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NURS305 > Week 6: Heart Failure > Flashcards

Week 6: Heart Failure Flashcards

1
Q

what is heart failure

A

long-term chronic condition that gets worse over time

  • inability of myocardium to pump enough blood to meet body needs
  • abnormal clinical syndrome involving impaired cardiac pumping or filling, or both
  • heart failure is a response to cardiac dysfunction
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2
Q

what are the most common causes of heart failure (11)

A
  • coronary artery disease: MI
  • hypertension
  • valvular disease: rheumatic disease
  • congenital heart disease
  • pulmonary: HTN (right sided), PE
  • infiltrative disorders
  • pericardial disease (Restrictive)
  • inflammatory (myocarditis)
  • cardiomyopathy
  • dysrhythmias
  • medication non-compliance
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3
Q

review the normal circulation through the heart

A
  1. superior/inferior vena cava
  2. right atrium
  3. tricuspid valve
  4. right ventricle
  5. pulmonary valve
  6. pulmonary artery to lungs
  7. left atrium
  8. mitral valve
  9. left ventricle
  10. aortic valve
  11. aorta to body
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4
Q

what are the 3 major systems that are recruited when myocardial injury occurs

A
  • sympathetic nervous system
  • Renin-Angiotensin-Aldosterone System
  • Natriuretic peptide system
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5
Q

what are the 4 compensation mechanisms

A
  1. elevation in SNS activity
  2. neural-hormonal response
  3. dilation of ventricle (Frank starling mechanism)
  4. ventricular hypertrophy
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6
Q

what does an elevation in SNS activity do

A

increases heart rate and contractility

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7
Q

what does the neural-hormonal response do

A
  • increases blood volume and elevates preload
  • increase in salt and water retention (RAAS)
  • posterior pituitary gland secretes ADH
  • production of endothelin - potent vasodilator
  • proinflammatory cytokines are released by heart causing hypertrophy, contractile dysfunction, and cell death
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8
Q

what does the Frank starling mechanism do

A
  • dilation of the ventricle
  • increase pressures result in increased volume at the end of diastole
  • increased stretch initially adaptive - eventual overstretch results in ineffective contraction
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9
Q

what is ventricular hypertrophy

A
  • increase in muscle mass and cardiac wall thickness in response to overwork and strain
  • develops overtime, generally following persistent or chronic dilation
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10
Q

what is the counter-regulatory mechanism

A

natriuretic peptide system
- impacts salt and water handling, pressure regulation, and may influence myocardial structure and function

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11
Q

natriuretic peptide system: what is BNP and ANP and what do they do

A

brain natriuretic peptide: natriuretic hormone primarily release from the heart - particularly the ventricles

atrial natriuretic peptide: hormone released by myocardial cells in atria

both are released in response to wall stress and volume expansion
both have diuretic, natriuretic, and hypotensive effects
both inhibit RAAS and impair systemic and renal sympathetic activity

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12
Q

what happens when the SNS, RAAS, NP systems regulate an issue for a prolonged amount of time? there are 4 outcomes

A

become maladaptive
- elevation of diastolic pressures transmitted to the atrial/pulmonary/systemic venous circulation promotes congestion and edema
- increase in LV afterload (vasoconstriction) can both directly depress cardiac function and enhance rate of deterioration of myocardial function
- increases in contractility, heart rate, and LV afterload can worsen or provoke coronary ischemia
- catecholamines, angiotensin 2, and aldosterone promote the loss of myocytes through apoptosis, and cause myocardial hypertrophy and fibrosis

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13
Q

explain acute vs chronic heart failure

A

acute
- sudden onset, no compensatory mechanisms
- days or hours

chronic
- ongoing process, months to years
- progressive worsening of ventricular function
chronic neuro-hormonal activation that results in ventricular remodelling

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14
Q

what are some clinical manifestations of chronic heart failure

A
  • fatigue
  • dyspnea
  • tachycardia
  • edema
  • nocturia
  • depression
  • chest pain
  • weight changes
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15
Q

explain left vs right heart failure

A

left
- left ventricular dysfunction
- disturbance of the contractile function of the left ventricle, resulting in low cardiac output state

right
- ineffective right ventricular contractile function
- backwards flow

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16
Q

explain systolic vs diastolic heart failure

A

systolic
- abnormality of the heart muscle that markedly decreases contractility during systole (ejection) and lessens the quantity of blood that can be pumped out of the heart

diastolic
- abnormality of the heart muscle that makes it unable to relax, stretch, or fill during diastole, ejection fraction can be normal

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17
Q

what are the 3 clinical heart failure syndromes

A
  1. heart failure reduced ejection fraction: HFrEF
  2. heart failure preserved ejection fraction: HFpEF
  3. heart failure mid-range ejection fraction: HFmEF
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18
Q

what are the 3 considerations for HFrEF

A

Heart failure reduced ejection fraction
- formally called systolic dysfunction (inability to pump)
- left ventricular ejection fraction < 40%
- aggressively treated with medical therapy and cause for etiology determined ASAP

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19
Q

what are the 3 considerations for HFpEF

A

Heart failure preserved ejection fraction
- Formally called diastolic dysfunction – inability to relax
- LVEF > 50%
- Treatment of symptoms

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20
Q

what are the 3 considerations for HFmEF

A

Heart failure mid-range ejection fraction
- “New” classification of patients.
- LVEF 40-49%
- Treatment pathway still under review, may be individualized

