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Cardiovascular System > Acute Myocardial Infarction- Zahger > Flashcards

Acute Myocardial Infarction- Zahger Flashcards

1
Q

What are the two ECG options for acute coronary syndrome?

A

ST elevation of non-ST elevation acute coronary syndrome

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2
Q

What are the biochemical marker outcomes that distinguish acute coronary syndrome with no ST elevation?

A

NSTEMI: NQMI or QwMI, or unstable Angina

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3
Q

How is an STeMI more dangerous than a non-STeMI

A

Larger infarct size if untreated, usually complete arterial occlusion, worse prognosis early on, common lethal ventricular arrhythmias, possible mechanical complications.

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4
Q

What are the dangers of a non-STeMI

A

Prevalence increases with age, worse prognosis in first year but can get worse if not treated. Many more admissions/year.

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5
Q

Pathological definition of myocardial infarction

A

Myocardial necrosis resulting from a transient or permanent decrease in coronary perfusion.

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6
Q

Flowcharg of acute MI

A

Rupture of atheromatous plaque, platelet aggregation, formation of fibrin clot, acute arterial occlusion (complete or incomplete), severe myocardial ischemia, wave front of necrosis over 6h from subendocardium (most vulnerable) to epicardium.

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7
Q

What is the appearance of an angiogram in an acute obstruction of the RCA?

A

Cut off dye, complete occlusion.

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8
Q

How does the wavefront phenomenon impact survival?

A

Early intervention means less myocardium necrosed.

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9
Q

What are the determinants of the infarct size?

A

Locatino of occlusino, severity, duration and persistence, collateral flow, metabolic state of myocardium (anemia, fever, thyrotoxicosis, preconditioning).

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10
Q

How does the location of an occlusion affect infarct size?

A

If large proximal artery more damage than distal small vesssel.

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11
Q

What is the difference between a 99% and a 100% occlusion

A

Better outcome from subtotal occlusion because at least some flow gets by. Many MI are preceded by plaque lysis and then reprofusion, rethrombosis, etc. If pain is intermittant, it means that maybe occlusion has been intermittent, so even if 14h, could be myocardium to save.

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12
Q

How does metabolic state affect infarct size?

A

Increased O2 demand so necrosis progresses faster.

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13
Q

How does preconditioning affect infarct size?

A

Repeating episodes of short ischemia prior to MI. Decreases eventual infarct size by metabolic mechanism. Protected more than those with brand new episode.

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14
Q

What follows cessation of flow in an infarct in the myocardium?

A

Immediate impairment of relaxation (because needs ATP to relax) followed by systolic dysfunction. Akinesis-dyskinesis of infarct area, hyperkinesis of remote myocardium.

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15
Q

What is the effect in myocardium/heart if large cumulative damage in MI?

A

Depressed cardiac output, elevated filling pressure, elevated pulmonary venous pressure, decreased tissue perfusion. Infarct expansion, increased wall stress, dilatation and remodeling, late development of HF (d/t LV damage).

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16
Q

Precipitating factors of development of atherosclerosis into MI?

A

Physical or mental stress leading to plaque disruption if untrained (middle aged person running to bus), surgery, infeection, hypoxia, fever, inflammation, pharmacological agents/illicit drugs.

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17
Q

How does Circadian Rhythm precipitate MI?

A

Early morning more prone to MI because of surge of catecholamines to get out bed.

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18
Q

What percentage of MI cases have antecedent angina?

A

2/3

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19
Q

Where is MI pain usually located?

A

Retrosternal, may radiate to shoulders, arms, neeck, back, lower jaw (may be limited to those site). Any pain from umbilicus to lower jaw.

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20
Q

Associated complaints with MI

A

Dyspnea, nausea/vomiting, diaphoresis, cold sweat, weakness palpitations, left hand numbness/tinging.

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21
Q

What proportion of MI cases are silent?

A

10%

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22
Q

What are differential diagnoses with MI?

A

Pericarditis, aortic dissection, pulmonary embolism, esophagitis, peptic disease, cholecystitis, musculoskeletal pain.

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23
Q

What distinguishes pericarditis from MI?

A

May have friction rub, fever, pleuritic pain worsens with inspiration.

