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Cardiovascular System > Chronic Ischemic Heart Disease > Flashcards

Chronic Ischemic Heart Disease Flashcards

1
Q

What is ischemic heart diseases and what is its most common manifestation?

A

A condiition of imbalance between myocardial oxygen supply and demand

Most common manifestation = angina pectoris

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2
Q

What influences myocardial oxygen supply?

A

Coronary perfusion pressure

Coronary vascular resistance

External compression

Intrinsic regulation

Local metabolites

Endothelial factors

Neural innervation

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3
Q

What influences myocardial oxygen demand?

A

Wall stress

Heart rate

Contractility

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4
Q

What percentage of oxygen is extracted from blood that travels through the coronary circulation?

A

75%

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5
Q

Myocardial oxygen supply depends on…

A

Oxygen content of blood and coronary blood flow

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6
Q

Coronary flow is directly proportional to _____ _______ and inversely related to _____ _______ ______

A

perfusion pressure; coronary vascular resistance

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7
Q

Perfusion pressure in the heart is dependent on _______ pressure

A

diastolic

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8
Q

What is the resting coronary flow?

What percentage of cardiac output is this?

A

225ml/min

4-5% of cardiac output

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9
Q

When is flow fastest?

A

Diastole > Systole

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10
Q

What processes allow autoregulation of flow?

A
  • Metabolic factors (adenosine, lactate, pH)
  • Sympathetic nervous system
    • alpha-1 receptors - constriction and increased HR
    • beta-2 receptors - dilation (minor)
    • Over ridden by metabolic regulation
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11
Q

Smaller arteries derived from epicardial arteries supply which part of the heart?

A

Supply the inner layers of muscle and feed the subendocardial plexus

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12
Q

Why is flow to the endocardium limited during systole

A

Compressive forces are greater in the subendocardium

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13
Q

How does increased heart rate and contractility affect oxygen requirement

A

Increases oxygen requirement

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14
Q

How is wall stress calculated?

A

Laplace’s law

Wall stress = Pxr/2h

Pressure x radius/(2x thickness)

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15
Q

What is wall stress?

A

Tangential force acting on the myofibers tending to pull them apart

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16
Q

What is coronary flow reserve?

A

The maximal increase in blood flow achievable above normal resting flow (increase in demand for oxygen causes arterioles to dilate)

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17
Q

What percentage of obstruction is enough to overcome the saving effects of coronary flow reserve?

A

>90% obstruction - distal perfusion pressure is not able to maintain normal resting blood flow

(>70% obstruction - distal perfusion pressure is not sufficient to sustain increased flow during periods of increased demand)

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18
Q

What factors decrease myocardial distribution of blood flow with an obstruction during exertion?

A
  • Reduced perfusion pressure
  • Elevated LV end-diastolic pressure with exertion impedes subendocardial flow
  • Increased heart rate decreases time during diastole (when subendocardium recieves blood flow)
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19
Q

What ECG changes are associated with subendocardial ischemia?

A

ST-segment depression

T wave inversion

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20
Q

What are collateral blood vessels and what is there function?

A
  • Vascular channels that interconnect epicardial arteries
  • Help to supply blood flow to ischemic regions caused by stenosis or occlusion of epicardial arteries
  • Normally closed and non-functional because of lack of pressure gradient to drive flow
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21
Q

How does endothelial dysfunction contribute to ischemia?

A
  • Inappropriate vasoconstriction due to imparied release of endothelial vasodilators
  • Loss of normal anti-thrombotic properties
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22
Q

What are the main consequences of Ischemia?

A
  • Inadequate oxygenation
    • Reduced generation of ATP
    • consequent elevation in diastolic pressure → Pulmonary congestion
  • Local accumulation of meataboic waste products
    • Can activate peripheral pain receptors
    • Precipitates arrhythmias
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23
Q

What is stable angina in ischemic syndromes?

