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PTRS 826 Exam 1 > Cardiac Muscle Dysfunction > Flashcards

Cardiac Muscle Dysfunction Flashcards

1
Q

Describe the key features of CMD (4)

A
  • Results from abnormality of structure or function
  • Impairs the heart’s ability to pump or receive blood
  • Exercise tolerance/funtional ability mild/mod reduced
  • Decreased QoL
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2
Q

Term: Resistance the ventricle feels as it empties

A

Afterload

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3
Q

Define chronic heart failure?

A

When the congestion or edema causing CHF is controlled

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4
Q

List Ejection fraction for the following conditions:

  1. Normal
  2. CMD
  3. CHF
A
  1. 60-70%
  2. 30-40%
  3. < 30%
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5
Q

List seconday issues due to CMD (6)

A
  • Angina and myocardial ischemia (inad O2 supply/demand)
  • Cardiac arrhythmia (decreased myocardial function)
  • HTN (places strain on the L ventricle)
  • Ventricle hypertrophy (due to HTN)
  • Myocardial stiffness (due to HTN)
  • Renal insufficiency
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6
Q

List the most common cause of CMD and its effect on the heart

A
  • MI

An MI can be due to artery spasm, ebolism, injury. Once an MI occurs there is subsequent scar formation. The scar tissue in the heart leads to decreased stretch with filling and decreased/altered line of squeeze with contraction. Overall the heart has decreased contractility

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7
Q

Describe the effect on HTN on EE

A

With HTN there is increased resistance for the heart. This requires increased EE due to the increased work of the heart mm to maintain/pump adequate cardiac output

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8
Q

Describe the difference in heart hypertrophy due to pathology vs. athletic conditioning

A

Pathologic: tissue is laid down on the inside of the ventricle, taking up space for filling and stiffening the heart

Athletic training: tissue laid down on the outside of the ventricle; pumping is more effeicient, SV is larger

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9
Q

Describe how ventricular hypertrophy progresses

A

With prolonged HTN the heart has increased EE > the ventricle hypertrophy > Myocardium stiffens > the ventricle weakens/deteriorates > the ventricle dilates (can’t squeeze) > CHF

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10
Q

Describe the tx options for HTN (2)

A
  1. Medications (ACE inhibitors, Ca blockers, beta blockers, diruetics)
  2. Regular exercise (Stimulate vasodilation at rest; Drop: SBP by 10; DPB by 6-8)
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11
Q

List the tx options for cardiac arrhythmia (4)

A
  • Medication
  • Pacemaker
  • Ablation (removing arrhythmatic cells)
  • ICD (implantatble cardiac defibrillator)
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12
Q

Describe the effect of renal insufficiency on the heart

A

Fluid retention/overload increases the pressure the heart must overcome

**Side note: Goal of tx is to decrease reabsorption as opposed to just removing the excess fluid

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13
Q

List the tx options for renal insufficiency (3)

A
  • Lasix (diuretic)
  • Monitor electrolyte levels (Na and K)
  • Dialysis (severe cases)
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14
Q

Term: a disorder affecting heart muscle; inadequate pumping of the heart

A

Cardiomyopathy

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15
Q

Condition: enlarged heart

A

Cardiomyopathy

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16
Q

List the subtypes of cardiomyopathy (2)

A
  1. Ischemic (results from coronary artery disease)
  2. Non-ischemic (disease of the heart mm itself)
    - dilated
    - hypertrophic
    - restrictive
17
Q

List the demographic of those with dilated cardiomyopathy (3)

A
  • Idiopathic
  • Middle aged ppl
  • Men > women

Side note: require transplant

18
Q

Describe the physiology of dilated cardiomypathy (3)

A
  • Dilated L ventricle and atrium decrease the elastic qualities of the heart, decreased recoil
  • Bulging of interventricular septum from left to right
  • Thin ventricular walls > myocardial mitochondria dysfunction > increased EE > heart failure
19
Q

List the demographics of hypertrophic cardiomyopathy (3)

A
  • Inherited (autosomal dominant)
  • onset at 10-25 yo
  • prinicipal cause of sudden death
20
Q

Describe the the hypertrophy that occurs in hypertrophic cardiomyopathy

A

The increased size of the heart is inappropriate for the hemodynamic load

It’s characterized by diastolic dysfunction and increased LV diastolic pressure (eventually increased LA/PA/pulmonary capillary pressure; hypercontractile LV)

