IM 3B– CARDIOLOGY: ACUTE CORONARY SYNDROME 2
Dr. Rondilla
ST-SEGMENT ELEVATION MI
 Acute myocardial infarction (AMI) is one of the most common
diagnoses in hospitalized patients in industrialized countries.
 Mortality is approximately fourfold higher in elderly patients
(over age 75) as compared with younger patients.
 When patients with prolonged ischemic discomfort at rest are
first seen, the working clinical diagnosis is that they are suffering
from an acute coronary syndrome
The 12-lead electrocardiogram (ECG)
• pivotal diagnostic and triage tool
• center of the decision pathway for management
• permits distinction of those patients presenting with ST-
segment elevation from those presenting without ST-segment
elevation
Serum cardiac biomarkers
• distinguish unstable angina (UA) from non-ST-segment
• assess the magnitude of an ST-segment elevation myocardial
infarction (STEMI)
PATHOPHYSIOLOGY : R OLE OF A CU TE P LA QU E R UPT UR E
• STEMI usually occurs when coronary blood flow decreases
abruptly after a thrombotic occlusion of a coronary artery
previously affected by atherosclerosis
• Slowly developing, high-grade coronary artery stenoses do not
typically precipitate STEMI because of the development of a
rich collateral network over time
• STEMI occurs when a coronary artery thrombus develops
rapidly at a site of vascular injury
• This injury is produced or facilitated by:
o Cigarette smoking
o Hypertension
o Lipid accumulation
o STEMI
o surface of an atherosclerotic plaque  disrupted 
exposing contents to the blood + local or systemic
response  thrombogenesis
• Mural thrombus
o forms at the site of plaque disruption, and the involved
coronary artery becomes occluded
• Histologic studies indicate that the coronary plaques prone to
disruption are those with a rich lipid core and a thin fibrous
cap
• After an initial platelet monolayer forms at the site of the
disrupted plaque, various agonists promote platelet activation
o Collagen
o ADP
o Epinephrine
o Serotonin
• agonist stimulation platelets thromboxane A2 (a potent
local vasoconstrictor)  further platelet activation +
conformational change in the glycoprotein IIb/IIIa receptor
develops a high affinity for soluble adhesive proteins potential
resistance to fibrinolysis
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 • Frequent location of the pain
• Platelet monolayer forms at the site o f the disrupted plaque o beneath the xiphoid and epigastrium
1 o Patients’ denial
o responsible for the common mistaken impression of
• Various agonists (collagen, ADP, epinephrine, serotonin) promote indigestion
2
platelet activation o Pain may radiate as high as the occipital area but not
below the umbilicus
• stimulation of platelets and thromboxane A2 • often accompanied by weakness, sweating, nausea, vomiting,
• activation of platelets by agonists promotes a conformational change in anxiety, and a sense of impending doom
3 the glycoprotein IIb/IIIa receptor • The pain of STEMI can simulate pain from:
o Acute pericarditis
• receptor develops a high affinity for soluble adhesive protein (i.e.,  Radiation of discomfort to the trapezius
integrins) such as fibrinogen o Pulmonary embolism
4
o Acute aortic dissection
o Costochondritis
• platelet cross-linking and aggregation o Gastrointestinal disorders
5 • Pain is not uniformly present in patients with STEMI
• The proportion of painless STEMIs is greater in patients with
diabetes mellitus, and it increases with age
• The amount of myocardial damage caused by coronary • In the elderly, STEMI may present as sudden-onset
occlusion depends on: breathlessness, which may progress to pulmonary edema
1. the territory supplied by the affected vessel • Other less common presentations, with or without pain:
2. whether or not the vessel becomes totally occluded • sudden loss of consciousness
3. the duration of coronary occlusion • confusional state
4. the quantity of blood supplied by collateral vessels to the • sensation of profound weakness
affected tissue • appearance of an arrhythmia
5. the demand for oxygen of the myocardium whose blood • evidence of peripheral embolism
supply has been suddenly limited • merely an unexplained drop in arterial pressure
6. endogenous factors that can produce early spontaneous
lysis of the occlusive thrombus Physical Findings
7. adequacy of myocardial perfusion in the infarct zone • Anxious and restless - unsuccessfully to relieve the pain by
when flow is restored in the occluded epicardial coronary moving about in bed, altering their position, and stretching
artery • Pallor
• Patients at increased risk for developing STEMI include those • Perspiration
with multiple coronary risk factors and those with UA • Coolness of the extremities
• Less common underlying medical conditions predisposing • Substernal chest pain persisting for >30 min + diaphoresis 
patients to STEMI : strongly suggests STEMI
o hypercoagulability • Many patients have a normal pulse rate and blood pressure
o collagen vascular diseas within the first hour of STEMI
o cocaine abuse • Anterior infarction
o intracardiac thrombi / masses that can produce coronary o ¼ of patients with sympathetic nervous system
emboli hyperactivity
o tachycardia and/or hypertension
CLINICAL PRESENTATIO N o Abnormal systolic pulsation caused by dyskinetic bulging
 In up to one-half of cases, a precipitating factor appears to be of infarcted myocardium
present before STEMI, such as vigorous physical exercise, o may develop in the periapical area within the first days of
emotional stress, or a medical or surgical illness. the illness and then may resolve
• commence at any time of the day or night • Inferior infarction
• circadian variations o ½ of patients with parasympathetic hyperactivity
o clusters are seen in the morning within a few hours of o bradycardia and/or hypotension
awakening • Other physical signs of ventricular dysfunction
• Pain is the most common presenting complaint in patients o Fourth and third heart sounds
with STEMI. o Decreased intensity of the first heart sound
o deep and visceral o Paradoxical splitting of the second heart sound
o Heavy • Dysfunction of the mitral valve apparatus
o squeezing o transient midsystolic or late systolic apical systolic murmur
o crushing may be present
o stabbing or burning • Pericardial friction rub
 It is similar in character to the discomfort of angina pectoris but o may be heard in patients with transmural STEMI at some
commonly occurs at rest, is usually more severe, and lasts time
longer. o Carotid pulse

