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
Q

If you survive an MI, what might your heart have afterwards?

A

Scar tissue that will hurt the contractility of your heart

26
Q

What are the treatment options for IHD MI?

A

Stents
Coronary artery bipass
Clot busting drugs such as streptokinase

27
Q

What are MI complications?

A
  • 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
Q

What is the most common cause of sudden cardiac death?

A

IHD (80-90%)

29
Q

What are the 2 classes of Cardiomyopathies?

A

Primary = disease primarily or solely confined to the heart muscle.

Secondary = myocardium is involved as part of a systemic disorder.

30
Q

What are the 3 functional patterns of Cardiomyopathies?

A
  • Dilated
  • Hypertrophic
  • Restrictive
31
Q

Describe a Dilated Cardiomyopathy….

A

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
Q

Describe a Hypertrophic Cardiomyopathy…

A

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
Q

Describe a restrictive Cardiomyopathy…

A
  • 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.