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HMS Homeostasis I > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Normal A-aDO2

A

0.3 x age or below

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2
Q

How do you treat ischemic heart disease?

A
  • Sublingual Nitroglycerin
  • Beta blocker
  • Calcium channel blocker
  • Ranolazine
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3
Q

stunned myocardium

A

Tissue that, after suffering an episode of severe acute, transient ischemia (but not necrosis), demonstrates prolonged systolic dysfunction even after the return of normal myocardial blood flow.

In general, the magnitude of stunning is proportional to the degree of the preceding ischemia, and this state is likely the pathophysiologic response to an ischemic insult that just falls short of causing irreversible necrosis.

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4
Q

Hibernating myocardium

A

Tissue that manifests chronic ventricular contractile dysfunction due to a persistently reduced blood supply, usually because of multivessel CAD. In this situation, irreversible damage has not occurred and ventricular function can promptly improve if appropriate blood flow is restored.

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5
Q

Stable angina

A

Predictable, transient chest discomfort during exertion or emotional stress. It is generally caused by fixed, obstructive atheromatous plaque in one or more coronary arteries

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6
Q

Stunned and hibernating myocardium contrast poorly when imaged (e.g., by echocardiography or contrast angiography) and can appear . . .

A

. . . indistinguishable from irreversibly infarcted heart muscle. However, they can be differentiated from necrotic regions by special imaging studies

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7
Q

Whether myocardium is simply stunned or hibernating vs infarcted influences the decision of whether or not to. . .

A

. . . undertake mechanical reperfusion procedures (percutaneous or surgical), because stunned or hibernating myocardium would be expected to improve with mechanical revascularization, whereas truly infarcted myocardium would not.

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8
Q

Flavors of angina

A
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9
Q

Silent ischemia

A

Episodes of cardiac ischemia sometimes occur in the absence of perceptible discomfort or pain. Can occur in patients who on other occasions experience typical symptomatic angina, or it may be the only manifestation of CAD.

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10
Q

Syndrome X

A

Patients with typical symptoms of angina pectoris who have no evidence of significant atherosclerotic coronary stenoses on coronary angiograms.

Some of these patients may show definite laboratory signs of ischemia during exercise testing

It is thought to be the result of pathology of resistance vessels or microvascular dysfunction, neither of which can be visualized on coronary angiography. Tends to have better prognosis than typical CAD.

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11
Q

Levine sign

A

Clenched first over sternum, as if defining the constricting discomfort by that tight grip. Indicates angina

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12
Q

Pathophysiologic findings of acute myocardial ischemia

A
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13
Q

Ischemia on ECG

A
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14
Q

Standard Exercise Testing

A

During this test, the patient exercises on a treadmill or a stationary bicycle to progressively higher workloads and is observed for the development of chest discomfort or excessive dyspnea.

The heart rate and ECG are continuously monitored, and blood pressure is checked at regular intervals. The test is continued until angina develops, signs of myocardial ischemia appear on the ECG, a target heart rate is achieved.

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15
Q

‘markedly positive’ (as opposed to just ‘positive’) exercise stress test

A
  1. ischemic ECG changes develop in the first 3 minutes of exercise or persist 5 minutes after exercise has stopped
  2. the magnitude of the ST segment depressions is >2 mm
  3. the systolic blood pressure abnormally falls during exercise
  4. high-grade ventricular arrhythmias develop
  5. the patient cannot exercise for at least 2 minutes because of cardiopulmonary limitations
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16
Q

Nuclear Imaging Studies

A

Radionuclide (commonly either a technetium-99m-labeled compound or thallium-201) is injected intravenously at peak exercise, after which imaging is performed. The radionuclide accumulates in proportion to the degree of perfusion of viable myocardial cells. Therefore, areas of poor perfusion appear as ‘cold spots’

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17
Q

Pharmacologic Stress Tests

A

For patients unable to exercise (e.g., those with hip or knee arthritis), pharmacologic stress testing can be performed instead using various agents, including the inotrope dobutamine (which increases myocardial oxygen demand by stimulating the heart rate and force of contraction) or the vasodilators dipyridamole or adenosine.

