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Cardiopulmonary PT > Cardiac Muscle dysfunction > Flashcards

Cardiac Muscle dysfunction Flashcards

1
Q

What does CMD result from?

A

Abnormality of structure or function

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2
Q

How does CMD affect the heart?

A

Impairs heart’s ability to pump or receive blood

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3
Q

How does CMD affect function?

A

Exercise tolerance and functional abilities are mild/moderately reduced: myocardial ischemia/infarction, angina, cardiac arrhythmias, dyspnea

Decreased quality of life

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4
Q

T/F: CMD is the most common cause of congestive heart failure?

A

True

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5
Q

How is CHF manifested?

A

As pulmonary congestion, or pulmonary edema

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6
Q

What is the difference between chronic heart failure and congestive heart failure?

A

Chronic heart failure: person is living with heart failure

CHF: person has edema involved

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7
Q

What are the characteristics of CMD?

A 
Ejection fraction: 30-40%
Angina and myocardial ischemia
Cardiac arrhythmias
MI
HTN
Cardiac arrhythmias
Renal insufficiency (acute/chronic)
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8
Q

What is cause for angina and myocardial ischemia in CMD?

A

Brought on by inadequate O2 supply/demand to heart

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9
Q

What do cardiac arrhythmias lead to?

A

Decreased myocardial function

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10
Q

What is the most common cause of CMD?

A

Myocardial infarction

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11
Q

What are causes for MI?

A

Chronically sustained ischemia to myocardium.

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12
Q

What are possible ways for chronic sustained ischemia to myocardium leading to an MI?

A

Coronary artery spasm (smooth muscle)
Sudden thrombotic occlusion (cell death)
Dysfunction of left or right ventricle or both from injury
Scar formation and decreased contractility occur

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13
Q

What is treatment for MI?

A

Fix underlying cause of infarction (surgical procedure, medications)

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14
Q

What happens to the cardiac muscle with chronic uncontrolled HTN?

A

Increased atrial pressure= strain of left ventricle: LVH, increased energy expenditure
Ventricle hypertrophies to compensate increased afterload
Myocardium stiffens: systolic and/or diastolic dysfunction
Left ventricle weakens and dilates: CHF

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15
Q

T/F: with chronic uncontrolled HTN there is increased energy expenditure in the heart because the muscles have to work harder to maintain adequate pump/cardiac output?

A

True

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16
Q

What is treatment for HTN?

A

Medications such as ACE inhibitors, Ca channel blockers, diuretics, and beta blockers
Regular exercise training

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17
Q

T/F: regular exercise training can reduce BP by 20 mmHg (systolic) and 15 mmHg diastolic?

A

False: reduces systolic 10 mmHg and 6-8 mmHg

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18
Q

T/F: if you stop exercise your blood pressure will stay the same?

A

False. Exercise needs to be maintained through life

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19
Q

What are cardiac arrhythmias and how is it a characteristic of CMD?

A

Decreased myocardial function: too rapid or slow which affects muscle function

Impaired atrioventricular conduction

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20
Q

What is treatment for cardiac arrhythmias?

A

Medications, pacemaker, ablation, ICD

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21
Q

What is renal insufficiency?

A

Fluid overload

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22
Q

What is treatment goal for renal insufficiency?

A

Decrease reabsorption of fluid (not just adjust fluid control) from kidney and rid the body of fluid (diuresed)

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23
Q

What is treatment for renal insufficiency?

A

Lasix (diuretic)
Monitor electrolyte levels for too high (further retention) or too low (cardiac arrhythmias)
Dialysis for severe cases

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24
Q

What is cardiomyopathy?

A

Disorder affecting the heart muscle: inadequate pumping of heart, contraction, relaxation

Primary/secondary causes

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25
Q

What does the heart do in cardiomyopathy?

A

It loses its ability to pump effectively. It becomes larger as it tries to compensate for its weakened condition

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26
Q

What are 2 categories of cardiomyopathy?

