollution2. URTI3. Altered conciousness4. Tracheal intubation5. Prolonged immobility6. lowered immune system7. malnutrition, DHN,8. Chronic Diseases:DM, Heart dse, renal dse, cancer9. inhalation toxicity/ aspiration

Clinical Manifestationo Chest pain, irritability, apprehensiveness, irritability, restlessness,

nausea, anorexia, hx of exposureo Cough- productive , rusty/ yellowish/greenish sputum, splinting of

affected side, chest retration (infants)o Sudden increased fever, chills

o Nasal Flaring, circumoral cyanosis

o Tachypnea, vomiting

Pathophysiology

Caused by infectious or non-infectious agents, clotting of an exudate rich

fibrogen, consolidated lung tissue

Diagnostic Tests

CXR, sputum culture, Blood culture, increased WBC, elevated

sedimentation rate

Medical Surgical Mgt

AntibioticsRest

Nursing Mgt

1. Promote adequate ventilation- positioning, Chest physiotherapy,IPPB2. Provide rest and comfort3. Prevent potential complications4. Health teaching

-------------------------------------------------------------------------------------------------------------------


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Asthma

- increased responsiveness of the trachea and bronchi to various stimuli,with difficulty in breathing, caused by narrowing of airways

Types:

- Immunologic asthma occurs in childhood- Non-immunologic asthma occurs in adulthood and assoc w/ recurrent

resp infections.Usually >35 y/o

- Mixed, combined immunologic and non-immunologic

** Status Asthmaticus

- a life-threatening asthmatic attack in w/c symptoms of asthma continues andso not respond to treatment

Clinical Manifestation

History of rhinitis, allergies, family hx of asthmaIncreased tightness of chest, dyspnea

Tachycardia, tachypneaDry, hacking, persistent cough(+) wheezes, cracklesPallor, cyanosis, diaphoresis, Chronic barrel chest, elevated shoulders,distended neck veins, orthopnea

Tenacious, mucoid sputum

Pathophysiology

Bronchial smooth muscles constrictsBronchial secretions increaseMucosa swell and narrows airway passageHistamine is produced in the lungsBronchospasm, production of large amount of thick mucous andinflammatory response contribute to resp. obstruction

Diagnostic Tests

ABG (elevated PCO2, dec PO2 and pH)Vital capacity reduedForced expiratoryVolume decreasedResidual Volume increased

Medical Surgical Mgt

Steroids,

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Antibiotics,Bronchodilators, expectorantsO2, nebulization

Nursing Mgt

a. Promote pulmonary ventillationb. Facilitate expectorationc. Health teachingd. Breathing techniquese. Stress management

-------------------------------------------------------------------------------------------------------------------Chronic Obstructive Pulmonary Disease

o a group of conditions assoc. w/ chronic obstruction of airflow

entering or leaving the lungs

a. Major diseases

1. Pulmonary Emphysema airway is obstructed due to destroyedalveolar walls

2. Chronic Bronchitis- increased mucus production that obstructsairway

3. Asthma

b. Clinical Manifestation

Shortness of breath, productive cough, hypoxia, wheezes/rales,

decreased exercise tolerance

c. Diagnostic Tests

Same w/ asthma

d. Medical Surgical Mgt

Antibiotics, expectorants, O2 at low flow, nebulization

e. Nursing Mgt

a. Promote pulmonary ventillationb. Facilitate expectorationc. Health teachingd. Breathing techniquese. Stress management

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-------------------------------------------------------------------------------------------------------------------


a. Acute Respiratory Distress

Syndrome

- noncardiogenic pulmonary infiltrations resulting in stiff, wet lungs andrefractory hypoxemia in previously healthy adult. Arf w/o hypercapnia

b.Risk Factors:

a. Primary- Shock, multiple trauma- Infections- Aspirations, inhalation of chemical toxins- Drug overdose- DIC- Emboli, esp Fat embolib. Secondary- Overaggressive fluid administration- Oxygen toxicity

c. Clinical Manifestation

Restlessness, anxiety, hx of risk factors, severe dyspnea cyanosis,tachycardia, hypotension, hypoxemia, acidosis, crackles

d. Pathophysiology

Damage to alveolar capillary membrane

Increased Vascular Permeability to pulmonary edema

Impaired Gas exchange

Decreased surfactant prduction

Potential Atelectasis

Severe hypoxia

May lead to death

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e. Diagnostic Tests

CVP, Pulmonary Wedge Capillary Pressure, ABG

f. Medical Surgical Mgt

ICU, strict monitoring, O2, suction, bronchodilator, anitibiotics, ETventilator

g. Nursing Mgt

a. Assist in respirationsb. Prevent complicationsc. Environment, fluid balance, bleeding tendencies

d. Health teaching

2. Ventilation Therapy:

b. Mechanical Ventilation a

means of augmenting respiratory gas exchange using a

mechanical device, equipped to deliver negative or positive

pressure that can maintain ventilation and O2 delivery for a

prolonged period of time.