These pharmacologic interventions are coupled (in place of exercise) with nuclear imaging or echocardiography

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18
Q

Organic nitrates

A
  • ↓ Myocardial O2 demand
  • ↓ Preload (venodilatation)
  • ↑ O2 supply
  • ↑ Coronary perfusion
  • ↓ Coronary vasospasm
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19
Q

β-Blockers

A
  • ↓ Myocardial O2 demand
  • ↓ Contractility
  • ↓ Heart rate
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20
Q

Calcium channel blockers (agent specific)

A
  • ↓ Myocardial O2 demand
  • ↓ Preload (venodilatation)
  • ↓ Wall stress (↓BP)
  • ↓ Contractility (V, D)
  • ↓ Heart rate (V, D)
  • ↑ O2 supply
  • ↑ Coronary perfusion
  • ↓ Coronary vasospasm
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21
Q

Ranolazine

A

↓ Late phase inward sodium current

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22
Q

Calcium channel blockers (general description)

A

Antagonize voltage-gated L-type calcium channels, but the actions of the individual drugs of this group vary.

  • The dihydropyridines are vasodilators
  • Nondihydropyridines reduce contractility and slow HR
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23
Q

Short-acting vs long-acting calcium channel blockers

A

In meta-analyses of randomized trials, short-acting blockers have been associated with an increased incidence of MI and mortality. The adverse effect may relate to the rapid hemodynamic effects and blood pressure swings induced by the short-acting agents.

So use the long ones instead!!

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24
Q

Ranolazine mechanism

A

It is believed to inhibit the late phase of the action potential’s inward sodium current (INa+) in ventricular myocytes.

That late phase tends to be abnormally enhanced in ischemic myocardium, and the associated increased sodium influx results in higher-than-normal intracellular Ca++. This calcium overload is thought to result in impaired diastolic relaxation and contractile inefficiency.

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25
Q

Clopidogrel

A

A thienopyridine. Novel antiplatelet agents that block the platelet P2Y12 ADP receptor, thereby preventing platelet activation and aggregation.

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26
Q

When revascularization is pursued

A
  1. the patient’s symptoms of angina do not respond adequately to antianginal drug therapy
  2. unacceptable side effects of medications occur
  3. the patient is found to have high-risk coronary disease for which revascularization is known to improve survival
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27
Q

Percutaneous transluminal coronary angioplasty

A

A procedure performed under fluoroscopy in which a balloontipped catheter is inserted through a peripheral artery (usually, femoral, brachial, or radial) and maneuvered into the stenotic segment of a coronary vessel, then inflated to dilate the vessel and removed.

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28
Q

Placement of CA stent

A
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29
Q

Coronary Artery Bypass Surgery

A
30
Q

Concentric vs eccentric hypertrophy

A
31
Q

Concentric left ventricular hypertrophy due to systemic hypertension often results in. . .

A

. . . Increase in “upstream” pressure in the pulmonary capillaries, which may lead to pulmonary edema

32
Q

Acute Coronary Syndrome

A

Characterized by unstable angina and high risk of heart attack

33
Q

Things that cause heart attack

A
  1. Thrombosis
  2. Embolism
34
Q

Heart Attack vs Heart Failure vs Cardiac Arrest

A

All different

Heart attack is local ischemia and infarction

Heart failure (diastolic or systolic) is inability to meet circulatory demands

Cardiac Arrest is HR of 0

35
Q

The continuum of acute coronary syndromes

A

Ranges from Unstable Angina at one end to ST elevation MI (STEMI) at the other

Non-ST elevation MI (NSTEMI) is somewhere in the middle

Unstable Angina > NSTEMI > STEMI

36
Q

Endogenous protection from occlusive thrombosis (5)

A

(1) Inactivation of thrombin by antithrombin (AT), the effectiveness of which is enhanced by binding of AT to heparan sulfate.
(2) Inactivation of clotting factors Va and VIIIa by activated protein C (protein C*), an action that is enhanced by protein S. Protein C is activated by the thrombomodulin (TM)–thrombin complex.
(3) Inactivation of factor VII/tissue factor complex by tissue factor pathway inhibitor (TFPI).
(4) Lysis of fibrin clots by tissue plasminogen activator (tPA).
(5) Inhibition of platelet activation by prostacyclin and NO.