A

Ischemic: results from coronary artery disease
Nonischemic: disease of heart muscle itself, dilated, hypertrophic, restrictive

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27
Q

What is the most common cause of CHF?

A

Dilated cardiomyopathy

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28
Q

What populations normally get dilated cardiomyopathy?

A

Middle aged people

Men more than women (2.5 to 1)

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29
Q

what is cause of dilated cardiomyopathy?

A 
Idiopathic in most cases
Familial (30-40%)
Viral infection
Chronic, excessive consumption of alcohol
Toxins (cobalt)
Cancer drugs
Pregnancy and childbirth
Long term alcohol use
Cigarette smoking
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30
Q

What is treatment for dilated cardiomyopathy?

A

transplantation

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31
Q

What are characteristics of dilated cardiomyopathy?

A

Dilated left ventricle and left atrium.
Bulging interventricular septum from left to right
Thin ventricular walls
Myocardial mitochondria dysfunction: energy

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32
Q

What structural changes occur in dilated cardiomyopathy?

A

Increased left ventricular mass
Normal or reduced left ventricular wall thickness
Increased left ventricular cavity size.
Ineffective/inefficient pump: poor cardiac output, end diastolic pressure not going up, bad squeeze.

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33
Q

T/F: in dilated cardiomyopathy normal activities will be easy for people

A

False; normal activities are harder

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34
Q

What is cause of hypertrophic cardiomyopathy?

A

Most are inherited (>100 mutations in 10 proteins)

Autosomal dominant trait

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35
Q

Who normally gets hypertrophic cardiomyopathy?

A

Most common early onset (10-25 years)

Principal cause of sudden death: young healthy individuals, athletes

36
Q

What are characteristics of hypertrophic cardiomyopathy?

A

Hypertrophy is inappropriate for hemodynamic load.
Proper myocardial mitochondira function
Characterized by diastolic dysfunction
Increased LV diastolic pressure: eventually increased LA,PA, and pulmonary capillary pressures

37
Q

What are structural changes in hypertrophic cardiomyopathy?

A

Severe thickening of interventricular septum.
Thickening of the left ventricular wall.
Tiny left ventricular chamber/ventricular cavity size

38
Q

T/F: with hypertrophic cardiomyopathy the problem is that the heart will get a good squeeze but it can’t fill with blood so no blood will get out?

A

True

39
Q

How does hypertrophic cardiomyopathy impair function?

A

Exaggerated pump function (hypercontractile systolic function)
Poor heart relaxation (diastolic dysfunction)

40
Q

What are causes and characteristics of restrictive cardiomyopathy?

A 
Rare form (5%)
Worst prognosis
Characterized by diastolic function

Does not appear to be inherited

41
Q

What are the forms of restrictive cardiomyopathy?

A

Amyloidosis: abnormal protein fibers accumulate
Sarcoidosis: inflammatory, forms lumps in lungs
Hemochromatosis: iron overload of body

42
Q

What is the restrictive cardiomyopathy that has abnormal protein fibers (amyloid) accumulate in the heart’s muscle?

A

Amyloidosis

43
Q

What is the restrictive cardiomyopathy that is an inflammatory disease that causes the formation of small lumps in organs (lungs)?

A

Sarcoidosis

44
Q

What is restrictive cardiomyopathy where there is iron overload of the body, usually due to a genetic disease

A

Hemochromatosis

45
Q

What happens to heart muscle tissue in restrictive cardiomyopathy?

A

Stiffened walls of the ventricles with loss of flexibility due to infiltration by abnormal tissue

46
Q

What are signs of CHF?

A 
Chest X-ray
EF
Cold, pale, cyanotic extremities
Abnormal heart sounds
Sinus tachycardia
Abnormal breathing patterns
Peripheral edema
Crackles/rales
Systolic BP with controlled expiratory maneuver
Jugular vein distention
Decreased exercise tolerance
Decreased quality of life
47
Q

What will you see on X-ray with person with CHF?