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  often decreased in volume, reflecting reduced stroke o skeletal muscle disease
volume o trauma – intramuscular injection
• Temperature elevations up to 38°C may be observed during • MB isoenzyme of CK
the first week after STEMI o advantage over total CK that it is not present in significant
• The arterial pressure is variable concentrations in extracardiac tissue
• In most patients with transmural infarction, systolic pressure o more specific
declines by approximately 10–15 mmHg from the preinfarction • Nonspecific reaction to myocardial injury is associated with
state o Polymorphonuclear leukocytosis
o Appears within a few hours after the onset of pain
LABORATORY FINDINGS o Persists for 3–7 days
o White blood cell count often reaches levels of 12,000–
• STEMI progresses through the following temporal stages
15,000/μL
1. Acute first few hours–7 days
• Erythrocyte Sedimentation rate
2. Healing 7–28 days
o rises more slowly than the white blood cell count, peaking
3. Healed ≥29 days
during first week and sometimes remaining elevated for 1
• The laboratory tests of value in confirming the diagnosis may
or 2 weeks
be divided into four groups:
1. ECG
2. Serum cardiac biomarkers
3. Cardiac imaging
4. Nonspecific indices of tissue necrosis and inflammation

ELECTROCARDIOGRAM
• Initial stage  total occlusion of an epicardial coronary artery
 ST-segment elevation
• Most patients initially presenting with ST-segment elevation
evolve Q waves on the ECG
• A small proportion of patients initially presenting with ST-
segment elevation will not develop Q waves
o obstructing thrombus is not totally occlusive
o obstruction is transient
o if a rich collateral network is present

SERUM CARDIAC BIOMARKERS

• Serum cardiac biomarkers are released from necrotic heart
muscle after STEMI
• Cardiac biomarkers become detectable in the peripheral blood
once the capacity of the cardiac lymphatics to clear the
interstitium of the infarct zone is exceeded and spillover into
the venous circulation occurs
• The temporal pattern of protein release is of diagnostic
importance
• Criteria for AMI require a rise and/or fall in cardiac biomarker
values with at least one value above the 99th percentile of the
upper reference limit for normal individuals

