caridac problems

caridac problems

1. left sided HF

   • caused by HTN, CAD, and valvular disease
   • decreased perfusion d/t poor cardiac output and pulmonary congestion d/t increased pressure in pulmonary vessels
   • systolic HF
     • reduced ejection fraction below 40%
       • blood accumulates in pulmonary vessels
     • preload increased, decreased contractility
     • afterload increased d/t increased peripheral resistance (HTN)
     • risk for: sudden cardiac death
   • diastolic HF
     • preserved left ventricular function
     • left ventricle doesn't relax during diastole
       • prevents ventricle from filling with sufficient blood for adequate output
     • ejection fraction is more than 40%
       • still ventricle becomes less compliant over time

2. right sided hf

   • caused be left ventricular failure, right ventricular MI, or pulmonary HTN
   • increased volume and pressure in venous system
     • peripheral edema

3. normals

   • ejection fraction 50-70%
   • tumor necrosis factor (TNF) and interleukins ( 1 and 6) will be increased after MI
   • BNP
     • promotes vasodilation and diuresis
     • higher in women
   • vasopressin (antidiuretic)
     • secreted by posterior pituitary with decreased cerebral perfusion
     • causes vasoconstriction and fluid retention
   • endothelin
     • secreted as endothelial cells stretch

4. high output HF

   • cardiac output is normal or above
   • caused by increased metabolic needs or hyperkinetic conditions (septice, high fever, anemia, hyperthyroidism)

5. classes

   • class 1
     • pt at high risk for hf
     • pt with cardiac structural abnormalities or remodeling with no symptoms
   • class 2
     • current or prior symptoms of HF
   • class 3
   • class 4
     • pt with refractory end-stage HF

6. compensatory mechanisms

   • sympathetic nervous system stimulation
     • most immediate
     • increase HR and BP from vasoconstriction
   • Renin-angiotensin system (RAS) activation
     • from decreased perfusion to kidneys
     • increased antiotensin 2
       • retain Na and water
       • arginine vasopressin
     • increased aldosterone
       • endothelin
       • cytokines (tumor necrosis factor
     • leads to hypertrophy and dilation of ventricle, genetically large cells, impaired contractility
   • other chemical responses
   • myocardial hypertrophy