LO 1 Myocardial infarction

Unstable angina & Non-STEMI Definition

Stable angina chest or arm discomfort that may not be described as

pain but is reproducibly associated with physical exertion or stress and is relieved within 5–10 min by rest and/or sublingual nitroglycerin

Unstable angina equivalent ischemic discomfort + 1 of 3 features:

occurs at rest (or with minimal exertion), lasting >10 min severe and of new onset (within the prior 4–6 weeks) occurs with a crescendo pattern

NSTEMI clinical features of UA develops evidence of myocardial

necrosis

Pathophysiology oxygen supply < +/ myocardial oxygen demand >

+ atherosclerotic coronary plaque plaque rupture or erosion with superimposed

nonocclusive thrombus dynamic obstruction (coronary spasm, as in Prinzmetal's

variant angina) progressive mechanical obstruction (rapidly advancing

coronary atherosclerosis) myocardial oxygen demand and/or decreased supply

(tachycardia, anemia)

History & physical examination chest pain (substernal region or sometimes in the

epigastrium radiates to the neck, left shoulder, and left arm)

Diaphoresis pale cool skin sinus tachycardia third and/or fourth heart sound basilar rales sometimes hypotension

Electrocardiogram ST-segment depression, transient ST-segment

elevation, and/or T-wave inversion 30-50%

Cardiac biomarkers CK-MB and troponin >

minor troponin elevations have been reported and can be caused by congestive heart failure, myocarditis, or pulmonary embolism false positive value

Diagnostic pathways

Short term management placed at bed rest with continuous ECG monitoring

for ST-segment deviation and cardiac rhythm Ambulation is permitted if

patient shows no recurrence of ischemia (discomfort or ECG changes)

does not develop a biomarker of necrosis for 12–24 h

Medical therapy Anti-ischemic & anti-thrombotic treatment

Anti-ischemic therapy Include bed rest, nitrates, beta blockers

Nitrates sublingually or by buccal spray (0.3–0.6 mg) Persist after three doses given 5 min apart IV nitroglycerin

(5–10 ug/min using nonabsorbing tubing) may be increased by 10 ug/min every 3–5 min pain relieved or systolic arterial pressure <100 mmHg

pain-free for 12–24 h Topical or oral nitrates replace the IV nitroglycerin

Beta blockers IV followed by oral beta blockers heart rate of 50–60

beats/min

Antithrombotic therapy

Invasive VS conservative strategy Invasive strategy (high risk patients / class I indication)

anti-ischemic and antithrombotic agents coronary arteriography is carried out within ~48 h of

admission coronary revascularization (PCI or coronary artery bypass

grafting

Conservative strategy anti-ischemic and antithrombotic watchfull waiting coronary arteriography

If rest pain or ST-segment changes recur

evidence of ischemia on a stress test

Risk stratification & prognosis

ST-segment elevation myocardial infarction

Pathophysiology coronary blood flow < + atherosclerotic thrombus atherosclerotic plaque disruption (by cigarette, HT, lipid

>) various agonists (collagen, ADP, epinephrine,

serotonin) platelet activation thromboxane A2 > local vasoconstrictor, further platelet activation conformational change in the glycoprotein IIb/IIIa receptor

high affinity to fibrinogen platelet cross-linking and aggregation

Factors VII and X are activated prothrombin ~ thrombin fibrinogen ~ fibrin further coagulation cascade

occlusion of coronary artery by thrombus

Clinical presentation precipitating factor

vigorous physical exercise, emotional stress, or a medical or surgical illness

Deep & visceral pain (heavy, squeezing, and crushing; stabbing, burning) occurs at rest, more severe, and lasts longer central portion of the chest and/or the epigastrium,

occasion it radiates to the arms, abdomen, back, lower jaw, and neck

weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom

when it begins during a period of exertion does not usually subside with cessation

Physical findings anxious and restless, attempting unsuccessfully to

relieve the pain (moving about in bed, altering their position, and stretching)

Pallor substernal chest pain > 30 min +

diaphoresis precordium is usually quiet, apical impulse difficult

to palpate murmur due to dysfunction of the mitral valve Transmural STEMI

pericardial friction rub is heard systolic pressure declines by approximately 10–15

mmHg

laboratory findings Electrocardiogram

total occlusion of an epicardial coronary artery ST-segment elevation + Q waves on the ECG