A

A predictable transient chest discomfort with exertion or emotional stress due to a fixed, obstructive plaque in one or more arteries

Causes innapropriate vasoconstriction contributing to reduced oxygen supply

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24
Q

What is unstable angina associated with ischemic syndromes?

A
  • Sudden increase in ischemic episodes, occuring with lesser degrees of exertion
  • Results from rupture of an unstable plaque with subsequent platelet aggregation and thrombosis
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25
Q

What is variant angina in ischemic syndromes?

A
  • Episodes of focal coronary artery spasm in the absence of atherosclerotic lesions
  • Also known as Prinzmetal’s angina
  • Often occurs at rest
26
Q

What is silent ischemia?

What is syndrome X?

A

Silent Ischemia: episodes of cardiac ischemia that sometimes occur in the absence of discomfort or pain

Syndrome X: Patients with typical signs of angina who have no evidence of significant athersclerotic stenoses

27
Q

Describe the quality and location of discomfort associated with chronic stable angina

A
  • Pressure, discomfort, tightness, burning, heaviness in chest
  • Usually diffuse, most often located in the retrosternal area or precordium
28
Q

What are some accompanying symptoms with Chronic stable angina?

A

Tachycardia, diaphoresis, nausea - due to sympathetic and parasympathetic activation

29
Q

What are the ECG readings associated with chronic stable angina?

A

During ischemia, ST segment depression and T wave inversion

Sometimes ST segments elevations are seen indicative of more severe transmural ischemia (intense vasospasm of variant angina)

30
Q

How do you diagnose chronic stable angina?

A

Stress testing - provocative exercise or pharmacological stress tests

Standard exercise stress test - monitor ECGs during treadmill exercise

Pharmacological stress test - uses dobutamine (increases myocardial O2 demand) or adenosine (coronary vasodilation)

31
Q

How are lesions visualized in chronic stable angina?

A

Visualized radiographically following the injection of a radiopaque contrast media into the artery

32
Q

Goals of IHD therapy

A

Decrease frequency of anginal attacks

Prevent acute coronary syndromes such as MI

Slow disease progression and prolong survival

33
Q

Anti- Angina therapy

A

Decrease O2 demand

Increase O2 supply

34
Q

Nitrates MOA

A
  • Enzymatically denitrated in smooth muscle - converted to NO
  • NO activates guanylyl cyclase increasing cGMP
  • cGMP activates protein kinase
  • Kinase phosphorylates targets leading to decreased calcium and phosphorylation of myosin
35
Q

What effects do Nitrates have on the ischemic heart?

A
  • Increase venous capacitance (decrease preload)
  • Small reduction in systemic arterial blood pressure
  • Coronary dilator
36
Q

How do nitrates cause reflex tachycardia

A

Increased contractility due to reduction in blood pressure

37
Q

How is nitroglycerin inactivated?

A

High capacity organic nitrate reductase in the liver - low bioavailability due to extensive 1st pass metabolism

38
Q

Which nitrate is metabolized to its active form?

A

Isosorbide dinitrate is metabolized by liver to mononitrate form: Mononitrate is biologically active

39
Q

How are nitrates administered?

A

Administered sublingually as rapid dissolvable tablets or aerosol spray - fast onset and short duration of action

40
Q

How are nitrates used in cronic therapy?

A

Nitrates provide prophylaxis against angina episodes in patients with more than occaisonal angina

41
Q

What are differences between Isosorbide Dinitrate, Isosorbide Mononitrate and Nitroglycerin?

A
  • Isosorbide Dinitrate
    • 25% orally bioavailable
    • Metabolized to mononitrate form that is active
  • Isosorbide Mononitrate
    • No 1st pass metabolism
    • Half life is about 5 hours
  • Nitroglycerin
    • Orally as controlled release tablets
    • Available as a patch and ointment/paste applied to skin
42
Q

How are Nitrates associated with tolerance?