Cardiac-specific troponin T and cardiac-specific troponin I

• amino-acid sequences different from those of the skeletal
muscle forms of these proteins
• not normally detectable in the blood of healthy individuals
but may increase after STEMI to levels many times higher than CARDIAC IMAGING
the upper reference limit
• measurement is of considerable diagnostic usefulness
Echocardiography
• preferred biochemical markers for MI
• Abnormalities of wall motion on two-dimensional
• with improvements in the assays, it is now possible to detect
echocardiography
concentrations <1 ng/L in patients without ischemic-type
• are almost universally present
chest discomfort
• Early detection of the presence or absence of wall motion
abnormalities by echocardiography
Creatine Phopsphokinase
o can aid in management decisions, such as whether the
• CK rises within 4–8 h, generally returns to normal by 48–72 h
patient should receive reperfusion therapy
• Important drawback of total CK measurement is its lack of
• Echocardiographic estimation of left ventricular (LV) function
specificity for STEMI
o useful prognostically
• CK may be elevated with

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 o detection of reduced function serves as an indication for
therapy with an inhibitor of the renin-angiotensin-
aldosterone system
• May also identify
1. RV infarction
2. Ventricular aneurysm
3. Pericardial effusion
4. LV thrombus
• Doppler echocardiography
o useful in the detection and quantitation of two serious
complications of STEMI:
1. Ventricular septal defect
2. Mitral regurgitation

Radionuclide imaging techniques

• available for evaluating patients with suspected STEMI
• used less often than echocardiography because they are more
cumbersome and lack sensitivity and specificity in many clinical
circumstances

INITIAL MANAGEMENT
PRE HOSPITAL CARE
• The prognosis in STEMI is largely related to the occurrence of
two general classes of complications:
1. electrical complications (arrhythmias)
2. mechanical complications (“pump failure”)
• Most out of hospital deaths from STEMI are due to the sudden
development of ventricular fibrillation
• The vast majority of deaths due to ventricular fibrillation occur
within the first 24 h of the onset of symptoms, and of over half
occur in the first hour

Major elements:
1. recognition of symptoms by the patient and prompt seeking
of medical attention
2. rapid deployment of an emergency medical team capable of
performing resuscitative maneuvers, including defibrillation

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3. expeditious transportation of the patient to a hospital facility
that is continuously staffed by physicians and nurses skilled in
managing arrhythmias and providing advanced cardiac life
support
4. expeditious implementation of reperfusion therapy • Rapid inhibition of cyclooxygenase-1 in platelets followed by
a reduction of thromboxane A2 levels is achieved by:
The greatest delay usually from onset of pain and the patient’s o buccal absorption of a chewed 160–325-mg tablet
decision to call for help o followed by daily oral administration of aspirin in dose of
75–162 mg

Oxygen
 Arterial O2 saturation is normal
o supplemental O2 is of limited of any clinical benefit
o not cost-effective
 Hypoxemia is present
o O2 should be administered by nasal prongs or face mask
(2–4 L/min) for the first 6–12 h after infarction
o the patient should then be reassessed to determine if
there is a continued need for such treatment

MANAGEMENT IN THE EMERGENCY DEPARTMENT

Goals for the management of patients with suspected STEMI
1. Control of cardiac discomfort
2. Rapid identification of patients who are candidates for urgent
reperfusion therapy
3. Triage of lower-risk patients to the appropriate location in the
hospital
4. Avoidance of inappropriate discharge of patients with STEMI

Overarching goal
CONTROL OF DISCOMFORT
• Minimize the time from first medical contact to initiation of
reperfusion therapy Sublingual nitroglycerin
• This may involve transfer from a non-PCI hospital to one that is • can be given safely to most patients with STEMI
PCI capable, with a goal of initiating PCI within 120 min of first • Up to three doses of 0.4 mg should be administered at about
medical contact 5-min intervals
• capable of decreasing myocardial oxygen demand
Aspirin o by lowering preload
• Essential in the management of patients with suspected STEMI • increasing myocardial oxygen supply
• Effective across the entire spectrum of acute coronary o by dilating infarct-related coronary vessels or collateral
syndromes vessels