Cardiac imaging early detection of the presence or absence of wall

motion abnormalities by echocardiography high-resolution cardiac magnetic resonance imaging radionuclide imaging techniques

Serum cardiac biomarkers Cardiac-specific troponin T (cTnT) and cardiac-specific

troponin I (cTnI) >20 times higher than the upper reference limit

Creatine phosphokinase (CK) rises within 4–8 h and generally returns to normal by 48–72 h (CK activity >=2.5 suggest MI)

Initial management Prehospital care

Management in the emergency department Aspirin, buccal absorption of a chewed 160–325 mg

tablet Hypoxemia O2 by nasal prongs or face mask (2–4

L/min) for the first 6–12 h reassessed

Control of discomfort Sublingual nitroglycerin (three doses of 0.4 mg at about 5-

min intervals) Morphine IV (2–4 mg every 5 min) IV beta blockers

metoprolol, 5 mg every 2–5 min for a total of 3 doses 15 min oral regimen is initiated of 50 mg every 6 h for 48 h 100 mg every 12 h

Management strategies reperfusion therapy (PCI or fibrinolytics)

LO 2 Cardiogenic shock & pulmonal edema

Cardiogenic shock & pulmonary edema life-threatening conditions that should be

treated as medical emergencies

Etiology severe left ventricular (LV) dysfunction

pulmonary congestion and/or systemic hypoperfusion

Cardiogenic shock systemic hypoperfusion due to severe

depression of the cardiac index [<2.2 (L/min)/m2]

sustained systolic arterial hypotension (<90 mmHg)

elevated filling pressure [pulmonary capillary wedge pressure (PCWP) > 18 mmHg]

Most common etiologies acute myocardial infarction cardiomyopathy or myocarditis cardiac tamponade

RV failure Refractory sustained

bradyarrhythmias Toxic metabolic

Beta blocker/CCB overdose

Severe acidosis & hypoxemia

Other etiologies Post cardiac arrest Refractory sustained

tacchyarrhythmias Pulmonary embolus Severe valvular heart

disease Critical aortic / mitral

stenosis Acute severe aortic /

mitral regurgitation

Incidence leading cause of death of patients hospitalized

with MI LV failure accounts for ~80% of the cases of CS

complicating acute MI fell from 20% in the 1960s but has plateaued at

~8% for >20 years typically associated with ST elevation MI (STEMI)

Pathophysiology Large infarctions and

shock SIRS Inflammatory

cytokines, inducible nitric oxide synthase shock

Pump failure Poor tissue perfusion

lactic acidosis Pulmonary edema

hypoxemia vicious cycle of worsening MI & hypotension

Risk factors acute MI older age female sex prior MI diabetes anterior MI location reinfarction soon after

MI

Timing 1/4 of MI patients

develop CS rapidly (within 6 hour of MI onset)

3/4 later on the 1st day

Subsequent onset of CS reinfarction, marked infarct

expansion, a mechanical

complication

Clinical findings Continuing chest pain

& dyspnea Pale, apprehensive,

diaphoretic Altered consciousness weak and rapid pulse

90–110 beats/min Systolic BP <90 mmHg

+ narrow pulse pressure (<30 mmHg)

quiet precordium + weak apical pulse

Tachypnea, Cheyne-Stokes respirations

jugular venous distention

S1 is usually soft, and an S3 gallop may be audible

Acute, severe MR and VSR systolic murmurs

LV failure causing CS rales

Oliguria urine output < 30 mL/h

Laboratory findings WBC count > with left

shift BUN & creatinin >> Hepatic transaminase

>> Lactic acid > Arterial blood gases

hypoxemia and metabolic acidosis

creatine phosphokinase, troponin I & T >

ECG acute MI with LV

failure Q waves and/or >2-mm

ST elevation in multiple leads

LBBB 1,5 of infarct

anterior severe left main

stenosis global ischemia severe (e.g., >3 mm)

ST depressions in multiple leads

Chest X ray pulmonary vascular

congestion pulmonary edema CS results from a first

MI heart’s size is normal

Echocardiogram left-to-right shunt in

patients with VSR Pulmonary embolism

Proximal aortic dissection with aortic regurgitation or tamponade

Pulmonary artery catheterization

Prognosis wide range of expected death rates

age, severity of hemodynamic abnormalities, severity of the clinical manifestations of hypoperfusion, and the performance of early revascularization

