1
Q
heart failure
A
- impaired cardiac pumping, filling or both
- 23.4% mortality rate
2
Q
characteristic of heart failure
A
- reduced exercise tolerance
- diminished quality of life
- shortened life expectancy
3
Q
risk factors of heart failure
A
- coronary artery disease
- hypertension
- diabetes
- smoking
- obesity
- high serum cholesterol
4
Q
pathophysiology of heart failure
A
- interference in normal mechanisms regulating CO, preload, afterload, cardiac contractility and HR
- any alteration in these factors leads to decreased ventricular function
5
Q
categories of heart failure
A
- reduced ejection fraction (REF)
- preserved ejection fraction (PEF)
6
Q
REF
A
- 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%)
7
Q
PEF
A
- diastolic HF
- inability of ventricles to relax and fill during diastole
- results in decreased stroke volume and CO
- results from left ventricular hypertrophy
8
Q
compensatory mechanisms of heart failure
A
- sympathetic nervous system (SNS) activation
- neuro-hormonal responses
- ventricular dilation
- ventricular hypertrophy
9
Q
sympathetic nervous system (SNS) activation and heart failure
A
- increased catecholamines, increase HR, myocardial contractility, peripheral vasoconstriction
- results in increased cardiac workload and need for O2
10
Q
neuro-hormonal responses to HF
A
-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
11
Q
ventricular dilation
A
- chambers enlarge due to elevated pressure
- muscle fibres become overstretched and lose ability to contract effectively
12
Q
ventricular hypertrophy
A
- 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
13
Q
counter-regulatory mechanisms and HF
A
- 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
14
Q
left sided HF
A
- 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
15
Q
right sided HF
A
- backs up into body
- results in peripheral edema, hepatomegaly, splenomegaly, jugular venous congestion
- primary cause is LSHF
16
Q
CM of decompensated HF
A
- 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
17
Q
CM of chronic HF
A
- fatigue
- dyspnea
- paroxysmal nocturnal dyspnea
- cough
- tachycardia
- edema
- nocturia
- skin changes
- behavioural changes
- chest pain
- weight changes
18
Q
complications of HF
A
- 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
19
Q
HF dx
A
- 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)
20
Q
acute decompensated HF nursing management
A
- 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
21
Q
chronic HF collaborative care
A
- referral to specialist
- non-pharmacologic therapies – O2, self-management teaching
- devices – pacemakers, implantable cardioverter-defibrillator, mechanical circulatory support
- transplant
22
Q
CHF drug therapy
A
- loop diuretics
- thiazide diuretics
- ACE inhibitors
- neprilysin inhibitor
- B-adrenergic blockers
- mineral corticoid receptor antagonists
23
Q
loop diuretics and CHF
A
act on ascending loop of Henle to promote excretion of sodium, chloride, and H20. risk of hypokalemia
24
Q
thiazide diuretics and CHF
A
inhibit sodium reabsorption from distal tubule promoting excretion of sodium and H20. tx edema and HTN
25
ACE inhibitors and CHF
(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
26
neprilysin inhibitor and CHF
combination of angiotensin receptor II blocker and new class of HF medication
27
B-adrenergic blockers and CHF
block negative effects of SNS including increased HR, risk for reduced myocardial contractility, bradycardia, fatigue, asthma, exacerbation, edema
28
mineral corticoid receptor antagonists
(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)
29
CHF nutritional therapy
- 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
30
nursing diagnosis for HF
- 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