-The volume of air delivered by the ventilator is relativelyconstant, assuring consistent adequate breaths despite varyingairway pressure.

c. Types:

1. Pressure cycled it permits air to flow into theclients lungs until a predetermined pressure is reached.-the volume of air or O2 can vary as the clients airwayresistance changes.

Birds

Bennett

2. Volume cycled delivers a predetermined volumeof gas into the patients lungs with each breath.-preset volume of air, ordered by the physician.

Engstron Bennett

Ohio and Emerson

d. Indications:

continues decrease in oxygenation (paO2)

increase in arterial carbon dioxide levels (paCO2)

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persistence of acidosis (decrease in blood pH)

e. Respiratory conditions

needing the aid of the mechanical ventilators:

post operative thoracic or abdominal surgery drug overdose

neuromuscular disease

inhalation injury

COPD

multiple trauma

shock

multi-system failure

coma

e. Mode or Breath Pattern:

- what causes the ventilator to cycle from inspiration

Mandatory (controlled) - which is determined by the respiratory rate.

Assisted (as in assist control) - synchronized intermittent mandatoryventilation, pressure support.

Spontaneous - no additional assistance in inspiration, as in CPAP.

CMV - Conventional controlled ventilation, without allowances forspontaneous breathing.

Many anesthesia ventilators operate in this way.

Assist-Control - Where assisted breaths are facsimiles of controlled

breaths. Intermittent Mandatory Ventilation - which mix controlled breath

and spontaneous breath.

Pressure Support - Where the patient has control over all aspects ofhis/her breath except the pressure limit.

Positive End Expiratory Pressure (PEEP) a method of maintaining apressure higher than the atmospheric pressure in the lungs in the end ofeach expiration.

Continues Positive Airway Pressure (CPAP) a non mechanicalmeans of ventilation. It provides a continues positive airway pressure inthe lungs at the end of expiration.

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Bennett MA-1 Bennett Puritan

=====================================================

3. SHOCK

- is defined as failure of the circulatory system to maintain adequateperfusion of vital organs.

A. Pathophysiology of Shock

The three major components of the circulatory system are the heart,

large blood vessels and microcirculation. As long as two of these factors

canmaintain a satisfactory compensatory action, adequate blood

circulation can be maintained even if the third factor is not functioning

normally.

However, if compensatory mechanisms fail or if more than one of these

three factors necessary for adequate circulation malfunction, circulatry

failure results and shock develops.

(see matrix and stages)

B. Classification of Shock

Classification Etiology

1. Hypovol Blood loss: Massive Trauma, GI Bleeding,

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emic Shock

- due to inadequatecirculationg bloodvolume

Ruptured AorticAneurysm, Surgery, Erosion of

Vessesl due to lesion, tubes or other devices,DIC

Plasma loss: Burns, Accumulation of intra-abdominal fluid,

malnutrition, severe dermatitis,DIC

Crystalloid loss: Dehydration, ProtractedVomiting, Diarrhea, nasogastric suction

2. Cardiogenic Shock

- due to inadequatepumping action ofthe heart becauseof primary cardiacmuscle dysfunctionor mechanicalobstruction of bloodflow caused by MI orvalvular insufficiency

Myocardial disease: Acute MI, MyocardialContusion,

Cardiomypathies

Valvular Disease or injury: Ruptured AorticCusp, Ruptured

Papillary muscle, Ballthrombus

External Pressure on the Heart interferes with heart

filling or emptying:Pericardial Tamponade due to Trauma,

aneurysm,cardiac surgery, pericarditis,

massivepulmonary embolus, tension

pneumothorax

Cardiac Dysrhtymias: Tachyarrhythmias,Bradyarrythmias,

Electromechanicaldissociation

3. Neurogenic Shock- interferencewith nervous

system control ofthe blood vessels

Spinal: Spinal anesthesia, spinal cord injury

Vaso-vagal reaction: Severe pain, severeemotional stress

4. Anaphylactic Shock- severehypersensitivity

reactionresulting in

Allergy to food, medicines, dye, insect bites orstings

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massivesystemicvasodilation.

