Transcript Chapter 22 – Cardiac Failure

Chapter 22
Cardiac Failure
Acute Pulmonary Edema
Increased
Venous Return
Insufficient
Pumping
Buildup of
Blood in
Lungs
Increased
Capillary
Pressure
Buildup of Fluid
in Lungs
Peripheral
Vasodilation
Diminished O2
Transport
Treatment for Pulmonary Edema
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Tourniquets on arms and legs
Bleeding the Patient
Diuretic (e.g. furosemide)
Pure O2 to breathe
Cardiotonic drug (e.g. ouabain) to
strengthen the heart
Cardiac Reserve
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Maximum amount that the CO can
increase.
Generally 300-400%.
Can be 500-600% in athletes.
Can be zero for diseased heart.
Exercise Test
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Put on a treadmill
Look for
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Shortness of breath
Muscle fatigue
Increased heart rate.
Graphical Analysis of Cardiac
Output
AV Fistula
Normal
Normal
Venous
Return
Heart Defects
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Patent Ductus Arteriosis (PDA)
Tetralogy of Fallot
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(Left to Right Shunt)
Blue Baby
4 abnormalities
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Aorta (partially) originates from RV
Stenosed Pulmonary artery
Blood from the RV passes through a septal hole
Right Ventricular Hypertrophy
German Measels is a common cause of heart
defects.
Extracorporeal Circulation
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Methods:
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Bubbling O2 through blood
Dripping blood over a large surface
Passing blood over rotating discs
Passing blood through thin membranes or porous
tubes
Problems: Hemolysis, Clotting, Bubbles, Emboli
of antifoam agent, need for large quantities of
blood, need for heparin (inteference with
hemostasis).
Cardiac Hypertrophy Caused by
Congenital and Valve Diseases
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Generally occurs with all defects
Part of heart affected depends on type of
defect
Extreme hypertrophy can cause heart
failure
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Coronary vasculature does not increase
Fibrosis often develops (especially
subendocardial)
Ischemia can cause anginal pain.