Chronic Angina Flashcards

1
Q

Clinical manifestations of stable angina

A

Strangling and anxiety, pressure, pain, constriction, heaviness, some mild or no pain, pressure and numbess upon exercise and then gone while resting. Older patients less pressure/pain more uneasiness.

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2
Q

Site of angina

A

Retrosternal, radiates into neck and lower jaw (never upper jaw) or into epigastrium (right upper quadrant)-dyspepsia, SOB, burping. Often confused with cholecystitis.

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3
Q

Differential diagnoses with angina

A

Esophageal disorders (spasm, reflux, also helped by nitro), heartburn (related to food and posture), biliary colic, costochondral pain (Titze’s syndrome), aortic dissection

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4
Q

Morning angina

A

Only in morning and not the rest of the day because heart learns to cope. Pericarditis (stabbing, postural, breathing), pulmonary embolus (pleuritic, SOB), AMI

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5
Q

Tietze’s syndrome

A

Intense sensitivity for pain but very localized to costochondral area. Very uncomfortable.

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6
Q

Physical exam of chronic angina

A

Usually appear normal, signs of atheroma (xanthomata- xanthelasma on eyelids), hypertension, peripheral vascular disease (weak peripheral pulses, cardiac conditions (aortic stenosis, HOCM-hypertrophic cardiomyopathy)

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7
Q

Cardiac appearance on physical exam

A

Ischemia (diastolic dysfunction, raised LVEDP, transient S4 esp lying on side, decreased compliance), Papillary muscle dysfunction (not typical, makes click, NESC, late SM)

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8
Q

What are the two options for anginal cause?

A

Increased demand or decreased supply.

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9
Q

What are the causes of increased myocardial oxygen demand?

A

Heart rate increase, increased systolic BP/afterload, contractility. Ex: increased sympathetic tone

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10
Q

What is the wall of la Place for wall tension?

A

T=Pxr/2h

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11
Q

Factors that influence coronary blood flow

A

Aortic diastolic pressure, coronary pressure beyond stenosis, LVEDP, heart rate (slow-longer diastole), coronary flow reserve

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12
Q

What is the only organ that gets perfused during diastole but not systole?

A

The heart. Important regarding pulse pressure.

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13
Q

How does decreased compliance affect the heart filling?

A

Makes relaxation more difficult and pressures in diastole higher.

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14
Q

How does reduced time effect curves of systolic pressure and diastolic pressure?

A

If shortened by half, area under curve will be reduced by about half, making diastolic pressure time index reduced by half.

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15
Q

How does increased end diastolic pressure effect curves of systolic pressure and diastolic pressure?

A

If increased to half of Systolic pressure, will decrease DPTI by half

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16
Q

DPTI and SPTI

A

Diastolic and systolic pressure time index. Ratio between them should be about 0.8 otherwise get ischemia.

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17
Q

What are the changes that decrease supply causing angina?

A

Emotion, cold, thrombus (fat affects arterial wall), smoking (reduced vessel radius, etc.), Primzmetal angina (vasospasm most common in women, crazy Q waves)

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18
Q

What signs are there of mixed variable threshold?

A

Increased heart rate, decreased afterload (systolic BP), contractility difficult to measure. Indicates worsening condition.

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19
Q

Double product

A

Area under diastolic and systolic pressure: DPTI and SPTI

20
Q

Canadian Cardiovascular Society Grading of Severity of the AP

A

Class I: strenuous or prolonged activity, Class II: strenuous activity brisk uphill walk, Class III: everyday activities, Class IV: at rest or minimal activity

21
Q

What tests are used to measure ischemia?

A

First: history. Then tests to measure severity. Resting EKG, stress test (ergometry), radionucleotide stress (thallium), pharmaceutical (dopamine/dipyridamole), echocardiogram/radionucleotide.

22
Q

Angina diagnosis in resting EKG and causes

A

Normal in 50% of patients, if there is CAD may see old MI, resting ST-T changes nonspecific, ST depression (rare, indicates severe disease), LBBB (always underlying disease, cardiomyopathy, HTN, CAD, etc), LVH (hypertension, AS, HOCM)

23
Q

Bayes Theorem

A

Sensitivity, sensitivity and predictive accuracy of a test depends on its prevalence in the population. In low risk, more false positives, in high risk, more sensitive.

