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22 Cards in this Set

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Compensatory Mechanism
*ventricular dilation
*^SNS stimulation
*neurohormonal activation
Ventricular dilation
*^'s preload which initially ^ CO
*overtime, it gets overstretched and < effective
*it also requires more O2 which can lead to hypoxia
Remodeling
*overtime, these changes cause changes in structure, function, and gene experssion of the myocardial cell
*as cardiac cells die, they are replaced with "mutant" cardiac cells that are bigger and die quicker than normal
*the result is a weak, hypertrophied heart
Right sided heart failure
"think Liver"
*increased pressure and vol in the RV transcends upward to the vena cava and down to the portal system causing venous congestion to the liver
Diagnosis of heart failure
*echocardiogram (ejection fraction)
*EKG
*chest xray
*ABG
*Liver enzymes (right side ^)
*BUN/Cr
Left sided heart failure
*^ LV pressure are transmitted to pulm circ which ^ pulm cap Hydrostatic pressure. When this exceeds oncotic pressure, the fluid moves with the alveolar
*SOB, DOE, PND, orthopnea, crackles, sputum prod (white frothy),tachypnea, wheezing, S3
Medical management; improving pump performance
*oxygen therapy
*digoxin (for persons still symptomatic despite ACE and Beta therapy)
*Inotropes (dobutamine, IV only)
Neurohormonal Activation
*^ in NE (vasoconstr & tachy)
*^ in cytokines released
*stim. of renin-angiotensis (^fluid ret. & BP)
Medical management; reducing myocardial workload
*< preload-diuretics
*< afterload:
-venous dilators-NTG and isordil
-arterial dilators-hydralazine (apresoline)
-arterial and venous dilator-sodium nitroprusside (nipride IV only
Other treatments of heart failure
*ventricular assist devices (VADs)
*intra-aortic balloon pumps (IABP)
*heart transplantation
Angiotensin-convertin enzyme (ACE inhibitors)
*blocks production of angiotensin II (potent vasoconstrictor), increases renal blood flow, lessens neurohormonal effects of heart failure, lessen remodeling and increase survival
*all persons with heart failure s/b on an ACE inhib.
Abnormal loading conditions (affect preload and/or afterload)
*anything that increases pressure of volume of the load of the ventricles
*valvular abnormalities
*fluid overload
*hypertension
*pulmonary hypertension
Nursing care of person with heart failure
*dietary management
*bedrest
Cause of Heart failure
*2/3 caused by CHD
*1/3 caused by abnormal loading conditions, abnormal muscle function, or conditions/diseases that limit ventricular filling
Frank-Starling Mechanism
*force of heartbeat is determined by length of fibers
*the more you stretch, the greater the force
*the more fluid in L. ventricle, the > the force
*overtime, >distension leads to hypertrophied L. vent
*leads to < forceful contraction
*this decreases SV
*HR x SV = CO
Performance of heart is dependent on 4 components
*contractility
*preload
*afterload
*heart rate
Increased SNS stimulation
*constriction (^ afterload)
*tachycardia and ^ myocardial contractility
*at first helpful, overtime, ^ myocardial workload and O2 demands
Limited Ventricular Filling
*constrictive pericarditis
*cardiac tamponade
Beta-adrenergic antagonists
*Atenelol, lopressor
*inhibit the effects of the SNS and < mortality
Abnormal muscle function (affects contractility)
*MI
*Myocarditis (viral, fungal, bacterial, parasitic or toxic)
*cardiomyopathy
*ventricular aneurysm
Pathophysiology
When demand is greater than supply, compensatory mechanisms are activated. The body does this to help improve CO, but if it continues it leads to abnormal cardiac growth and reconfiguration (remodeling) of the heart
Conditions that may precipitate heart failure
*conditions that increase O2 demand (stress, infection, anemia, thyroid disorders, pregnancy and Paget's)
*thiamine deficiency (reduces contractility)
*chronic pulmonary or liver disease