A

Complete tolerance can develop if used continually for more than a few hours - reverses rapidly (24 hours after stopping drug)

43
Q

How do you overcome tolerance in treatment with Nitrates?

A

Use smallest effective dose

Schedule nitrate-free period of at least 8 hours to reduce or prevent tolerance particularly with patches

44
Q

Adverse effects of nitrates

A
  • Due to cardiovascular actions
    • Headache
    • Hypotension
    • Reflex tachycardia
    • Flushing
45
Q

How do ß-adrenergic receptor blockers work?

A
  • Exert anti-anginal effect primary by reducing oxygen demand
    • Decrease the force of ventricular contraction and heart rate due to blockade of effects of endogenous catecholamines on ß1 receptors
46
Q

What are non-selective ß-blockers?

What are the selective ß blockers?

A
  • Non-selective
    • Propanolol; timolol
  • ß1-selective antagonists
    • Metoprolol, atenolol
47
Q

What are ß-blockers effects on the ischemic heart?

A
  • Decrease oxygen demand
  • Small increase in oxygen supply to ischemic areas
  • Decrease cardiac output → increase in preload that can result in increased wall tension
48
Q

ß-blockers - adverse effects and contraindications

A
  • Patients with significant obstructive airway disease
  • Not used in patients with acutely decompensated heart failure
  • Patients with marked bradycardia or heart block
  • Patients with insulin treated diabetes
  • Adverse effects: fatigue, sexual dysfunction
49
Q

Two types of calcium channel blockers?

A

Dihydropyridines and Non-Dihydropyridines

50
Q

What drugs are Dihydropyridines? What do they do?

A

Nifedipine and amlodipine

  • Potent vasodilators
  • Decrease oxygen demand
  • Increases oxygen supply by coronary vasodilation
  • Potent agents for relief of vasospasm
51
Q

What drugs are non-dihydropyridines? What do they do?

A

Verapamil and diltiazem

  • Vasodilators (less potent than dihydropyridines)
  • Decrease oxygen demand by reducing the force of contraction and heart rate
  • Verapamil, diltiazem
52
Q

Adverse effects of calcium channel blockers (and the specific drugs for each)

A
  • Headache, flushing
  • Decrease contractility (V, D)
  • Bradycardia (V, D)
  • Edema (especially N, D)
  • Constipation (especially V)
53
Q

There are potential benefits of combining a ______ with a __ ________

A

Nitrate with a ß blocker

ß blockers prevent reflex increase in heart rate and contractility produced by nitrates

Nitrates prevent potential increase in wall tension produced by ß blockers

54
Q

Care should be taken in combining a ß blocker with a ________________

A

nondihydropyridine calcium blocker

Additive negative inotropic effect can cause excessive cardiodepression

55
Q

What is the function and MOA of Ranolazine?

A

Decreases the frequency of anginal episodes and increases exercise capacity

Inhibits the late sodium current (INa+) in cardiac myocytes (blocks ion channel allowing calcium to come into cell)

56
Q

What types of medical therapy are used to prevent acute cardiac events?

A

Antiplatelet therapy - platelet aggregation and thrombosis are key elements in the pathophysiology of acute MI and unstable angina

Lipid-regulating therapy - HMG-CoA reductase inhibitors (statins)

57
Q

In antiplatelet therapy if asprinin is contraindicated, what else can be used?

A

ADP P2Y12 receptor blockers

58
Q

How is revascularization achieved?

A

Percutaneous coronary intervention (PCI)

Coronary artery bypass graft surgery (CABG)

59
Q

What is PCI?

A

Percutaneous Coronary intervention (including percutaneous transluminal coronary angioplasty (PTCA))

Coronary stents including drug-eluting stents reduce the rate of restenosis (also balloon tipped catheters)

60
Q

What is CABG?

A

Involves grafting portions of a patient’s native blood vessel to bypass an obstructed artery

  • Use of native veins
  • Arterial grafts

Cardiovascular System (35 decks)

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