Chapter 19

Question 1

Heart Failure

Answer 1

• 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

Question 2

Pathogenesis and diagnosis of HF

Answer 2

• 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

Question 3

Systolic Dysfunction

Answer 3

• 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

Question 4

Diastolic Dysfunction

Answer 4

• 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

Question 5

Compensatory Mechanisms and Remodeling

Answer 5

• 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

Question 6

Sympathetic Nervous System (SNS) Activation

Answer 6

• 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

Question 7

Increased Preload

Answer 7

• 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

Question 8

Myocardial Hypertrophy and Remodeling

Answer 8

• 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

Question 9

Clinical manifestations of HF

Answer 9

• 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

Question 10

Left sided HF

Answer 10

• 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

Question 11

Clinical Manifestations of Left Sided HF (only backwards effects)

Answer 11

• dyspnea
• dyspnea on exertion
• orthopnea
• paroxysmal nocturnal dyspnea
• cough
• respiratory crackles (rales)
• hypoxemia
• high left-atrial pressure
• cyanosis

Question 12

Right SIded HF

Answer 12

• 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

Question 13

Clinical Manifestations of Right Sided HF

Answer 13

• edema
• ascites
• jugular veins distended
• impaired mental functioning,
• hepatomegaly
• splenomegaly
• hepatojugular reflux test

Question 14

Biventricular HF

Answer 14

• 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

Question 15

Classes and Stages of HF

Answer 15

• 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

Question 16

Treatment of HF

Answer 16

• 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 `

Question 17

Cardiac Dysrhythmias

Answer 17

• 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

Question 18

3 major types of Cardiac Dysrhythmia

Answer 18

• abnormal rates of sinus rhtythm
• abnormal sites (ectopic) of impulse initiation
• disturbances in conduction pathways

Question 19

Dysrhythmia Mechanisms

Answer 19

• 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

Question 20

Automaticity

Answer 20

• 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