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24
Q

What distinguishes pulmonary embolism from MI?

A

Chest X-ray, oscultation

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25
Q

How does an MI patient appear in a physical exam?

A

Distressed, pale, diaphoretic, may vomit, may have low grade fever.

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26
Q

What is the heart rate of an MI patient?

A

Slow if inferior (vagal stimulation), fast otherwise.

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27
Q

What is the blood pressure of a patient with an MI?

A

Any possible. Inferior: low BP (vagal tone).

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28
Q

What heart sounds are heard in MI patients?

A

S4 in most from poor compliance, S3 if systolic dysfunction, murmurs of MR or VSD, pericardial friction rub if pericarditis, pulmonary congestion possible.

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29
Q

When does myoglobin peak after MI?

A

Within 1-2h. Nonspecific but if negative can rule out.

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30
Q

When is the CK-MB peak after MI?

A

After 24h

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31
Q

When does CK-MB begin to rise after MI?

A

3-4h

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32
Q

When does CK-MB return to normal after MI?

A

Within 3-4 days

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33
Q

When does cardiac troponin peak after MI?

A

3-6h

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34
Q

How long does troponin stay in the system after MI?

A

7-14 days

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35
Q

What is the area under the CK-MB curve representative of?

A

Size of infarct

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36
Q

Biochemical trends after MI

A
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37
Q

What is the ST segment response to MI?

A

In STeMI: ST elevation in lead representing ischemic area (in anterior MI no waves coming at us), reciprocal changes in opposite wall. In nonSTeMI: ST depression in ischemic area, accompanied or replaced by T inversion, later may normalize.

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38
Q

What is the response of R waves after MI?

A

Progressive loss. In nonSTeMI: loss possible.

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39
Q

What is the response of Q waves following MI?

A

Negative deflection development

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40
Q

What is the response of T waves after MI

A

Inverstion followed by return of upright T waves later in some cases.

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41
Q

How is unstable angina distinguished from nonSTeMI?

A

Same EKG signs but different biochemical markers.

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42
Q

What are the diagnostic requirements to define MI?

A
  1. Rise and fall of troponin with corresponding sign, 2. ST elevation/angiography coronary thrombus of patient who died before troponin rise could be documented, 3. Following PCI (Percutaneous coronary intervention) a rise of troponin*3ULN, 4. Following CABG: a rise of troponin *5ULN and evidence of freshly occluded vessel or new Q waves.
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43
Q

What is periprocedural myocardial necrosis

A

Smaller rise in troponin not sufficient for diagnosis of AMI following PCI or CABG

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44
Q

What is the necessary but insufficient component for diagnosing AMI?

A

Troponin

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45
Q

What are the possible signs of which one of must accompany a rise in troponin to define an MI?

A

Typical symptoms, ST-T changes, new Q waves, loss of normal regional contraction or viability on noninvasive testing.

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46
Q

Universal classification of MI: Type I

A

Spontaneous MI related to ischemia d/t a primary coronary event such as plaque erosion or rupture, fissuring or dissection.

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47
Q

Universal classification of MI: Type 2

A

MI secondary to ischemia d/t imbalance btween oxygen demand and supply (eg: coronary spasm, anemia, hypotension)

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48
Q

Universal classification of MI: Type 3

A

Sudden cardiac death with symptoms of ischemia, accompanied by enw ST elevation or LBBB, or verified coronary thrombus by angiography or autopsy but death before blood samples could be obtained.

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49
Q

Universal classification of MI: Type 4a

A

MI associated with PCI

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50
Q

Universal classification of MI: Type 4b

A

MI associated with verified stent thrombosis

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51
Q

Universal classification of MI: Type 5

A

MI associated with CABG

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52
Q

Complications of acute MI

A

Extension/ischemia, arrhythmia (tachyarrhythmias, bradyarrhythmias), pericarditis, expansion/andeurysm, RV infarct, mechanical, HF, mural thrombosis

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53
Q

What is the primary complication of AMI/the most common cause of early AMI death after AMI?

A

Ventricular fibrillation (tachyarrhythmias). Common during first hours.

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54
Q

What are the types of tachyarrhythmias?

