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Cardiopulmonary PT > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What are 5 types of cardiovascular diseases?

A 
Coronary artery disease
Ischemic heart disease
Hypertension
Peripheral vascular disease
Stroke (generally ischemic)
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2
Q

T/F: CVD remains leading cause of death in U.S.

A

True

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3
Q

What are clinical signs and symptoms of CAD?

A

Can have obstruction but doesn’t affect heart function.

Depends on severity of obstruction per vessel and the number of vessels involved

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4
Q

What are main coronary arteries to the heart?

A

Right coronary
LAD
Circumflex

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5
Q

What are determinants of myocardial blood flow?

A

Diastolic BP
Resistance
Vasomotor tone
LV end diastolic volume

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6
Q

What is atherosclerosis?

A 
Atherosis= fatty streak
Sclerosis= fibrotic

Active process involving molecular signals that produce altered cellular behavior as well as endothelial dysfunction and subsequent inflammatory response.

Lipid deposition is a fundamental part of this process

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7
Q

What is progression of atherosclerosis?

A

Fatty streaks: lipid deposits in aorta and coronary arteries
Fibrous plaque: increased levels of collagen, destruction of medial elastin, changes in composition of fibrous proteins (stable or unstable, progression based on risk factors)

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8
Q

What is the atherogenesis chain of effect (6 steps)?

A

1) endothelial injury with increased infiltration of atherogenic lipoprotein
2) Sub endothelial retention and modification of LDL, VLDL leads to intimal entry of monocytes and T lymphocytes
3) Subintimal diffusion of monocytes to macrophage which internalize LDL, transform into foam cells (First stage of fatty streak development)
4) Hemodynamic stress or inflammatory process activate Platelet-derived growth factor or PDGF which will stimulate Smooth Muscle Cells ending by having atherosclerotic plaque separated from blood by fibrous cap
5) Death of foam cells by necrosis or apoptosis lead to necrotic core formation
6) Rupture of fibrous cap, exposure of thrombogenic substrate, subsequent arterial thrombosis

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9
Q

What is etiology of HTN?

A

Essential/Primary: occurs in absence of disease, areteriole resistance
Non-essential/Secondary: occurs in presence of disease
Labile: comes and goes

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10
Q

What is PT implications for high BP?

A

Get medical clearance if resting SBP>200 mmHg or DBP >105 mmHg

Terminate exercise if SBP >250 or DBP >115

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11
Q

What are side effects for BP medication?

A

Orthostatic hypotension

With activity: drop in BP 20 mmHg SBP or 10 mmHg systolic AND diastolic

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12
Q

What are considerations for HTN and exercise?

A

avoid Valsalva

Aerobic exercise: 4-7x/week, 30-45 minutes, 60-85% HR max, RPE 12-16

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13
Q

What is presentation of Ischemic heart disease?

A

Depends on rate of progress of atherosclerosis and has different presentations

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14
Q

What are possible presentations of IHD?

A 
Chronic stable angina
Unstable angina
Myocardial infarction
Silent ischemia
Arrythmia
Sudden death
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15
Q

What are signs and symptoms of MI for men?

A

Pain radiating down left arm
Crushing pain: hard to breathe, elephant on chest
Sweating
Skin color

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16
Q

What are signs and symptoms of MI for women?

A

Unusual fatigue, sleep disturbances, SOA, indigestion, anxiety, chest discomfort

LV dysfunction found on functional study, arrhythmia (more VT or VF, but can be seen with atrial flutter or fib)
Syncope
Silent

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17
Q

What are precipitating factors and relieving factors for MI in women?

A

Precipitating: cold, exertion, anxiety, heavy meals, tachycardia, hypoglycemia
Relief: rest, NTG

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18
Q

What is stable angina?

A

Characterized by chest pain: transient hypoxia, relieved with change in activity or SLNG

Has well established onset: myocardial oxygen demand, rate pressure product

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19
Q

When is angina considered stable?

A

When characteristics remain unchanged for 60 days

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20
Q

What is unstable angina?

A

Presence of signs and symptoms of inadequate blood supply to myocardium: absent of demand

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21
Q

What are factors contributing to unstable angina?

A 
Circadian variation (4 hours) in catecholamine levels- increases HR and BP
Increased platelet activation
Pathologic changes in atherosclerotic plaques
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22
Q

What are clinical clues of unstable angina (when should you notify physician or nursing staff)?

A

Angina at rest
Typical angina occurs at lower exertion
Deterioration of previously stable pattern
Physiological changes: drop in HR or BP with usual exercise

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23
Q

What is prinzmetal angina?

A

Unusual syndrome of cardiac pain secondary to myocardial ischemia.
Exclusively at rest
ST segment elevation on EKG
Secondary to incrased coronary vasomotor tone or vasospasm

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24
Q

What is treatment for prinzmetal angina?

A

Combination of nitrates and calcium channel blockers

Beta blockers are usually avoided: alpha adrenergic activity, worsening vasoconstriction

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25
Q

What are two types of acute MI?

A

Transmural

Non-transmural (subendocardial): endocardium or endocardium to myocardium

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26
Q

What does STEMI stand for?

A

ST elevation MI

27
Q

What is definition of STEMI?

A

In at least two contiguous leads.
> 2mm in leads V1, V2, V3
>1 mm in all other leads

28
Q

What does STEMI indicate?

A

Occlusion in a large vessel, and large area at risk.

Cardiac emergency requiring either thrombolytic therapy, or immediate cardiac catheterization

29
Q

What is NSTEMI?

A

Findings of MI without ST elevation on EKG

Not always, but may represent smaller area, or high grade lesion, without total occlusion

30
Q

Where would you see localization of infarction of right coronary artery?

