heart failure

Question 1

heart failure

Answer 1

• impaired cardiac pumping, filling or both
• 23.4% mortality rate

Question 2

characteristic of heart failure

Answer 2

• reduced exercise tolerance
• diminished quality of life
• shortened life expectancy

Question 3

risk factors of heart failure

Answer 3

• coronary artery disease
• hypertension
• diabetes
• smoking
• obesity
• high serum cholesterol

Question 4

pathophysiology of heart failure

Answer 4

• interference in normal mechanisms regulating CO, preload, afterload, cardiac contractility and HR
• any alteration in these factors leads to decreased ventricular function

Question 5

categories of heart failure

Answer 5

• reduced ejection fraction (REF)
• preserved ejection fraction (PEF)

Question 6

REF

Answer 6

• most common
• heart cant pump blood effectively
• impaired contractile function, increased afterload (hypertension), cardiomyopathy, mechanical abnormality
• LV loses ability to generate enough pressure to eject blood through aorta
• reduction in ejection fraction EF <40% (normal is >55%)

Question 7

PEF

Answer 7

• diastolic HF
• inability of ventricles to relax and fill during diastole
• results in decreased stroke volume and CO
• results from left ventricular hypertrophy

Question 8

compensatory mechanisms of heart failure

Answer 8

• sympathetic nervous system (SNS) activation
• neuro-hormonal responses
• ventricular dilation
• ventricular hypertrophy

Question 9

sympathetic nervous system (SNS) activation and heart failure

Answer 9

• increased catecholamines, increase HR, myocardial contractility, peripheral vasoconstriction
• results in increased cardiac workload and need for O2

Question 10

neuro-hormonal responses to HF

Answer 10

-kidneys respond to decreased blood flow by producing more renin

-renin increases causes adrenal cortex to release aldosterone, resulting in more sodium and H2O retention, increased peripheral vasoconstriction and increased BP

-posterior pituitary gland responds to decreased cerebral perfusion pressure and secretes ADH creating increased BV

Question 11

ventricular dilation

Answer 11

• chambers enlarge due to elevated pressure
• muscle fibres become overstretched and lose ability to contract effectively

Question 12

ventricular hypertrophy

Answer 12

• increase muscle mass and cardiac wall thickens in response to overwork
• muscle has poor contractility requiring more O2 to perform
• coronary artery circulation becomes poor and heart is prone to dysrhythmias

Question 13

counter-regulatory mechanisms and HF

Answer 13

• natriuretic peptides (atrial and brain) are hormones produced in response to increased BV
• regulate renal, cardiovascular and hormonal effect
• cardiac decomposition occurs when mechanism can no longer maintain CO and tissue perfusion becomes insufficient

Question 14

left sided HF

Answer 14

• think “lungs”
• ventricular dysfunction causes blood to back up to left atrium and pulmonary veins
• fluid extravasation from pulmonary capillary bed into interstitium and then into alveoli leads to pulmonary congestion and edema
• upon inspection: crackles, wheezing, diminished lung sounds

Question 15

right sided HF

Answer 15

• backs up into body
• results in peripheral edema, hepatomegaly, splenomegaly, jugular venous congestion
• primary cause is LSHF

Question 16

CM of decompensated HF

Answer 16

• pulmonary edema – increase in respiratory rate and decreased partial pressure of arterial O2
• increase in pulmonary venous pressure causes fluid to leak into interstitial space tachypnea and SOB
• increased fluid moves into alveoli which disrupts gas exchange – respiratory acidosis
• anxious, pale, cyanotic, clammy, cold, dyspnea, orthopnea, wheezing, coughing, blood-tinged sputum
• auscultation; crackles, wheezing, bronchi

-rapid HR and elevated BP

Question 17

CM of chronic HF

Answer 17

• fatigue
• dyspnea
• paroxysmal nocturnal dyspnea
• cough
• tachycardia
• edema
• nocturia
• skin changes
• behavioural changes
• chest pain
• weight changes