A

Ventricular fibrillation, ventricular tachycardia, ventricular premature beats, atrial fibrillation

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55
Q

What are the types of bradyarrhythmias?

A

Sinus dysfunction, AV block, junctional rhythm. Require pacing when symptomatic. More common in inferior MI

56
Q

What are some mechanisms of heart failure post MI?

A

Extensive (acute or cumulative) damage to LV myocardium (if substantial scarring, substantial CO at risk), mitral regurgitation (some patients have HF even though LV is performing well since the mitral valve is leaking), ongoing ischemia, RV infarction, mechanical complications, arrhythmias

57
Q

Definition of cardiogenic shock

A

A decrease in cardiac output d/t cardiac causes to the extent that tissue perfusion is impaired. Most serious form of HF.

58
Q

What percentage of AMI patients suffer cardiogenic shock?

A

About 6%

59
Q

What are the symptoms and signs of cardiogenic shock?

A

Decreased CO, pulmonary congestion, cold extremities, diaphoresis, hypotension, tachycardia, confusino, oliguria.

60
Q

What is the mortality rate of untreated cardiogenic shock?

A

About 100%

61
Q

What is the treatment for cardiogenic shock?

A

IABP, rapid vascularization (positive inotropes if necessary). Major principle: stabilize patient.

62
Q

What is the mortality rate of treated cardiogenic shock?

A

50%

63
Q

What is IABP (intra-aortic balloon pump)/IAB inflation/deflation?

A

In diastole, inflates and prevents blood from going up aorta and makes sure it goes into coronaries. In systole, creates a vacuum in the aorta, and sucking mechanism makes it easier for ventricle to eject blood.

64
Q

Pathophysiology of cardiogenic shock from systolic dysfunction.

A

Decreased cardiac output and stroke volume, decreased systemic perfusion and hypotension, decreased coronary perfusion pressure, compensatory vasoconstriction, fluid retention, ischemia–>progressive myocardial dysfunction.

65
Q

Pathophysiology of cardiogenic shock from diastolic dysfunction.

A

Increased LVEDP and pulmonary congestion, hypoxemia to ischemia to progressive myocardial dysfunction.

66
Q

Mechanical complications of AMI

A

Rupture of papillary muscle, cordae tendinae, severe MR. Free wall rupture, rupture of ventricular septum. Must be fixed quickly.

67
Q

What sort of MI most frequently causes mitral regurgitation?

A

Infero-posterior MI

68
Q

What are the consequences of severe mitral regurgitation post MI?

A

Sudden hypotension and pulmonary congestion (backwards flooding), a new murmur possible, not always audible (chronic situation).

69
Q

How is a post-MI mitral regurgitation diagnosed?

A

Echo (TEE)

70
Q

What is the treatment for mitral regurgitation post MI?

A

Vasodilators, mechanical ventilation, IABP, catheterization, surgery. Make it easier for ventricle to eject forward and not back.

71
Q

In which patients is rupture of ventricular septum more common?

A

Multivessel disease

72
Q

What is the result of rupture of ventricular septum?

A

New onset of heart failure and systolic murmur.

73
Q

How is ventricular septum rupture diagnosed?

A

Left-right shunt by echo or cath.

74
Q

What is the treatment for rupture of the ventricular septum?

A

Vasodilators, IABP, catheterization, surgery.

75
Q

What is the mortality rate of untreated ventricular septum rupture?

A

85% following right heart failure.

76
Q

What is the second most common cause of death of AMI in the hospital?

A

Free wall rupture

77
Q

What is the most common cause of death of AMI in the hospital?

A

Cardiogenic shock

78
Q

When does free wall rupture usually happen?

A

30-50% on the day of MI, mostly 1st week otherwise.

79
Q

What risk factors are there for free wall rupture?

A

Age, female, hypertension, first MI

80
Q

What is the usual presentation of free wall rupture?

A

EKG appears normal-sudden electromechanical dissociation. Ineffective CPR, shortness of breath, chest pain.

81
Q

What percentage of free wall rupture patients have a subacute rupture?

A

30%. Allows for rapid intervention.

82
Q

How is free wall rupture diagnosed?

A

Sudden shock, venous congestion, clear lungs, pericardial fluid on echo, blood on tap.

83
Q

What is the treatment for free wall rupture?

