Congestive Heart Failure #9 (2/2/16) Flashcards

1
Q

What is congestive Heart failure?

A

Failure to pump an adequate amount of blood to supply the metabolic requirements of the organs.

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2
Q

What happens if the heart cannot keep up with metabolic demand?

A

Compensatory mechanisms: Activation of neurohumoral systems.

  • Release of norepinephrine with increased HR and Contractility.
  • Activation of Renin-angiotensin system with water/salt retention (increased circulatory volume)
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3
Q

What is the Frank-starling mechanism?

A

A compensatory mechanism where increased end diastolic filling stretched the cardiac muscle fibers to get them to contract more forcefully causing increased cardiac output.

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4
Q

What is Myocardial hypertrophy?

A

A compensatory mechanism where there is an increase in muscle fiber size, resulting in thickening of ventricular wall without increase in size of lumen.

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5
Q

T or F, compensatory mechanism usually work.

A

False, they usually fail due to increased oxygen requirements of myocardium, but without increase capillary supply resulting in ischemia.

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6
Q

What are the causes of left sided heart failure?

A
  • Ischemic Heart Disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
  • Valvular disease
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7
Q

What are the causes of Right sided heart failure?

A
  • Left side heart failure
  • pulmonary hypertension
  • valve disease
  • Septal defects with left to right shunts.
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8
Q

What are the clinical manifestations of congestive heart failure?

A

Left side failure:

  • Pulmonary edema and congestion, resulting in dyspnea
  • Chronic cough
  • Orthopnea

Right side failure:
- Cerebral hypoxia

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9
Q

What are some clinical manifestations of Right ventricular failure?

A
  • Congestion of the liver “Nutmeg liver” and spleen.

- Edema (pitting) of subcutaneous tissues, particularly the lower extremities.

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10
Q

How common is Congenital heart failure?

A

Not very 6-8/1000

*may have abnormal connections, shunts, absence of normal connections.

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11
Q

What are the 2 causes of Congenital heart failure?

A

Cyanotic and noncyanotic

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12
Q

What are the 3 forms of Noncyanotic congenital heart disease?

A
  1. Atrial septal defect (ASD) = 2nd most common congenital malformation.
  2. Ventricular septal defect (VSD) = Most common of cardiac malformations 4/1000.
  3. Patent ductus arteriosus (PDA) = connects aorta and pulmonary artery, should close within a few days after birth.
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13
Q

What are the Cyanotic forms of Congenital Heart Disease?

A
  1. Tetralogy of Fallot: 4 anomalies
    - ventricular septal defect (VSD)
    - Narrowed Right ventricular outflow
    - Overriding the VSD by aorta
    - Right ventricular hypertrophy
  2. Transposition of the great arteries:
    - Right Ventricle empties into aorta
    - Left ventricle empties into pulmonary artery
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14
Q

Clinical sign of Cyanosis?

A

Swelling of hands

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15
Q

What is Ischemic Heart Disease?

A

Refers to a group of related disorders are all characterized by an imbalance between myocardial blood supply and myocardial oxygen demand (ischemia).

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16
Q

What is the primary cause of Ischemic Heart disease?

A

90% of the time its due to coronary artery atherosclerosis (coronary artery disease)
*Leading cause of death in US 500,000 annually.

17
Q

What are is the pathogenesis of Ischemic HD?

A
  • Coronary A. atherosclerosis >75% narrowing.
  • Coronary A. Thrombosis
  • Anemia
  • Pneumonia
  • Hypertension
18
Q

What is Angina? (associated with Ischemic HD)

A

Intermittent chest pain caused by transient, reversible myocardial ischemia.
*Stable Angina occurs predictably at certain levels of physical exertion.

19
Q

Describe Unstable Angina….

A

Usually last longer than stable angina, often precedes a more serious ischemia or MI.

20
Q

What is an Acute Myocardial infarct?

A

A heart attack = Necrosis of cardiac muscle caused by ischemia.

21
Q

Severe Ischemia lasting longer than _____ will cause irreversible myocyte injury and cell death.

A

20-40 minutes

22
Q

Myocardial ischemia also contributes to arrhythmias, why?

A

Because ischemic regions cause electrical instability/irritability that may lead to ventricular fibrillation

23
Q

What are the clinical manifestations of a IHD Myocardial infarct?

A
Chest pain
Vomiting
SOB
Low grade fever
Diaphoresis
24
Q

MI’s less than _______ old are not usually grossly apparent at autopsy.

A

12 hrs

*at 12-24hrs infarcted areas appears reddish blue

25
If you survive an MI, what might your heart have afterwards?
Scar tissue that will hurt the contractility of your heart
26
What are the treatment options for IHD MI?
Stents Coronary artery bipass Clot busting drugs such as streptokinase
27
What are MI complications?
- Arrhythmias - CHF/shock - Mural thrombus (which can lead to left sided embolism) - Mitral valve regurgitation (due to papillary muscle dysfunction) - Myocardial rupture (heart ripped/exploded) - Infarct expansion to involve right ventricle - Chronic Ischemic Heart disease
28
What is the most common cause of sudden cardiac death?
IHD (80-90%)
29
What are the 2 classes of Cardiomyopathies?
Primary = disease primarily or solely confined to the heart muscle. Secondary = myocardium is involved as part of a systemic disorder.
30
What are the 3 functional patterns of Cardiomyopathies?
- Dilated - Hypertrophic - Restrictive
31
Describe a Dilated Cardiomyopathy....
May be primary or secondary: - Genetic in 20-50% of cases - Dilation of all 4 chambers - Poor ventricular contractility - Nonspecific histology with fibrosis and myocyte hypertrophy.
32
Describe a Hypertrophic Cardiomyopathy...
A primary genetic Cardiomyopathy: - AD inheritance - Missence point mutation in one of several sarcomeric gene loci. - Stiff ventricles prevent adequate filling. - Histology myocyte disarray with fibrosis.
33
Describe a restrictive Cardiomyopathy...
- Wall of ventricle becomes stiffer with impaired filling during diastole. - Can be idiopathic or secondary to systemic conditions that affect the myocardium-radiation fibrosis, amyloidosis, hemochromatosis, sarcoidosis.