5. SepticShock- systemicreactionvasodilation dueto infection

Gram-negative septicemia but also caused byother organisms

MATRIX: PATHOPHYSIOLOGY OF SHOCK

CIRCULATORY SYSTEM

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HEART LARGE BLOOD VESSELS

MICROCIRCULATION

Myocardial disease Blood loss Plasma loss

Crystalloid loss

External Pressure on the Heart interferes with heart filling or emptying

S inal cord in ur


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Compensated Decompensated

(body is able to maintain tissue (systemic circulation &microcirculationperfusion to the vital organs) no longer work in unison)

C. Stages of Shock

1. Nonprogressive Stage - cardiac output is slightly decreasedbecause of loss

of actual or relative blood volume.

- body responds to compensate for the

hypovolemia

to maintain blood pressure.

cardiac output sympatheticstimulation

capillary blood flow epinephrine and

hydrostatic pressure within norepinephrinereleased

capillaries lower thansurrounding tissues vasoconstriction

fluid moves from tissues tachycardia systemic vascularinto vascular system resistance

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Non-progressive

Stage

vasoconstriction continues microcirculationNormal State

decreased venous return decreased circulation ofdeoxygenated blood

Inadequate tissue perfusion

Pro ressive Sta e

Cellular IschemiaNecrosis

Organ FailureDEATH


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circulating volume blood pressuremaintained

2. Progressive Stage - the compensatory mechanisms are notadequate to

compensate for the loss of blood volume.- blood declines to a very low level that is not

adequate

to maintain blood flow to the cardiac musclethus

heart begins to deteriorate.

persistent compensatory vasoconstriction

dilation in microcirculation

venous return

cardiac output

arterial blood pressure

venous poolingcoronary artery

tissue perfusionfillingpooling of bloodin microcirculation damage to microcirculationmyocardial

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functionaccumulation of cellular hypoxia and release ofmetabolites in cell vasoactive substances

metabolic acidosis capillary permeability

venous return

3. Irreversible Stage occurs if the cycle of inadequate tissueperfusion is

not interrupted

- cellular ischemia and necrosis lead to organ

failure

D. Physiologic Manifestations of Shock

Early signs

1. tachycardia2. tachypnea3. oliguria

Late signs

4. cold moist skin5. color ashen: pallor

6. hypotensive, tachycardia

E. Effects of Shock in Different Organs

a.Respiratory system

- shock leads to hypoxia, with blockage of normal aerobicmetabolism.

- lactic acid accumulates, resulting to tissue acidosis.

b. Cardiovascular System1. Myocardial deterioration2. Disseminated Intravascular Coagulation

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c. Neuroendocrine System1. General Adaptation Response

- neuroendocrine responses during shock are defensivereactions that

occur during the bodys stage of resistance2. Adrenal Response

- increase in adrenocortical mineralocorticoid hormonesoccurs

- helps increase intravascular fluid volume by stimulating thekidneys

to retain sodium and water3. Pituitary response

-ADH is released and carried to the kidneys where it causesthe body

to retain water4. Metabolic Response

- during the initial phase of shock, the bodys small stores ofavailable

carbohydrates are rapidly depleted. Protein and fats arethen

metabolized to meet bodys energy requirements.

d. Immune System- all forms of shock depresses the macrophages located both in the

bloodstream and tissues.- A person in a state of shock is more susceptible to bacterial

endotoxins.

e. GI Sysytem- vagal stimulation to the GI tract slows down or stops, resulting to

absenceof peristalsis

- liver loses ability to detoxify and may release vasoactivesubstances .

- during shock, pooling of blood occurs in the liver or portal bed

f. Renal System1. Altered Capiillary blood pressure and glumerular filtration2. Renal Ischemia

F. Medical Surgical Management

1. Improve oxygenation- supplemental oxygen is administered to protect againsthypoxemia- via O2 cannula, ET tude, tracheostomy tube

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2. Restore and maintain adequate perfusion

3. Administer vasoactive medications or emergency drugs

- Atropine, dopamine, epinephrine, isoproterenol ( to increaseStroke volume), Lidocaine( for

dysrrhythmias), Metaraminol ( promotes vasoconstriction),Levophed, Na bicarbonate

4. Assist circulation-use of intra aortic balloon pump, medical anti shock trousers(MAST suit)- modified trendelenberg position- administer blood products properly typed and crossmatched

5. Fluid replacement Colloid or balanaced salt solution, colloidsolution, blood,

6. Prevent complications such as renal impairment and GI bleeding

G. Nursing Intervention

1. Assessment:

Vital signs, Airway, breathing, circulation, LOC, state ofhydration, Pane, presence of any laceration or deformity(if any)

2. Diagnosis

Ineffective airway clearance, impaired gas exchange,decreased cardiac output, etc..

3. Planning

Plans of intervention R/T diagnosis and state of theclient

4. Intervention

Assess and monitor client, stop bleeding (if present),Administer medications and fluids, Refer accordingly,position client appropriately, maintain safety of thepatient

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5. Evaluation

abc revised

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