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Intravenous nitroglycerin
• Used if there is return of chest discomfort after favorable
response to sublingual nitroglycerin
• accompanied by other evidence of ongoing ischemia
o Further ST-segment or T-wave shifts
Avoided if:
• low systolic arterial pressure (<90 mmHg)
• clinical suspicion of RV infarction
o inferior infarction on ECG
o elevated jugular venous pressure
o clear lungs
o Hypotension
• With use of phosphodiesterase-5 inhibitor for erectile
dysfunction within the preceding 24 hours
• idiosyncratic reaction to nitrates, sometimes occurs but can
usually be reversed promptly by the rapid administration of
intravenous atropine
Morphine
• very effective analgesic for the pain associated with STEMI
• may reduce sympathetically mediated arteriolar and venous
constriction
• venous pooling may reduce cardiac output and arterial
pressure
• has a vagotonic effect
• routinely administered by repetitive (every 5 min) intravenous
injection of small doses (2–4 mg)
• rather than by the subcutaneous administration of a larger
quantity because absorption may be unpredictable by the latter
route
• may cause bradycardia or advanced degrees of heart block,
particularly in patients with inferior infarction
• Side effects usually respond to atropine (0.5 mg intravenously)
• Hemodynamic disturbances usually respond promptly to
o elevation of the legs
o volume expansion with intravenous saline
Beta blockers
• useful in the control of the pain of STEMI
• control pain effectively in some patients
o diminishing myocardial O2 demand and hence ischemia
• there is evidence that intravenous beta blockers reduce the
risks of reinfarction and ventricular fibrillation
• patient selection is important when considering beta blockers
for STEMI
• Oral beta blocker therapy should be initiated in the first 24 h
for patients who DO NOT have any of the following:
1. Signs of heart failure
2. Evidence of a low-output state
3. Increased risk for cardiogenic shock
• Other relative contraindications to beta blockade
o PR interval greater than 0.24 seconds
o second- or third-degree heart block
o active asthma, or reactive airway disease
Metoprolol
• 5 mg every 2–5 min for a total of three doses
o provided the patient has a
 heart rate >60 beats/min
 systolic pressure >100 mmHg
 a PR interval <0.24 s
 rales that are no higher than 10 cm up from the
diaphragm
 Fifteen minutes after the last intravenous dose an
oral regimen is initiated of 50 mg every 6 h for 48 h,
followed by 100 mg every 12 h
Calcium Antagonists
• little value in the acute setting
• evidence that short-acting dihydropyridines may be associated
with an increased mortality risk
MANAGEMENT STRATEGIE S
12-lead ECG
• primary tool for screening patients and making triage decisions
• Candidate for reperfusion therapy
o ST-segment elevation of at least 2 mm in two contiguous
precordial leads
o ST-segment elevation of at least 1 mm in two adjacent
limb leads
LIMITATION OF INFARCTION SIZE
 The quantity of myocardium that becomes necrotic as a
consequence of a coronary artery occlusion is determined by
factors other than just the site of occlusion
 Up to one-third of patients with STEMI may achieve
spontaneous reperfusion of the infarct-related coronary
artery within 24 h and experience improved healing of infarcted
tissue
Ischemic Penumbra
 While the central zone of the infarct contains necrotic tissue
that is irretrievably lost, the fate of the surrounding ischemic
myocardium (ischemic penumbra) may be improved by:
o timely restoration of coronary perfusion
o reduction of myocardial O2 demands
o prevention of the accumulation of noxious metabolites
o blunting of the impact of mediators of reperfusion injury
Protection of the ischemic myocardium
• maintenance of an optimal balance between myocardial O2
supply and demand through pain control:
o treatment of congestive heart failure (CHF)
o minimization of tachycardia and hypertension
• extends the “window” of time for the salvage of myocardium by
reperfusion strategies
Glucocorticoids and nonsteroidal anti-inflammatory agents with
the exception of Aspirin
• should be avoided in patients with STEMI
• impair infarct healing
• increase the risk of myocardial rupture
• may result in a larger infarct scar
• increase coronary vascular resistance
• reducing flow to ischemic myocardium
PRIMARY PERCUTANEOUS CORONARY INTERVENTION
• usually angioplasty and or stenting without preceding
fibrinolysis
• effective in restoring perfusion in STEMI when carried out on an
emergency basis in the first few hours of MI
• advantage of being applicable to patients who have