A 
Cardiac silhouette (size and shape increased)
Fluid in lungs
48
Q

What is ejection fraction in person with CHF?

A
49
Q

What is cause of cold, pale, extremities in person with CHF?

A

Increased sympathetic activity

50
Q

What are the abnormal heart sounds in CHF?

A

S3 occurs when LV is non-compliant and poor relaxation during diastole
Hallmark sign of CHF

51
Q

What is cause of sinus tach in CHF?

A

Increased sympathetic activity

52
Q

What does breathing pattern look like in person with CHF?

A

Quick, shallow breaths even with change in position

53
Q

How does peripheral edema effect the body in CHF?

A

Inadequate blood flow to periphery: promotes decreased fluid excretion, fluid retention, weight gain > 3lbs

54
Q

Why do you hear crackles/rales with CHF?

A

heard on inspiration and at lung base

Hear it because of alveolar opening in presence of pulmonary edema

55
Q

What are symptoms of CHF?

A

Dyspnea
Paroxysmal nocturnal dyspnea
Orthopnea

56
Q

What are causes of dyspnea in patients with CHF?

A

Poor gas transport: acute/chronic pulmonary edema
Abdominal ascites: peripheral edema, and limitation in diaphragmatic descent
Ventilatory muscle weakness

All contribute to inadequate oxygen supply: increased tidal volume and respiratory rate

57
Q

What is paroxysmal nocturnal dyspnea?

A

Sudden SOB upon wakening from sleep

58
Q

What is cause of paroxysmal nocturnal dyspnea?

A

Supine position increases venous return: this overloads the poorly functioning heart, increases pulmonary edema

59
Q

What do patients who awaken with orthopnea occur?

A

Relief with upright position

Prefer to sleep with pillows, HOB propped up or in chair

60
Q

What are NY Heart Association Classification?

A

Class 1: cardiac disease w/o limitations
Class 2: Cardiac disease slight limitation (physical activity results in fatigue, palpitations, dyspnea, angina pain
Class 3: Cardiac disease marked limitation (less than ordinary activity causes symptoms above)
Class 4: Cardiac disease but inability to perform physical activity w/o discomfort (symptoms may be felt at rest, physical activity intensifies symptoms)

61
Q

If a person is okay at rest but less than ordinary activities cause symptoms what level are they at?

A

Level 3

62
Q

If a person is doing activity and their heart pitter patters what class would they be?

A

Class 2

63
Q

What is pathophysiology of CHF?

A

Neurohumonal: sympathetic symptoms
Muscle wasting
Pulmonary/edema
Renal: water retention d/t decreased Q, urine (oliguria)

64
Q

For CHF what are the things we should look, listen, feel for?

A

Look: breathing pattern, color, edema, oximeter, JVD, changes in extremities, weight gain
Listen: breath and heart sounds, BP
Feel: edema, breathing pattern, pulse (rate, rhythm, force)

65
Q

What happens when oxygen saturation is 90 and partial pressure of oxygen is 60?

A

Tachycardia, tachypnea, restlessness

66
Q

What happens when oxygen saturation is 85 and partial pressure of oxygen is 50?

A

Incoordination, impaired judgement, labored respirations, confusion

67
Q

What happens when oxygen saturation is 80 and partial pressure of oxygen is 45?

A

Tachycardia, tachypnea, restlessness

Incoordination, impaired judgement, labored respirations, confusion

68
Q

Will someone have symptoms if their oxygen saturation and partial pressure O2 is 99-95 and 100-80 respectively?

A

No signs or symptoms

69
Q

What are medical interventions for CHF?

A

Directed at pathophysiologic cause.