Question 18

complications of HF

Answer 18

• pleural effusion – fluid leaking into pleural space
• dysrhythmias
• left ventricle thrombus – increased LV and decreased CO increase risk of thrombus formation
• hepatomegaly – venous system backing up into liver leading to impaired liver function, cirrhosis
• renal failure – decreased CO leads to hypoperfusion of kidneys

Question 19

HF dx

Answer 19

• echo (distinguish between HRrEF from HFpEF)
• measurement of BNP or N-terminal-pro-BNP (help distinguish dyspnea caused by HF)
• chest x-ray (distinguish pleural effusions from other caused of dyspnea)

Question 20

acute decompensated HF nursing management

Answer 20

• decrease intravascular volume – loop diuretics (reduce venous return = reduce preload = improved CO, improved LV function, decrease pulmonary vascular pressures, improves gas exchange
• decrease venous return – elevated head of bed with feet dangling
• decrease afterload – monitor VS (decreased systematic vascular resistance reduces afterload)
• improve gas exchange – morphine can reduce preload and afterload and decrease myocardial oxygen demand, administer O2 if sats <90%
• improving cardiac function – aggressive complex therapies including inotropic therapies and hemodynamic monitoring
• reduce anxiety

Question 21

chronic HF collaborative care

Answer 21

• referral to specialist
• non-pharmacologic therapies – O2, self-management teaching
• devices – pacemakers, implantable cardioverter-defibrillator, mechanical circulatory support
• transplant

Question 22

CHF drug therapy

Answer 22

• loop diuretics
• thiazide diuretics
• ACE inhibitors
• neprilysin inhibitor
• B-adrenergic blockers
• mineral corticoid receptor antagonists

Question 23

loop diuretics and CHF

Answer 23

act on ascending loop of Henle to promote excretion of sodium, chloride, and H20. risk of hypokalemia

Question 24

thiazide diuretics and CHF

Answer 24

inhibit sodium reabsorption from distal tubule promoting excretion of sodium and H20. tx edema and HTN

Question 25

ACE inhibitors and CHF

Answer 25

(end in pril)

block conversion of angiotensin I to II which reduces aldosterone levels, reduces vascular resistance, maintains tissue perfusion, ventricular filling pressure. risk for hypotension, chronic cough, renal insufficiency in high doses, angioedema

Question 26

neprilysin inhibitor and CHF

Answer 26

combination of angiotensin receptor II blocker and new class of HF medication

Question 27

B-adrenergic blockers and CHF

Answer 27

block negative effects of SNS including increased HR, risk for reduced myocardial contractility, bradycardia, fatigue, asthma, exacerbation, edema

Question 28

mineral corticoid receptor antagonists

Answer 28

(potassium-sparing diuretics)

block sodium and H20 excretion as well as potassium excretion by blocking aldosterone. risk for additive effects with ACE inhibitors (monitor renal function and potassium)

Question 29

CHF nutritional therapy

Answer 29

• diet and weight
• DASH diet
• dietary restriction of sodium (<2g/day)
• stop using saltshaker, do not add salt to food, read food labels, ear fresh fruits and veggies
• recognize sociocultural value of food
• daily weight to monitor fluid retention
• weigh same time every day, before breakfast, wearing similar clothing
• Contact primary care provider if the patient experiences weight gain of 2 kg over a 2-day period or 2.5 kg over 5-day period

Question 30

nursing diagnosis for HF

Answer 30

• impaired gas exchange; respiratory monitoring, O2 therapy, positioning in semi-fowlers
• cardiac care; check pulses, cap refill, ins and outs, monitor for dyspnea, tachypnea, instruct pt about activity restriction
• hypovolemia management; monitor effects of meds, monitor potassium levels, daily weight, monitor respiratory status, monitor hemodynamic status
• activity intolerance; encourage alternating periods of rest and activity, teach pt to change positions slowly