contraindications to fibrinolytic therapy
• more effective than fibrinolysis in opening occluded coronary
arteries and, when performed by experienced operators in
dedicated medical centers
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• better short-term and long term clinical outcomes
• preferred when:
1. diagnosis is in doubt
2. cardiogenic shock is present
3. bleeding risk is increased
4. symptoms have been present for at least 2–3 h
5. clot is more mature and less easily lysed by fibrinolytic
drugs
• expensive in terms of personnel and facilities
• applicability is limited by its availability, around the clock, in
only in minority of hospitals
FIBRINOLYSIS
 If no contraindications are present, fibrinolytic therapy should
ideally be initiated within 30 min of presentation (i.e., doorto-
needle time ≤30 min)
• Principal goal of fibrinolysis - prompt restoration of full
coronary arterial patency
• Fibrinolytic agents:
o Tissue plasminogen activator (tPA)
o Streptokinase
o Tenecteplase (TNK)
o Reteplase (rPA)
• MOA: promoting the conversion of plasminogen to plasmin,
which subsequently lyses fibrin thrombi
• TNK and rPA are referred to as bolus fibrinolytics since their
administration does not require a prolonged intravenous
infusion
• Door to- needle time
o should ideally be initiated within 30 min of presentation
Thrombolysis in Myocardial Infarction (TIMI) grading system
Grade 0 complete occlusion of the infarct-related artery
Grade 1 some penetration of the contrast material beyond the
point of obstruction but without perfusion of the distal
coronary bed
Grade 2 perfusion of the entire infarct vessel into the distal
bed, but with flow that is delayed compared with that
of a normal artery
Grade 3 indicates full perfusion of the infarct vessel with
normal flow
Fibrinolysis
TIMI frame count
• angiographic assessment of the efficacy of fibrinolysis
• counting the number of frames on the cine film required for dye
to flow from the origin of the infarct-related artery to a
landmark in the distal vascular bed
TIMI myocardial perfusion grade
• determining the rate of entry and exit of contrast dye from the
microvasculature in the myocardial infarct zone
• tPA and the other relatively fibrin-specific plasminogen
activators, rPA and TNK
o more effective than streptokinase at restoring full
perfusion
• The current recommended regimen of tPA consists
o 15-mg bolus followed by 50 mg intravenously
o over the first 30 min
o followed by 35 mg over the next 60 min
• Streptokinase
o administered as 1.5 MU intravenously over 1h
• rPA
o administered in a double-bolus regimen consisting of a 10-
MU bolus given over 2–3 min
o followed by a second 10-MU bolus 30 min later
Clear contraindications to the use of fibrinolytic agents
1. History of cerebrovascular hemorrhage at any time
2. Non hemorrhagic stroke or other cerebrovascular event
within the past year
3. Marked hypertension (a reliably determined systolic
arterial pressure >180 mmHg and/or a diastolic pressure
>110 mmHg) at any time during the acute presentation
4. Suspicion of aortic dissection
5. Active internal bleeding (excluding menses)
Relative contraindications to fibrinolytic therapy
1. current use of anticoagulants (international normalized
ratio ≥2)
2. recent (<2 weeks) invasive or surgical procedure
3. prolonged (>10 min) cardiopulmonary resuscitation
4. bleeding diathesis
5. pregnancy
6. hemorrhagic ophthalmic condition
o hemorrhagic diabetic retinopathy
7. active peptic ulcer disease
8. history of severe hypertension that is currently adequately
controlled
9. should not receive streptokinase if that agent had been
received within the preceding 5 days to 2 years
Allergic reactions to streptokinase
• occur in ∼2% of patients who receive it
• minor degree of hypotension occurs in 4–10% of patients given
this agent
• marked hypotension rarely ,in association with severe allergic
reactions
Hemorrhage
• most frequent and potentially the most serious complication
• Hemorrhagic stroke is the most serious complication and occurs
in ∼0.5–0.9% of patients
o increases with advancing age
o with patients >70 years experiencing roughly twice the rate
of intracranial hemorrhage as those <65 years.
o Large-scale trials have suggested that the rate of
intracranial hemorrhage with tPA or rPA is slightly higher
than with streptokinase
INTEGRATED REPERFUSION STRATEGY
• Cardiac catheterization and coronary angiography should be
carried out after fibrinolytic therapy if there is evidence of either
1. Failure of reperfusion
a. persistent chest pain and ST-segment elevation >90
min), in which case a rescue PCI should be considered