37
Q

Things That Inactivate Clotting Factors

A

Antithrombin

Protein S

Protein C

Tissue factor pathway inhibitor (TFPI)

38
Q

Things that lyse thrombus

A

tPA ⇒ Plasmin

tPA comes from endothelium in response to pro-clotting signals

39
Q

Virchow’s Triad

A
40
Q

Relation of IFNγ to plaque rupture

A

T lymphocytes elaborate γ-interferon, which inhibits collagen synthesis by smooth muscle cells and thereby interferes with the usual strength of the cap.

41
Q

The normal platelet-associated vascular response

A

vasodilation!

Platelet products stimulate endothelial NO and prostacyclin release, the influences of which predominate over direct platelet-derived vasoconstrictor.

But. . . if you have a dysfunctional endothelium. . . the platelet vasoconstriction will win out. See Virchow’s triad.

42
Q

The distinction between NSTEMI and UA

A

Based on the degree of ischemia. If there is any necrosis, call it NSTEMI. If not, call it UA.

43
Q

If a young person with no CAD risk factors presents with apparent CAD and angina, you should consider. . .

A
  • Cocaine-induced vasospasm of coronary arteries
  • Coronary emboli from mechanical or infected cardiac valves
  • Inflammation from acute vasculitis
  • Connective tissue disease
  • Spontaneous coronary artery dissection in peripartum women
44
Q

What happens in an ischemic myocardiocyte?

A
  1. Lactic acid fermentation
  2. Dysregulation of Na/K ATPase (precipitates arrhythmia)
  3. Increase in intracellular calcium and activation of calpains and calpain-mediated apoptosis
45
Q

Histologic changes of MI

A
  • Wavy myofibers: Earliest irreversible change. Appear as intercellular edema separates the myocardial cells
  • Contraction bands: Seen near the borders of the infarct: sarcomeres are contracted and consolidated and appear as bright eosinophilic belts.
  • Neutrophil infiltration
  • Coagulative necrosis: Pyknotic nuclei and bland eosinophilic cytoplasm, eventually nuclei destroyed.
  • Eventually tissue remodeling and fibrosis
46
Q

The destruction of functional myocardial cells in infarction quickly leads to. . .

A

systolic dysfunction

(and sometimes diastolic, but usually systolic)

47
Q

ischemic preconditioning

A

Clinical relevance is that patients who sustain an MI in the context of recent angina experience less morbidity and mortality

For some reason, tissue seems to be more ‘tolerant’ of ischemia. Nobody really knows why. ¯_(ツ)_/¯

48
Q

Clinical presentation of unstable angina

A
  • Any angina at rest without provocation
  • Chronic stable angina with an acute increase in frequency or severity of angina
  • New onset of severe angina without history of CAD symptoms
49
Q

Up to ___ of patients who sustain an MI are asymptomatic during the acute event

A

Up to 25% of patients who sustain an MI are asymptomatic during the acute event

50
Q

How can you tell if someone is vasoconstricted?

A

Cool, clammy skin

Seen in PAD and in myocardial infarct

51
Q

S4

A

Sound of an atrial kick into a noncompliant ventricle

52
Q

S3

A

Indicative of volume overload in the presence of failing LV systolic function

53
Q

Diagnosis of Acute Coronary Syndromes

A

On basis of:

  • Presenting symptoms
  • Suggestive ECG (usually ST elevation)
  • Serum markers of cardiac necrosis (troponin)
54
Q

When we order a troponin test, what are we really measuring?