24
Q

What is ergometry useful for

A

Severity of disease, functional limitation, prognosis. Not good for screening because prevalence is so low.

25
Q

What is the predictive value of ergometry for ST depression with chest pain?

A

~95%

26
Q

What is the predictive value of ergometry for ST depression without chest pain?

A

~80%

27
Q

Predictors of mutlivessel disease in ergometry

A

Persistent ST depression after exercise (early onset ST depression), low exercise duration, abnormal BP response.

28
Q

What is a BP drop of over 30mmHg indicative of?

A

L heart disease

29
Q

What is radionucleotide/thallium used for?

A

Better screening test for CHD, MVD and stress test for those that can’t handle exercise. More accurate localisation of ischemia. Especially useful for abnormal baseline ECG. (LVH, LBBB)

30
Q

How is the radionucleotide test performed?

A
  1. Inject tracer in exercising patient, 2. patient exercises for a minute, 3. patient lied down in imaging machine, 4. tracer taken up by working muscle so ischemic areas appear black
31
Q

Results of thallium high risk predictors

A

Multiple areas of ischemia, lung uptake of tracer (HF), left ventricle dilatation on exercise: high risk.

32
Q

What is cardiac catheterization used for?

A

Definitive diagnosis, assessment of anatomy (1,2,3 vessel disease), LV function (done by echo more now)

33
Q

Who is more likely to have single vessel disease and who probably has multiple vessel disease?

A

Young patients usually only have single disease (like 40 yo smoker), older person has multiple disease because of longstanding HTN.

34
Q

How is chronic angina managed?

A

Treat precipitating causes, exercise itself improves endothelial function. Reduction in risk factors (nonpharmacological and drugs). Revascularization (PTCA, CABG)

35
Q

How does risk relate to increasing LDL-C conentration?

A

Increases exponentially. Important for treatment of CAD-acute and chronic.

36
Q

Pharmacological treatment for coronary artery disease

A

Nitrates, beta blockers, calcium antagonists, combination therapy

37
Q

How do nitrates improve CAD?

A

For symptoms, no improved risk, may develop dependence

38
Q

How do beta blockers affect CAD?

A

Reduced MVO2 (both in rest/exercise, decrease systolic BP and afterload, contractility), Improve coronary flow (increased diastolic perfusion, increased distal coronary perfusion, favorable epi-endo shift).

39
Q

What are potential unfavorable effects of beta blockeres

A

Increased heart size and preload, increased epicardial coronary constriction. Never proven. Asthmatics can’t take it. Fatigue, impotence.

40
Q

What are the 3 types of calcium antagonists?

A
  1. Phenylalkamines (verapamil), 2. Dihydropyridines (nifedipine, amlodipine), 3. modified benzothiazepines (diltiazem)
41
Q

Verapamil usage

A

Old drug, didn’t do much in low doses but great in high doses but no patent so no studies. Similar to beta blockers.

42
Q

Nifedipine usage

A

Pure arterial vasodilator. Not that useful for angina by itself, decreases infarct size. Not used for MI but good for angina to prevent spasms. Not a very useful drug.

43
Q

Usage of diltiazem

A

Not as good as verapamil but better than nifedipine for angina. Less useful than publicized.

44
Q

Types of Revascularization in CAD

A

PTCA (catheter based: Percutaneous Transluminal Coronary Angioplasty), now everyone gets PCI. CABG

45
Q

What is PTCA used for in CAD?

A

Symptomatic treatment, effects on mortality not clear in chronic (though clear improvement in acute), few randomized trials (vs CABG). Doesn’t really make patients live longer. Medical therapy just as good.

46
Q

What are the indications for CABG?

A

Left main coronary artery disease occluded over 50%. However, can be treated with PCI with just as good results and fewer complications. TVD (triple vessel disease) with proximal LAD and LV dysfunction.