2. coronary artery reocclusion
a. re-elevation of ST segments and/or
b. recurrent chest pain or
c. the development of recurrent ischemia
 recurrent angina in the early hospital course or
 positive exercise stress test before discharge), in
which case an urgent PCI
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HOSPITAL MANAGEMENT COMPLICATIONS AND THEIR MANAGEMENT
VENTRICULAR DYSFUNCTION
Activity Ventricular remodeling
• Patients with STEMI should be kept at bed rest for the first 6– • Left ventricle undergoes a series of changes in shape, size, and
12 h thickness in both the infarcted and noninfarcted segments
o increase the work of the heart during the initial hours of • Precedes the development of clinically evident CHF in the
infarction may increase the size of the infarct months to years after infarction
• Absence of complications • The overall chamber enlargement that occurs is related to the
o Within the first 24 h upright posture by dangling their size and location of the infarct, with greater dilation following
feet over the side of the bed and sitting in a chair infarction of the anterior wall and apex of the left ventricle
o Second or third day ambulating in their room with • ACE inhibitors and other vasodilators (nitrates)
increasing duration and frequency (shower or stand at the o Ameliorate progressive dilation and its clinical
sink to bathe) consequences
o Day 3 after infarction patients should be increasing their o Patients with an ejection fraction <40%
ambulation progressively to a goal of 185 m (600 ft) at least o whether or not heart failure is present, ACE inhibitors or
three times a day ARBs should be prescribed
Diet
• Nothing or only clear liquids by mouth for the first 4–12 h HEMODYNAMIC ASSESSMENT
o Risk of emesis and aspiration soon after STEMI • Pump failure is now the primary cause of in-hospital death from
• Diet Composition STEMI
o Total calories as fat ≤30% • Extent of infarction correlates well with the degree of pump
o Cholesterol content of ≤300 mg/d failure and with mortality, both early (within 10 days of
o Complex carbohydrates 50–55% of total calories infarction) and later
o not be unusually large • Pulmonary rales and S3 and S4 gallop sounds
o enriched with foods that are high in potassium, o Most common clinical sign
magnesium, and fiber, but low in sodium o Elevated LV filling pressure and elevated pulmonary
o Diabetes mellitus and hypertriglyceridemia restriction of artery pressure
concentrated sweets in the diet o characteristic hemodynamic findings
o findings may result from a reduction of ventricular
Bowel Management compliance (diastolic failure) and/or a reduction of stroke
• Bed rest and the effect of the narcotics Constipation volume with secondary cardiac dilation (systolic failure)
• Bedside commode
• Diet rich in bulk Killip (Made a classification that divides patients into 4 groups)
• Routine use of a stool softener Class (Mortality Rate)
o Dioctyl sodium sulfosuccinate (200 mg/d) Class I no signs of pulmonary or venous congestion
o If remains constipated laxative can be prescribed (0–5%)
• Safe to perform a gentle rectal examination on patients with Class II moderate heart failure
STEMI (10–20%) • rales at the lung bases
• S3 gallop
Sedation • tachypnea
• Many patients require sedation during hospitalization to • signs of failure of the right side of the heart
• venous and hepatic congestion
withstand the period of enforced inactivity with tranquility.
Class III severe heart failure
o Diazepam 5 mg (35–45%) • pulmonary edema
o Oxazepam 15–30 mg Class IV shock
o Lorazepam (0.5–2 mg) (85–95%) • systolic pressure <90 mmHg
 given three to four times daily • evidence of peripheral vasoconstriction
• Peripheral cyanosis
• mental confusion
PHARMACOTHERAPY
• oliguria
• Antiplatelet and anticoagulant therapy during the initial
phase of STEMI is based on extensive laboratory and clinical • Hemodynamic evidence of abnormal global LV function
evidence that thrombosis plays an important role in the o contraction is seriously impaired in 20–25% of the left
pathogenesis of this condition ventricle
• Primary goal of treatment with antiplatelet and anticoagulant • Cardiogenic shock
agents is to maintain patency of the infarct-related artery o Infarction of ≥40% of the left ventricle
• Secondary goal is to reduce the patient’s tendency to
thrombosis HYPOVOLEMIA
• Easily corrected condition that may contribute to the
hypotension and vascular collapse
• May be secondary to previous diuretic use, to reduced fluid
intake during the early stages of the illness, and/or to vomiting
associated with pain or medications