A

Immediate surgery.

84
Q

In what type of MI is pericarditis most common?

A

Transmural infarction

85
Q

What is the presentation of pericarditis?

A

Pleuritic chest pain, fever, friction rub, ST-T changes (some or all) during first days. Rub is diagnostic.

86
Q

What is another differential diagnosis for pericarditis?

A

Recurrent ischemia.

87
Q

Treatment of pericarditis?

A

High dose aspirin, steroids

88
Q

What is Dressler’s syndrome?

A

Late pericarditis, immune response to injury or cardiac surgery. Self-limiting.

89
Q

What percentage of infero-posterior infarction result in right ventricular infarction?

A

1/3, but clinically less

90
Q

What is the cause of right ventricular infarction shock?

A

Underfilling of left heart and septal movement into LV. RV thinner than the left so RV infarct balloons into LV and compromises LV. RV has to dilate out, prevents filling of LV. Since both ventricles are compromised, leads to shock.

91
Q

Diagnosis of right ventricular infarction

A

ST elevation in right chest leads, echo. Additional right side EKG leads.

92
Q

Treatment of right ventricular infarction

A

Reperfusion, fluids, positive inotropes

93
Q

Additional complications of AMI

A

LV aneurysm, recurrent ischemia, LV thrombus and emboli (stroke), late arrhythmias, pulmonary embolism (as a result of immobility)

94
Q

What is PCWP?

A

Pulmonary capillary wedge pressure, a stand-in for left atrial pressure.

95
Q

What happens when PCWP is high and there is low tissue perfusion?

A

Pulmonary edema. Give diuretics and vasodilators.

96
Q

What happens when PCWP is high and there is severe hyperperfusion?

A

Cardiogenic shock. Give vasodilators if normal BP or vasopressors if low BP.

97
Q

What happens if PCWP is low and there is severe hypoperfusion?

A

Hypovolemic shock. Give fluids.

98
Q

What should be done for prehospital AMI management?

A

Rapid defibrillation, thrombolytic therapy, particularly if prolonged evacuation, or facilitation of angioplasty by IIb/IIIa antagonists.

99
Q

Management of AMI in the ER

A

Bed rest, continuous EKG monitoring beginning within 10 mins of arrival, oxygen, venous access, analgesics as necessary (morphine), sublingual nitroglycerin (unless SBP

100
Q

Two modalities of reperfusion therapy

A

Pharmacologic (thrombolysis), primary (direct) angioplasty.

101
Q

What is the purpose of reperfusion therapy?

A

Rapid restoration of normal arterial flow and tissue perfusion, limiting infarct size.

102
Q

Indications for reperfusion therapy

A

Typical symptoms lasting

103
Q

What are some types of thrombolytic agents?

A

Streptokinase, tPA (tissue plasminogen activator, alteplase), Reteplase (rPA), Tenecteplace (TNK-tPA)

104
Q

How does streptokinase (STK) compare to tPA as a thrombolytic?

A

tPA is more potent but shorter acting and causes more hemorrhage and is a lot more expensive, has more fibrin specificity, but less antigenic (STK may cause antibody response and hypotension).

105
Q

Absolute contraindications for fibrinolysis in STeMI

A

Any prior intracranial hemorrhage, known cerebral vascular lesion (eg. arteriovenous malformation), knowon intracranial neoplasm (primary or metastatic), ischemic stroke within 3 months unless within 3 hours. Suspected aortic dissection, active bleeding or diathesis except menses, significant closed head/facial trauma within 3 months.

106
Q

Relative contraindications for fibrinolysis in STeMI

A

History of chronic, severe, poorly controlled hypertension (risk of intracranial hemorrhage), severe uncontrolled HTN on presentation, history of ischemic stroke over 3 months ago dementia or known pathology otherwise, traumatic or prolonged CPR or major surgery in an area of bleeding difficult to control.

107
Q

Relative contraindications for STeMI fibrinolgysis

A

Internal bleeding (5 days ago, only works once), pregnancy, active peptic ulcer, current anticoagulant use.

108
Q

What is the best emergency medication for AMI?

A

Aspirin and streptokinase together.