A

Location: inferior
EKG: 2, 3, aVF

31
Q

Where would you see localization of infarction of LAD (2 possible answers)?

A

Location: anteroseptal
EKG: V1-V3

Location: Anterior
EKG: V2-V4

32
Q

Where would you see localization of infarction of LAD or circumflex?

A

Location: lateral
EKG: 1, aVL, V5, V6

33
Q

Where would you see localization of infarction for posterior descending?

A

Location: posterior
EKG: V1-V2, tall broad initial R wave, ST depression, tall upright T wave

34
Q

What are corresponding EKG lines for inferior, anteroseptal, anterior, lateral, and posterior part of heart?

A 
Inferior: 2, 3, aVF
Anteroseptal: V1-V3
Anterior: V2-V4
Lateral: 1, aVL, V5, V6
Posterior: V1-V2, tall broad initial R wave, ST depression, tall upright T wave
35
Q

What artery corresponds with V1-V3 leads?

A

LAD

36
Q

What artery corresponds with V2-V4 leads?

A

LAD

37
Q

What artery goes with 2, 3, and aVF leads?

A

Right coronary

38
Q

What artery goes with 1, aVL, V5, and V6 leads?

A

LAD or circumflex

39
Q

What artery goes with V1-V2?

A

posterior descending

also will have tall broad initial R wave, ST depression, tall upright T wave

40
Q

What is treatment of MI (acute coronary syndrome)?

A

In ER- up to/through admission:
Morphine sulfate, beta blockers (also nitrates or calcium channel blockers), aspirin, EKG, blood draw for cardiac markers

41
Q

What does MONA stand for?

A

Morphine
Oxygen
Nitrates
Aspirin

42
Q

What are the cardiac markers they test for when looking at MI?

A

CK- total and MB
Troponins
Myoglobin
LDH

43
Q

What is onset, peak, return to normal for CK?

A

Onset: 3-4 hours
Peak: 33 hours
Return to normal: 3 day

44
Q

What is onset, peak, return to normal for troponins?

A

Onset: 3-12 hours
Peak: 18-24 hours
Return: up to 10 days

45
Q

What is onset, peak, return to normal for myoglobin?

A

Onset: 1-4 hours
Peak: 3-15 hours

46
Q

What is onset, peak, return to normal for LDH?

A

Onset: 12-24 hours
Peak: 72 hours
Return: 5-14 days

47
Q

What are cardiovascular risk factors and prevention techniques?

A 
Family history
Age
Diabetes: nutrition and exercise
Hypercholesterolemia: nutrition and exercise
Hypertension: nutrition and exercise
Smoking: stop
Obesity: nutrition and exercise
Inactivity/sedentary lifestyle: exercise
48
Q

What type of effect does physical activity have on prevention and treatment?

A

Clear cardio protective effect of physical activity and proatherogenic effect of inactivity.

No other therapeutic intervention has mulit-faceted potency and preventative efficacy of aerobic exercise

49
Q

What are exercise induced changes in myocardial function?

A

Effects on: HR, systolic BP, rate-pressure product, oxygen demand via decreased energy demand, changes in myocardial oxygen consumption (demand versus delivery)

50
Q

What does training help if there is damage in the central mechanism (heart)?

A

Heart is rate limiting factor.

Training will help with the periphery. We want to improve a-v O2 difference with training to have better oxygen exchange

51
Q

What may cause a reduction in cardiac output?

A

Chronotropic incompetence
LV dysfunction due to an MI
Transient ischemia
Cardiomyopathy that results in reduced EF, SV, and diastolic filling

52
Q

What is the cause of reduction in VO2?

A

Is seldom the result of decreased oxygen extraction but rather the result of decreased oxygen delivery

53
Q

What is peak VO2 in healthy versus patients with CAD?

A

healthy, active: between 35-70

In CAD patients: below 20

54
Q

What are disease specific effects on physiologic responses and fitness?

A

affects VO2, HR, and BP

55
Q

What is chronotropic incompetence?

A

Failure to reach 85% of APMHR in the absence of beta blockers or other medications with similar effects

56
Q

What is abnormal HR recovery?

A

Decrease in HR of

57
Q

What happens to BP because of heart disease?

A

In absence of beta blockers or ACE inhibitors, a failure of systolic BP to rise in proportion to exercise intensity

58
Q

What are surgical and pharmacological treatments?

A

Oxygen- increase oxygen saturation and delivery
Nitroglycerin- decrease myocardial oxygen demand, vasodilator
Aspirin/clopidrigrel- anti platelet
Heparin/enoxaparin- anti coagulation
Pain relief
Revascularization
Beta-blockers
Calcium channel blockers- if beta not working
ACE inhibitors- improve LV function
Statins- decrease production of cholesterol in liver, and anti-inflammatory

59
Q

What are phases of cardiac rehab?

A

Phase I or inpatient phase was introduced in the 1960s and consists of the early graded mobilization of the stable cardiac patient to the level of activity required to perform simple household tasks.

Phase II consists of outpatient monitored exercise and risk factor reduction. This multidimensional approach gained popularity in the 1970s and became well structured in the 1980s.

Phase III or maintenance phase consists of home- or gymnasium-based exercise with the goal of continuing the risk factor modification and exercise program learned during phase II.

60
Q

What is incidence of cardiac arrest?

A

295 000 cases of cardiac arrest in the US per year

7.9% survival to discharge

61
Q

What is cause of cardiac arrest?

A

60-70% of cardiac arrest occurs in individuals with CAD

62
Q

What is the only method for sustainable cardio protection?

A

Aerobic exercise

63
Q

What does regular exercise protect the heart against?

A

Arrhythmias
Stunning
Infarction
Remodeling

Cardiopulmonary PT (19 decks)

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