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CONGESTIVE HEART FAILURE TREATMENT
• Diuretic agents are extremely effective diminish pulmonary
congestion in the presence of systolic and/or diastolic heart failure
• LV filling pressure falls and orthopnea and dyspnea improve after the
intravenous administration of furosemide or other loop diuretics
• These drugs should be used with caution
• Can result in a massive diuresis with associated decreases in plasma
volume, cardiac output, systemic blood pressure, and, hence,
coronary perfusion
Nitrates
• used to decrease preload and congestive symptoms
• Oral isosorbide dinitrate
• Topical nitroglycerin ointment
• Intravenous nitroglycerin
• advantage over a diuretic of lowering preload through venodilation
without decreasing the total plasma volume
CARDIOGENIC SHOCK
• Prompt reperfusion, efforts to reduce infarct size and
treatment of ongoing ischemia and other complications of MI
appear to have reduced the incidence of cardiogenic shock from
2% to about 7%
• Only 10% of patients with this condition present with it on
admission, while 90% develop it during hospitalization
• cardiogenic shock have severe multivessel coronary artery
disease with evidence of “piecemeal” necrosis extending
outward from the original infarct zone
RIGHT VENTRICULAR INFARCTION
 One-third of patients with inferior infarction demonstrate at
least a minor degree of RV necrosis
 Clinically significant RV infarction causes signs of severe RV
failure
o jugular venous distention
o Kussmaul’s sign
o Hepatomegaly
 ST-segment elevations of right sided precordial ECG leads,
particularly lead V4R, are frequently present in the first 24 h in
patients with RV infarction
 Therapy consists of volume expansion to maintain adequate
RV preload and efforts to improve LV performance with
attendant reduction in pulmonary capillary wedge and
pulmonary arterial pressures
ARRHYTHMIAS
• Incidence of arrhythmias after STEMI is higher in patients seen
early after the onset of symptoms
• Mechanisms responsible for infarction-related arrhythmias
1. Autonomic nervous system imbalance
2. Electrolyte disturbances
3. Ischemia
4. Slowed conduction in zones of ischemic myocardium
• Most deaths from arrhythmia occur during the first few hours
after infarction, the effectiveness of treatment relates directly
to the speed with which patients come under medical
observation
Ventricular Premature Beat
• Infrequent, sporadic ventricular premature depolarizations
occur in almost all patients with STEMI and do not require
therapy
• Pharmacologic therapy is now reserved for patients with
sustained ventricular arrhythmias
• Prophylactic antiarrhythmic therapy (either intravenous
lidocaine early or oral agents later) is contraindicated for
ventricular premature beats in the absence of clinically
important ventricular tachyarrhythmias, because such
therapy may actually increase the mortality rate
• Beta-adrenoceptor blocking agents are effective in abolishing
ventricular ectopic activity in patients with STEMI and in the
prevention of ventricular fibrillation
• Hypokalemia and Hypomagnesemia are risk factors for
ventricular fibrillation in patients with STEMI
• To reduce the risk:
o serum potassium concentration should be adjusted to
approximately 4.5 mmol/L
o magnesium to about 2.0 mmol/L
Ventricular Tachycardia and Fibrillation
• First 24 h of STEMI, ventricular tachycardia and fibrillation can
occur without prior warning arrhythmias
• Routine prophylactic antiarrhythmic drug therapy is no longer
recommended
o Prophylactic use of lidocaine has not been shown to
reduce overall mortality from STEMI.
o In fact, in addition to causing possible noncardiac
complications, lidocaine may predispose to an excess risk
of bradycardia and asystole
• Sustained ventricular tachycardia that is well tolerated
hemodynamically should be treated with :
IV regimen of Amiodarone Procainamide
 bolus of 150 mg over 10 min  bolus of 15 mg/kg over 20–
 infusion of 1.0 mg/min for 30 min
6h and then 0.5 mg/min  infusion of 1–4 mg/min
• If it does not stop promptly, electroversion should be used
o Unsynchronized discharge of 200–300 J (monophasic
waveform)
o Approximately 50% of these energies with biphasic
waveforms is used immediately in patients with
ventricular fibrillation or when ventricular tachycardia
causes hemodynamic deterioration
• Ventricular tachycardia or fibrillation that is refractory to
electroshock may be more responsive after the patient is
treated with
Amiodarone Epinephrine
75–150-mg bolus 1 mg intravenously or 10 mL
of a 1:10,000 solution via the
intracardiac route
• Torsades des pointes
o May occur in patients with STEMI as a consequence of
other concurrent problems
 Hypoxia
 Hypokalemia
 Electrolyte disturbances
 Toxic effects of an agent being administered to the
patient
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 Primary ventricular fibrillation Ventricular fibrillation Supraventricular Arrhythmias
secondary to severe Sinus tachycardia Atrial flutter and
pump failure atrial fibrillation
• primary response to acute • mortality rate is  is the most common supraventricular • often secondary to
ischemia that occurs during the increased both in- arrhythmia. LV failure
first 48 h and is not associated hospital and during  If it occurs secondary to another
with predisposing factors such as long-term follow-up. cause
1. CHF • should be considered o anemia
2.Shock for electrophysiologic o Fever
3. bundle branch block study and implantation o heart failure
4.ventricular aneurysm of a cardioverter- o metabolic derangement
• long-term survival is excellent defibrillator (ICD)  primary problem should be treated
first
Accelerated Idioventricular Rhythm  Sympathetic overstimulation
 “slow ventricular tachycardia” treatment with a beta blocker is
 ventricular rhythm with a rate of 60–100 beats/min indicated
 often occurs transiently during fibrinolytic therapy at the time
of reperfusion • (+) Heart Failure – Digoxin is usually the treatment of choice
 benign and does not presage the development of classic • (-) Heart Failure – beta blockers, verapamil, or diltiazem are
ventricular tachycardia suitable alternatives for controlling the ventricular rate, as they
 Most episodes of AIVR do not require treatment if the patient is may also help to control ischemia.
monitored carefully • If the abnormal rhythm persists for >2 h with a ventricular rate
>120 beats/min, or if tachycardia induces heart failure, shock,
or ischemia (as manifested by recurrent pain of ECG changes),
a synchronized electroshock (100–200 J monophasic
waveform) should be used