A

Troponin consists of three subunits: TnC, TnI, and TnT. Although these subunits are found in both skeletal and cardiac muscles, the cardiac forms of troponin I (cTnI) and troponin T (cTnT) are structurally unique, and highly specific assays for their detection in the serum have been developed.

55
Q

Timecourse of biomarkers in MI

A
56
Q

CK-MB

A

Isoform of creatine kinase that is utilized mostly in the heart.

It should be noted that small amounts of CK-MB are found in tissues outside the heart, including the uterus, prostate, gut, diaphragm, and tongue.

57
Q

A patient comes in with acutely worsening CAD. What the heck do you do about it?

A
  • Set up continuous ECG
  • Bed rest
  • MONA
    • Morphine
    • Oxygen
    • Nitroglycerin
    • Aspirin
  • Metoprolol if indicated
58
Q

verapamil and diltiazem

A

Nondihydropyridine calcium channel antagonists

Decrease heart rate and contractility and act as venodilators

Reserved for those in whom ischemia persists despite β-blocker and nitrate therapies

They should not be prescribed to patients with LV systolic dysfunction, because clinical trials have shown adverse outcomes in such cases.

59
Q

Anticoagulants

A
  • Aspirin
  • Coumadin/warfarin
  • Heparin
  • Clopidogrel
  • glycoprotein (GP) IIb/IIIa receptor antagonists
60
Q

Fibrinoltyics

A
  • Recombinant tPAs: (alteplase, tPA), reteplase (rPA), and tenecteplase (TNK-tPA)
  • Streptokinase
61
Q

Successful reperfusion in acute MI is marked by

A
  • Relief of angina
  • Return of ST to baseline
  • Earlier-than-usual peaking of troponin and CK-MB
62
Q

Primary Percutaneous Coronary Intervention

A

Put a stent in there

Alternative to fibrinolysis

90 minute standard

63
Q

Adjunctive therapies for CAD patients

A
  • ACE inhibitors prevent LVH and CAD progression
  • Statins associated with lower mortality rates
64
Q

Possible complications of MI

A
65
Q

Congestive Heart Failure

A

Acute cardiac ischemia results in impaired ventricular contractility (systolic dysfunction) and increased myocardial stiffness (diastolic dysfunction), both of which may lead to symptoms of heart failure.

Signs and symptoms of such decompensation include dyspnea, pulmonary rales, and a third heart sound (S3).

66
Q

___ have particularly high rates of atherosclerotic cardiovascular disease

A

South Asians have particularly high rates of atherosclerotic cardiovascular disease

67
Q

Specific risk factors that increase atherosclerotic heart disease rates among South Asians

A
  • Higher rate of type 2 diabetes (insulin resistance is a contributing factor)
  • MetS cluster (increased abdominal adiposity, elevated blood pressure, high triglycerides, low high-density lipoprotein, high fasting blood glucose)
  • Higher rate of kidney disease
  • Higher genetic risk from CYP2C19
    *
68
Q

How to assess patient risk for heart disease

A
  • QRISK2 calculator
  • Use the International Diabetes Federation race-specific cut points for diagnosing MetS
  • Closely follow up pre-diabetic women for the development of full diabetes
  • Demonstate cultural competency when working with South Asian patients (culturally relevant diet, exercise, lifestyle recommendations)
69
Q

You are sending a patient home after recovering from an MI. What perscriptions do you want them to start to prevent a second MI?

A
  1. Aspirin
  2. Metoprolol
  3. Clopridogel or ACE inhibitor (depending on context. If thrombosis involved, clopridogel. If aldosterone antagonist indicated for heart failure, ACE inhibitor)
  4. High-dose statin
70
Q

Regions of heart supplied by specific coronary arteries

A
71
Q

Localizing ST elevations to respective coronary artery occlusions by ECG

A
72
Q

Localizing ST elevations to respective coronary artery occlusions by ECG

(table form)

A

HMS Homeostasis I (62 decks)

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