Flashcards in Chapter 19 Deck (20)
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1
Q
Heart Failure
A
- inability of the heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs
- results in congestion of blood flow in the systemic or pulmonary venous circulation, inability to increase cardiac output to meet the demands of activity or increased tissue metabolism
2
Q
Pathogenesis and diagnosis of HF
A
- potential consequence of most cardiac disorders
- most common cause is myocardial ischemia followed by hypertension and dilated cardiomyopathy
- common manifestations include dyspnea, pulmonary rales, cardiomegaly, pulmonary edema, S3 heart sound, and tachycardia
- results from the impaired ability if myocardial fibers to contract, relax, or both
3
Q
Systolic Dysfunction
A
- common etiology is MI
- reduced contractility evidenced by low ejection fraction and reduced inotropy during ventricular systole
- impaired contractility involves loss of cardiac muscle cells, Beta receptor down regulation, and reduced ATP production
4
Q
Diastolic Dysfunction
A
- Two main causes are coronary artery disease and hypertension
- disorder of myocardial relaxation such that the ventricle is excessively noncompliant and does not fill effectively
- low cardiac output, congestion, and edema formation with normal ejection fraction
5
Q
Compensatory Mechanisms and Remodeling
A
- helpful in restoring cardiac output toward normal
- over the long term they are detrimental to the heart
- Current management of HF is directed towards reducing the harmful consequences of SNS activation, increased preload, and myocardial hypertrophy
6
Q
Sympathetic Nervous System (SNS) Activation
A
- primarily a result of baroreceptor reflex stimulation, which detects fall in pressure
- CNS increases activity in the sympathetic nerves to the heart resulting in venoconstriction
- juxtaglomerular cells release renin, activating the RAAS cascade, resulting in increased sodium and water retention
- Remodeling: process of myocyte loss, hypertrophy of remaining cells, and interstitial fibrosis
7
Q
Increased Preload
A
- initially a consequence of reduced EF with resultant increase in residual ESV
- decreased CO to the kidney reduced glomerular filtration = fluid concentraion
- RAAS cascade activated = elevated blood volume
- Frank - Starling mechanism
- causes damage in HF
8
Q
Myocardial Hypertrophy and Remodeling
A
- results from a chronic elevation of myocardial wall tension (law of laplace)
- High systolic pressure in the ventricle needed to overcome a high afterload leading to hypertrophy
- neurohormonal factors have hypertrophic effect on the heart
- angiotensin II is involved in remodeling
9
Q
Clinical manifestations of HF
A
- left ventricular failure is most common
- often leads to right ventricular failure
- Forward failure = insufficient cardiac pumping manifested by poor CO
- Backwards failure = congestion of blood behind the pumping chamber
10
Q
Left sided HF
A
- most often associated with:
- backward effects, which result in accumulation of blood within the pulmonary circulation, pulmonary congestion, and edema
- forward effects, which result in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and orgnas
- acute cardiogenic pulmonary edema (flash pulmonary edema) which is a life threatening condition
11
Q
Clinical Manifestations of Left Sided HF (only backwards effects)
A
- dyspnea
- dyspnea on exertion
- orthopnea
- paroxysmal nocturnal dyspnea
- cough
- respiratory crackles (rales)
- hypoxemia
- high left-atrial pressure
- cyanosis
12
Q
Right SIded HF
A
- pulmonary disorders, increased pulmonary vascular resistance, high afterload, right ventricular hypertrophy (cor pumonale), right ventricular failure
- backward effects due to congestion in the systemic venous system
- forward effects cause low output to left ventricle leading to low CO
13
Q
Clinical Manifestations of Right Sided HF
A
- edema
- ascites
- jugular veins distended
- impaired mental functioning,
- hepatomegaly
- splenomegaly
- hepatojugular reflux test
14
Q
Biventricular HF
A
- most often result of primary left sided HF progressing to right sided HF
- Reduced CO
- pulmonary congestion due to left sided HF
- systemic venous congestion due to right sided HF
15
Q
Classes and Stages of HF
A
- FACES ( fatigue, activity limitation, congestion, edema, shortness of breath)
- diagnostic assessment includes XRAY and echocardiography
- b type naturetic peptide level
- severity of symptoms used to identify the 4 classes/ stages of HF
16
Q
Treatment of HF
A
- reduce preload (diuretics & ACE inhibitors)
- Improve CO (digitalis; must hold 60 bpm)
- inhibit SNS effects (beta blockers)
- Improve contractility (digitalis)
- reduce effects of ANG II (ACE inhibitors & ARBs)
- Pacemakers `
17
Q
Cardiac Dysrhythmias
A
- also called arrhythmias
- abnormality of the cardiac rhythm or impulse generation or conduction
- Are significant because they indicate an underlying pathophysiologic disorder and may impair normal CO
18
Q
3 major types of Cardiac Dysrhythmia
A
- abnormal rates of sinus rhtythm
- abnormal sites (ectopic) of impulse initiation
- disturbances in conduction pathways
19
Q
Dysrhythmia Mechanisms
A
- impulse generation: abnormalities in rate of impulse generation from a normal pacemaker or from impulse generation from an abnormal (ectopic) site
- dysrhytmias initiated by 3 types of depolarizing mechanisms: abnormal automaticity, triggered activity from depolarization, reentrant circuits
20
Q
Automaticity
A
- spontaneous generation of an action potential
- major causes include:
- failure to repolarize to normal resting membrane potential
- plasma membrane leakiness to sodium or calcium ions at rest
- hypokalemia