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Sinus Bradycardia
• Treatment of sinus bradycardia is indicated if hemodynamic
compromise results from the slow heart rate.
• Atropine is the most useful drug for increasing heart rate and
should be given intravenously in doses of 0.5 mg initially.
• If the rate remains <50–60 beats/min, additional doses of 0.2
mg, up to a total of 2.0 mg, may be given.
• Persistent bradycardia (<40 beats/min) despite atropine may be
treated with electrical pacing
• Isoproterenol should be avoided
• complication can usually be managed with aspirin (650 mg four
times daily)
• Anticoagulants potentially could cause tamponade in the
presence of acute pericarditis
Thromboembolism
• Complicates STEMI in ∼10% of cases
• Embolic lesions are found in 20% of patients in necropsy series
• Important contributing cause of death in 25% of patients with
STEMI
• Typically occurs in association with large infarcts (especially
anterior), CHF, and an LV thrombus detected by
echocardiography
• Arterial embolism presents as a major complication
o cerebral circulation  hemiparesis
o renal circulation is compromised hypertension
• Systemic anticoagulation should be undertaken in the absence
of contraindications
• Appropriate duration of therapy is unknown
• 3–6 months is probably prudent

Left Ventricular Aneurysm

• usually used to describe dyskinesis or local expansile
paradoxical wall motion
• True aneurysms are composed of scar tissue and neither
predispose to nor are associated with cardiac rupture
• The complications of LV aneurysm do not usually occur for
Atrioventricular and Intraventricular Conduction Disturbances
weeks to months after STEMI
• Anterior wall infarction
o CHF
o In-hospital mortality rate and the postdischarge
o Arterial embolism
mortality rate of patients who have complete
o Ventricular arrhythmias
atrioventricular (AV) block in association with anterior
• Apical aneurysms are the most common and the most easily
infarction are markedly higher than those of patients who
detected by clinical examination
develop AV block with inferior infarction
• Because a pseudoaneurysm often ruptures spontaneously, it
o heart block is usually related to ischemic malfunction of
should be surgically repaired if recognized
the conduction system, which is commonly associated with
extensive myocardial necrosis
 Temporary electrical pacing provides an effective means of
increasing the heart rate of patients with bradycardia due to AV
block
 Pacing does appear to be beneficial in patients with
inferoposterior infarction who have complete heart block
associated with:
o heart failure
o Hypotension
o marked bradycardia
o significant ventricular ectopic activity
 External noninvasive pacing electrodes should be positioned
in a “demand” mode for patients with :
o sinus bradycardia (rate <50 beats/ min) that is unresponsive
to drug therapy
o Mobitz II second-degree AV block
o third-degree heart block, or
o bilateral bundle branch block (e.g., right bundle branch
block plus left anterior fascicular block

OTHER COMPLICATIONS  PPT

Pericarditis  Harrison’s
• Pericardial friction rubs
• Pericardial pain
o pain radiating to either trapezius muscle
o rarely occurs with ischemic discomfort

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