Improve hearts pumping ability: beta block, vasodilator therapy
Control sodium intake: diet, heart healthy, low cholesterol and fat
Water retention: diuretics will increase urine output
Devices
Cardiac transplantation

70
Q

What should people with CHF avoid?

A

Antiarrhythmic agents: act as cardio depressants and have pro arrhythmic effects
Ca channel blockers: can worsen CHF, increase risk of CV events
Nonsteroid anti-inflammatory drugs: increases sodium retention, peripheral vasoconstriction

71
Q

What are devices that can be used as medical interventions for CHF?

A

Bi-ventricular pacing
ICD (implantable cardiac difibrillators)
Intraaortic balloon pump
Left ventricular assistive device

72
Q

When is and ICD used?

A

EF

73
Q

What does a intra aortic balloon pump do

A

Inflates during diastole, improves myocardial blood flow

74
Q

What does left ventricular assistive device do?

A

Helps maintain pumping ability of heart that can’t work on its own.
Sometimes used as “bridge to transplant”
Hospitalization ~7-10 days

75
Q

What is part of assessment for people with CMD?

A

When did sx begin?
Stable, worse, what brings on sx
Chest pain, claudication, SOBOE, sleeping hx
Activity level: FITT principle
Objective measures/labs: EKG, echo, blood gas levels, auscultation, 6MWT, questionnaires, physical appearance, RR, breathing pattern

76
Q

What is inpatient care for CMD?

A 
Flexibility exercises, cycle ergometry, treadmill ambulation
Energy conservation
Self management
Transfers
Education
77
Q

What are guidelines for geometry/treadmill?

A

30 minutes
3-5 days/week
2-4 weeks
50-70% peak cycle work rate

Improvements reported in decreased symptoms, improved HR and exercise tolerance

78
Q

What is done with home care PT for cardiac patients?

A

Flexibility exercises, cycle ergometry, walking
Self management of sx, diet, activity, energy conservation, ther ex/act
ADLs/IADLs

79
Q

What are parameters of home care exercises? improvements?

A

20-60 minutes
3-7 days/wk
2-6 months
50-80% peak cycle heart rate or O2

Improvements: decreased symptoms, improved HR, BP, exercise tolerance via GXT

80
Q

What methods of aerobic activity can be found with cardiac rehab centers?

A

Most use cycle erg
20-60 minutes, 3-7 days/wk, 2-57 months, 40-90% of peak cycle heart rate or VO2
Improvements reported in decreased symptoms, improved HR, BP, and exercise tolerance

81
Q

Can SLE be used for PT with CHF?

A

Unilateral exercise better than 2 legged: severe CHF, limited exercise tolerance, low cardiac output especially with exercise

82
Q

What are PT interventions for strength and breathing?

A

Strength: 10 reps for 2-4 months OR 60-80% of maximum voluntary contraction. Progress is slow

Breathing: inspiratory muscle training with hand held device, limited data on yoga (positive for decreasing dyspnea)

83
Q

What is criteria for modification or termination of exercise?

A 
Marked dyspnea or fatigue
RR >40 breaths/min
Development of S3 heart sound
Increase pulmonary crackles
Decrease in HR or BP of >10 bpm or mmHg during steady state or progressive exercise
Diaphoresis, pallor, or confusion
84
Q

What are other causes of CMD?

A

Heart valve abnormalities
SCI: transection to cervical spinal cord
Pericardial effusion

85
Q

How do heart valve abnormalities cause CMD?

A

Heart must contract more forcefully to expel Q because of the blocked/incompetent valves.
Leads to hypertrophy: decreased ventricular distensibility, diastolic dysfunction, incompetent valves associated with hypertrophy (regurgitated blood fills atria or ventricles)

86
Q

How does a SCI cause CMD?

A

Disconnect between cardiovascular system and control with SNS

87
Q

What does pericardial effusion cause CMD?

A 
Increased pressure (fluid fills pericardial sac)
Decreased diastolic function

Cardiopulmonary PT (19 decks)

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