21
Q

Describe the physiology of hypertrophic cardiomyopathy (3)

A
  • Severe thickening of the interventricular septum
  • Thickening of L ventricular wall (won’t relax/stretch/fill but good squeeze; ejects well just not much blood in ventricle)
  • Tiny left ventricular chamber
22
Q

Describe the demographics of restrictive cardomyopathy (4)

A
  • Worst prognosis
  • Not inherited
  • Characterized by diastolic dysfunction
  • Mutliple forms: amyloidosis, sarcoidosis, hemochromatosis
23
Q

Form of restrictive cardiomyopathy: abnormal protein fibers (amyloid) accumulate in the heart’s mm

A

amyloidosis

24
Q

Form of restrictive cardiomyopathy: an inflammatory disease that causes the formation of small lumps in organs (lungs)

A

Sarcoidosis

25
Q

Form of restrictive cardiomyopathy: an iron overload of the body, usually due to a genetic disease

A

hemochromatosis

26
Q

Describe the physiology of restrictive cardomyopathy (2)

A
  • Stiffened walls of the ventricles with lost of flexibility due to infiltration by abnormal tissue
  • Doesn’t want to fill or squeeze
27
Q

List the signs to look for CHF (10)

A
  • Chest x-ray report
  • Cold, pale, cyanotic extremities
  • Abnormal heart sounds (S3)
  • Sinus tachycardia (inc SNS > inc HR to comp for dec SV)
  • Abnormal breathing patterns (quick, shallow)
  • Peripheral edema (dec BF to periphery > inc fluid retention)
  • Crackles/rales
  • SBP with controlled expiratory maneuver
  • JVD
  • Decreased exercise tolerance and QoL
28
Q

List the symptoms of CHF (4)

A
  • Dyspnea (due to poor gas transport)
  • Paroxysmal noctural dyspnea
  • Orthopnea
  • Abdominal ascities
29
Q

Describe the difference between diphragmatic and pursed lip breathing

A

Diaphragmatic: belly breathing slows down breathing rate and increases gas exchange in the lungs

Pursed lip: slow down breathing by created a back pressure to open up alveoli and improve gas exchange (if fluid is the limiting agent)

30
Q

Describe the new york heart association classifications (1-4)

A

I: cardiac disease w/o limitation

II: cardiac disease w/slight limitation

III: cardiac disease w/marked limitation

IV: cardiance disease but inability to perfrom PA w/o discomfort

31
Q

Identify the new york heart association classification: PA results in fatigue, palpitation, dysnpnea (SOBOE), and anginal pain; no sx at rest

A

Class II

32
Q

Identify the new york heart association classification: “My heart pitter patters when I walk around Walmart.

A

Class II

33
Q

Identify the new york heart association classification: Less than ordinary activity causes fatigue, palpitations, SOBOE, and anginal pain; No sx at rest

A

Class III

34
Q

Identify the new york heart association classification: Symptoms are felt at rest and intensify with physical activity

A

Class IV

35
Q

Describe the components of CHF’s pathophysiology (4)

A
  • Neurohormonal (SNS)
  • Mm wasting (less active)
  • Pulmonary edema
  • Renal (due to lack of Q, kidneys think the body needs more fluid > water retention and oligurea)
36
Q

List the tx for CHF (3)

A

Tx directed by pathophysiologic cause

  • improve pumping ability (beta blocker, vasodilatory therapy)
  • control sodium intake
  • diuertics
37
Q

List the Criteria for Modification or termination of exercise (6)

A
  • Marked dyspnea/fatigue
  • RR > 40 b/m
  • Development of S3
  • Inc pulmonary crackles
  • Decrease in HR or BP > 10 unites
  • Diaphoresis, pallor, confusion
38
Q

List other causes of CMD (3)

A
  • Heart valve abnormalities
  • SCI (disconnect b/t CVS and control with SNS)
  • Pericardial effusion (increase pressure, decreased diastolic function)
39
Q

Describe how heart valve abnormalities can lead to CMD

A

blocked or incompetent valves causes the heart to contract more forcefully to expel Q > hypertrophy > cardiac stiffness > diastolic dysfunction

PTRS 826 Exam 1 (6 decks)

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