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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 510 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 46 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 1224 h

Medical therapy

Anti-ischemic & anti-thrombotic treatment

Anti-ischemic therapy

Include bed rest, nitrates, beta blockers

Nitrates

sublingually or by buccal spray (0.30.6 mg)


Persist after three doses given 5 min apart IV
nitroglycerin (510 ug/min using nonabsorbing tubing)
may be increased by 10 ug/min every 35 min pain
relieved or systolic arterial pressure <100 mmHg
pain-free for 1224 h Topical or oral nitrates replace the
IV nitroglycerin

Beta blockers

IV followed by oral beta blockers heart rate of 5060


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

Deep & visceral pain (heavy, squeezing, and


crushing; stabbing, burning)

vigorous physical exercise, emotional stress, or a medical


or surgical illness

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 1015
mmHg

laboratory findings

Electrocardiogram

total occlusion of an epicardial coronary artery STsegment 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 48 h and
generally returns to normal by 4872 h (CK activity
>=2.5 suggest MI)

Initial management

Prehospital care

Management in the emergency department

Aspirin, buccal absorption of a chewed 160325 mg


tablet
Hypoxemia O2 by nasal prongs or face mask (24
L/min) for the first 612 h reassessed
Control of discomfort

Sublingual nitroglycerin (three doses of 0.4 mg at about 5min intervals)


Morphine IV (24 mg every 5 min)
IV beta blockers

metoprolol, 5 mg every 25 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

Other etiologies

Post cardiac arrest


Refractory sustained
tacchyarrhythmias
Pulmonary embolus
Severe valvular heart
disease

Critical aortic / mitral


stenosis
Acute severe aortic /
mitral regurgitation

RV failure
Refractory sustained
bradyarrhythmias
Toxic metabolic

Beta blocker/CCB
overdose
Severe acidosis &
hypoxemia

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

90110 beats/min

Systolic BP <90 mmHg


+ narrow pulse
pressure (<30 mmHg)
quiet precordium +
weak apical pulse

Tachypnea, CheyneStokes 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 hearts 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

Electrocardiography

ST elevation and evolving Q waves is usually diagnostic of acute


MI

Brain natriuretic peptide levels > heart failure as the


etiology
X ray

systolic and diastolic ventricular dysfunction and valvular lesions

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

Nitrates

Sublingual nitroglycerin (0.4 mg x 3 every 5 min) IV


nitroglycerin, commencing at 510 ug/min

Morphine

Furosemide <=0.5 mg/kg

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

Physical Methods

IV recombinant brain natriuretic peptide (nesiritide)


potent vasodilator + diuretic (refractory patients & not
recommended in ischemia or MI)
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 0.250.75 ug/kg per min)


stimulate myocardial contractility + peripheral and
pulmonary vasodilation

Digitalis Glycosides

Intraaortic Counterpulsation

IABP

Treatment of Tachyarrhythmias and AtrialVentricular Resynchronization

rarely used at present

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 46 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
6090 s of CPR before the first shock

intubation with an endotracheal tube


insertion of an intravenous line