Independent risk factors advanced age; depressed cardiac index, ejection

fraction, and BP; more extensive coronary artery disease; and renal insufficiency

Pulmonary edema Etiology

Cardiogenic & non cardiogenic

Pathophysiology (cardiogenic) Cardiac abnormality pulmonary venous &

hydrostatic pressure > fluids exit the capillary interstitial & alveolar edema pleural effusion breathing discomfort

Clinical findings rapid onset of dyspnea at rest, tachypnea,

tachycardia, and severe hypoxemia Rales and wheezing

due to airway compression from peribronchial cuffing Hypertension

due to release of endogenous catecholamines

Other examinations Echocardiography

systolic and diastolic ventricular dysfunction and valvular lesions Electrocardiography

ST elevation and evolving Q waves is usually diagnostic of acute MI

Brain natriuretic peptide levels > heart failure as the etiology

X ray peribronchial thickening, prominent vascular markings in the

upper lung zones, and Kerley B lines patchy alveolar filling (in perihilar distribution) diffuse alveolar

infiltrates Swan-Ganz catheter

high pressure PCWP

Treatment Oksigen therapy Positive pressure ventilation Diuretics

Furosemide <=0.5 mg/kg Nitrates

Sublingual nitroglycerin (0.4 mg x 3 every 5 min) IV nitroglycerin, commencing at 5–10 ug/min

Morphine 2- to 4-mg IV boluses

ACE-I A low dose of a short-acting agent may be initiated and

followed by increasing oral doses

Other Preload-Reducing Agents IV recombinant brain natriuretic peptide (nesiritide)

potent vasodilator + diuretic (refractory patients & not recommended in ischemia or MI)

Physical Methods Patients without hypotension should be maintained in

the sitting position with the legs dangling along the side of the bed

Inotropic and Inodilator Drugs dopamine and dobutamine bipyridine phosphodiesterase-3 inhibitors (inodilators)

milrinone (50 g/kg followed by 0.25–0.75 ug/kg per min) stimulate myocardial contractility + peripheral and pulmonary vasodilation

Digitalis Glycosides rarely used at present

Intraaortic Counterpulsation IABP

Treatment of Tachyarrhythmias and Atrial-Ventricular Resynchronization a primary tachyarrhythmia may require cardioversion patients with reduced LV function and without atrial

contraction / with lack of synchronized atrioventricular contraction atrioventricular sequential pacemaker

Stimulation of Alveolar Fluid Clearance IV Beta-adrenergic agonist treatment decreases

extravascular lung water

LO 3 Cardiac arrest

Cardiac arrest

Etiology

Clinical characteristics presaged by days to months of

> angina, dyspnea, palpitations, easy fatigability, and other nonspecific complaints

Clinical transition acute change in cardiovascular status preceding cardiac

arrest by up to 1 h HR >, advanced grades of PVCs to evolve, nonsustained

or sustained VT that generates VF Progression to biologic death

VF or asystole without CPR within the first 4–6 min has a poor outcome

few survivors among patients who had no life support activities for the first 8 min after onset

In the setting of acute MI distinguish Primary cardiac arrests

Occurs in the absence of hemodynamic instability success rate for immediate resuscitation 90%

secondary cardiac arrests those which occur in patients in whom abnormal

hemodynamics dominate the clinical picture before cardiac arrest

70% of patients with secondary cardiac arrest succumb immediately or during the same hospitalization

Treatment Initial evaluation & basic life support

observations of the state of consciousness, respiratory movements, skin color, and the presence or absence of pulses in the carotid or femoral arteries call 911

severe stridor + persistent pulse aspiration Heimlich maneuver

precordial blow, or "thump," delivered firmly occasionally revert VT or VF, but there is concern about converting VT to VF only when monitoring and defibrillation are available

head is tilted back and the chin lifted Mouth-to-mouth respiration Chest compression

arms remaining straight, 100x per minute, depress sternum 4-5 cm

AED ACLS

defibrillation/cardioversion and/or pacing VF or VT is established monophasic 300 J / biphasic 120–

150 J escalated to a maximum of 360 J monophasic (200 J biphasic)

if the first shock fails 5 cycles of CPR be carried out before repeated shocks

if 5 min has elapsed between the onset of cardiac arrest 60–90 s of CPR before the first shock

intubation with an endotracheal tube insertion of an intravenous line