109
Q

Signs of reperfusion bedside

A

Rapid resolution of symptoms, of ST elevation (>70% decline=successful, 30-70% is partial), rapid rise of cardiac markers, reperfusion arrhythmias (IVR accelerated with no adverse reprucussions, temporary)

110
Q

Pros of thrombolytic therapy

A

Universally acailable, no special expertise/equipment necessary, rapid administration including prehospital.

111
Q

Cons of thrombolytic therapy

A

Imperfect reperfusion rates, incomplete recanalization. Risk of bleeding, particularly intracranial. Almost always have residual coronary artery tightening, will need to be stented later to prevent occlusion.

112
Q

Pros of direct (primary) PCI

A

High reperfusion rates, good recanalization especially with stents, low bleeding risk

113
Q

Cons of direct (primary) PCI

A

Mandatory delay (more time for angiography than IV drip), expertise and equipment needed, not universally available.

114
Q

What is the maximal accepted time for thrombolysis from door to needle?

A

30 minutes

115
Q

What is the maximal accepted time for PPCI from door to balloon?

A

90 minutes

116
Q

STeMI treatment flowchart

A
117
Q

Is PCI performed after non reperfused MI?

A

No

118
Q

What medications can be given for AMI?

A

Antiplatelets, antirhombotics, ACE inhibitors, beta blockers, Statins, Nitrates, Ca channel blockers

119
Q

Oral antiplatelet medication for AMI

A

Aspirin reduces 30d mortality by 25%. Long term. Clopidogrel only for one year unless aspirin intolerant, then used instead.

120
Q

IV platelet GP IIb/IIIa receptor antagonists

A

More potent platelet inhibitors than aspirin or clopidogrel. Mainly effective in reducing PCI complications.

121
Q

Available anticoagulant therapy agents

A

Unfractionated heparin, LMWHeparin, Fondaprinux, Bivalirudin

122
Q

How is unfractionated heparin used?

A

For STeMI patients before primary PCI, with thrombolysis or in a nonreperfused MI. Given in NSTE ACS to reduce complications until angiography or discharge.

123
Q

What are the benefits of LMWHeparin?

A

More potent thrombin inhibitor, stable anticoagulation, no need for lab monitoring, less thrombocytopenia, easier to administer.

124
Q

What is the choice antithrombotic post-MI and when is it not good?

A

Enox/enoxaparin

125
Q

What is fondaparinux?

A

Synthetic factor Xa inhibitor, one step further than heparin, smaller molecule. Doesn’t affect thrombin just factor Xa. Reduces bleeding, reduces mortality but not standard of care because problem for cath lab patients.

126
Q

What is bivalirudin?

A

Direct thrombin inhibitor, good agent for STeMI and NSTeMI. Better than combination of heparin and GPIIb/IIIa inhibitor.

127
Q

What is the standard medical management of AMI?

A

ACE inhibitors always in absence of contraindications, beta blockers for anyone with LV systolic dysfunction unless contraindication.

128
Q

What is the effect of ACE inhibitors?

A

Stops ventricular remodeling (from volume expansion) and dilation and thus HF.

129
Q

Which AMI patients should receive statins?

A

All regardless of LDL.

130
Q

What is the decrease in mortality from statins?

A

20-25%

131
Q

Which AMI patients should receive calcium channel antagonists?

A

Patients with contraindications for beta blockers (asthmatics) to treat ischemia or tachycardia.

132
Q

Which AMI patients receive nitrates?

A

Especially with large MI for 24-48h. Not with RVMI nor hypotension. Mostly symptomatic, no mortality benefit.

133
Q

What is the role of coronary angiography post STeMI in high risk patients?

A

Recurrent ischemia, hemodynamic instability, heart failure, significant LV dysfunction, ischemia on predischarge non-invasive testing

134
Q

What is the more general strategy for coronary angiography post STeMI?

A

Cath most patients to define anatomy and perform revascularization if possible (artery hypothesis). Unproven with STeMI but better in nonSTeACS. Proven to have better endpoints.

135
Q

Determinants of post MI prognosis

A

Age, extent of cumulative myocardial damage, extent of residual ischemia, extent of coronary disease, arrhythmias, comorbidity (esp diabetes).

Cardiovascular System (28 decks)

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