Chronic Ischemic Heart Disease Flashcards Preview

Cardiovascular System > Chronic Ischemic Heart Disease > Flashcards

Flashcards in Chronic Ischemic Heart Disease Deck (60):
1

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

A condiition of imbalance between myocardial oxygen supply and demand

Most common manifestation = angina pectoris

2

What influences myocardial oxygen supply?

Coronary perfusion pressure

Coronary vascular resistance

External compression

Intrinsic regulation

Local metabolites

Endothelial factors

Neural innervation

3

What influences myocardial oxygen demand?

Wall stress

Heart rate

Contractility

4

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

75%

5

Myocardial oxygen supply depends on...

Oxygen content of blood and coronary blood flow

6

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

perfusion pressure; coronary vascular resistance

7

Perfusion pressure in the heart is dependent on _______ pressure

diastolic

8

What is the resting coronary flow?

What percentage of cardiac output is this?

225ml/min

4-5% of cardiac output

9

When is flow fastest?

Diastole > Systole

A image thumb
10

What processes allow autoregulation of flow?

  • 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

 

11

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

Supply the inner layers of muscle and feed the subendocardial plexus

12

Why is flow to the endocardium limited during systole

Compressive forces are greater in the subendocardium

13

How does increased heart rate and contractility affect oxygen requirement

Increases oxygen requirement

14

How is wall stress calculated?

Laplace's law

Wall stress = Pxr/2h

Pressure x radius/(2x thickness)

A image thumb
15

What is wall stress?

Tangential force acting on the myofibers tending to pull them apart

16

What is coronary flow reserve?

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

A image thumb
17

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

>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)

18

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

  • 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)

19

What ECG changes are associated with subendocardial ischemia?

ST-segment depression

T wave inversion

A image thumb
20

What are collateral blood vessels and what is there function?

  • 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

21

How does endothelial dysfunction contribute to ischemia?

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

A image thumb
22

What are the main consequences of Ischemia?

  • 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

23

What is stable angina in ischemic syndromes?

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

24

What is unstable angina associated with ischemic syndromes?

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

25

What is variant angina in ischemic syndromes?

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

A image thumb
26

What is silent ischemia?

What is syndrome X?

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

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

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

28

What are some accompanying symptoms with Chronic stable angina?

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

29

What are the ECG readings associated with chronic stable angina?

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)

A image thumb
30

How do you diagnose chronic stable angina?

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

How are lesions visualized in chronic stable angina?

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

32

Goals of IHD therapy

Decrease frequency of anginal attacks

Prevent acute coronary syndromes such as MI

Slow disease progression and prolong survival

33

Anti- Angina therapy

Decrease O2 demand

Increase O2 supply

34

Nitrates MOA

  • 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

What effects do Nitrates have on the ischemic heart?

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

36

How do nitrates cause reflex tachycardia

Increased contractility due to reduction in blood pressure

37

How is nitroglycerin inactivated?

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

38

Which nitrate is metabolized to its active form?

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

39

How are nitrates administered?

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

40

How are nitrates used in cronic therapy?

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

41

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

  • 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

How are Nitrates associated with tolerance?

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

 

43

How do you overcome tolerance in treatment with Nitrates?

Use smallest effective dose

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

44

Adverse effects of nitrates

  • Due to cardiovascular actions
    • Headache
    • Hypotension
    • Reflex tachycardia
    • Flushing

45

How do ß-adrenergic receptor blockers work?

  • 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

What are non-selective ß-blockers?

What are the selective ß blockers?

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

 

47

What are ß-blockers effects on the ischemic heart?

  • 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

ß-blockers - adverse effects and contraindications

  • 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

Two types of calcium channel blockers?

Dihydropyridines and Non-Dihydropyridines

50

What drugs are Dihydropyridines? What do they do?

Nifedipine and amlodipine

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

51

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

Verapamil and diltiazem

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

 

52

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

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

 

53

There are potential benefits of combining a ______ with 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

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

nondihydropyridine calcium blocker

Additive negative inotropic effect can cause excessive cardiodepression

55

What is the function and MOA of Ranolazine?

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

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

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

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

ADP P2Y12 receptor blockers

58

How is revascularization achieved?

Percutaneous coronary intervention (PCI)

Coronary artery bypass graft surgery (CABG)

59

What is PCI?

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

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

A image thumb
60

What is CABG?

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

  • Use of native veins
  • Arterial grafts

A image thumb