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21
Q

what are the complications of heart failure

A
  • pleural effusions
  • dysrhythmias
  • left ventricular thrombosis
  • hepatomegaly
  • renal failure
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22
Q

explain the process of heart failure diagnosis

A
  1. suspected heart failure
  2. examine clinical history and physical assessment
    - history: symptomos, functional limitation, prior cardiac disease, risk factors, comorbidities
    physical: vitals, weight, volume, heart, lung, abdomen, vascular
  3. do initial investigations
    - chest radiograph
    - electrocardiogram
    - B-type natriuretic peptide
    - lab work (CBC, electrolytes, renal function, urinalysis, glucose, thyroid)
  4. assess ventricular function
    - echocardiogram
  5. additional diagnostic investigations
    - radionuclide imaging
    - cardiac catheterization
    - cardiopulmonary exercise testing
    - CMI, ST, endomyocardial biopsy
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23
Q

what are the clinical manifestations of right sided heart failure

A
  • fatigue, weakness
  • hypotension (severe disease)
  • fluid overload
  • weight gain
  • anorexia
  • peripheral edema, +/- JVP
  • decreased saO2
  • murmurs
  • ascites/anasarca (massive, generalized body edema)
  • hepatomegaly
  • right heaves
  • renal impairment
  • tachypnea
  • tachycardia
24
Q

what are the clinical manifestations of left sided heart failure

A
  • Fatigue, weakness
  • Hypertension
  • Hypotension – reflects severe disease
  • Fluid overload
  • Weight gain
  • Pulmonary edema (crackles)
  • Decreased SaO2
  • Extra heart sounds (S3 and S4 )
  • Peripheral edema
  • Left Heaves
  • Renal impairment
  • Tachypnea
  • Tachycardia
  • Nocturia
  • Dyspnea
  • Orthopnea
25
what are some abnormal from baseline assessments we would observe in heart failure?
- evidence of severely compensated HF (hypotension, renal function, altered mentation) - dyspnea at rest - worsened congestion, event without dyspnea at rest - s&s of pulmonary/systemic congestion even in weight gain absence - major electrolyte disturbance - associated comorbid conditions: pneumonia, pulmonary embolism, diabetic ketoacidosis, acute coronary syndrome or symptoms of transient ischemic attack/stroke - repeated implantable cardioverter defrib firings - previously undiagnosed HF with s&s of systemic/pulmonary congestion - hemodynamically significant arrhythmia including new onset of a.fib with rapid ventricular respose
26
what are the grades of ejection fraction and the corresponding %?
Grade 1 (normal) - >50% Grade 2 (mild) - 41-49% Grade 3 (moderate) - 30-41% Grade 4 (severe) <30%
27
what are the 9 lab works done for HF
1. BNP: brain natriuretic peptide - elevated in pt with kidney failure - elevated in CAD, valvular heart disease, pulmonary hypertension, sepsis 2. CBC: anemia, polycythemia, leukocytosis 3. electrolytes: Na, K 4. renal function 5. liver function, hepatic congestion 6. troponin, CK 7. glucose 8. thyroid function 9. blood gases
28
what are the 7 diagnostic assessments of HF
1. ECG 2. chest radiograph 3. echocardiography 4. exercise testing 5. stress test 6. MRI - cardiac 7. cardiac catheterization
29
what does an ECG look for
evidence of ischemia, infarction, arrhythmia (ex. a.fib)
30
what does a chest radiograph look for
assesses signs of pulmonary edema, cardiomegaly, alternative diagnoses (Ex. pneumonia)
30
what does an echocardiography look for
ejection fraction - if cardiac or valvular function is not know - follow up to compare to previous
31
what are the 4 classifications of heart failure
Class 1 - no symptoms - can perform ordinary activities with no limitations Class 2 - mild symptoms - occasional swelling - somewhat limited in ability to exercise - no symptoms at rest Class 3 - noticeable limitations in ability to exercise - comfortable only at rest Class 4 - unable to do any physical activity without discormfort - symptoms at rest
32
what are the goals of therapy (9)
1. Improve left ventricular function by decreasing intravascular volume 2. Decreasing preload 3. Decreasing afterload 4. Improving gas exchange and oxygenation 5. Increasing CO 6. Reduce anxiety 7. Patient education and support 8. Improve quality of life 9. Reduce morbidity
33
what are the 9 key collaborative care interventions?
1. patient education and support 2. referral to special care program 3. nonpharm therapies - diet, exercise and activity, oxygen therapy, self-management 4. control CAD, HTN, cholesterol and diabetes 5. drug therapies: medication management VASTLY improves outcomes 6. devices - cardiac resynchronization therapy - implantable cardioverter -defibrillator - mechanical circulatory support 7. valve replacement 8. cardiac transplantation 9. follow up care
34
what are important aspects in patient education and support (6)
1. appropriate follow up - routine visits, referrals, palliative care 2. support group/rehab program 3. medication education 4. adherence 5. daily monitoring 6. lifestyle modifications - smoking cessation, diet, exercise
35
what are some ways to reduce risks of developing heart failure (lifestyle & medicinal)
lifestyle - regular physical activity - healthy weight - no smoking - healthy eating medicinal - treat high blood pressure - control diabetes - maintain healthy cholesterol levels - take heart protective meds as prescribed
36
management of HF: Nutrition
- obtain dietary history - patients have decreased appetite and nausea, so small frequent meals may be more appropriate - individualized - sodium restriction (<2-3g/day, severe = <1.5g/day) - fluid restriction (1.5-2L/day)
37
management: exercise and activity
- provide adequate rest and recovery time between procedures: cluster care - increasing dyspnea with exertion - restrict activity during breathlessness - increase activity according to tolerance - repositioning if at bed rest - stable: exercise 3-5 days for 30-45 min at a time - cardiac rehab programs
38
what are the 3 principles of pharmacologic therapy?
- start low, go slow - one med at a time - re-evaluate symptoms, status, v/s, adverse effects, and lab values
39
when are all efforts in treating HF patients 2-fold
1. reduce HR to <70bpm 2. respire normal sinus rhythm if not already
40
which med do we start with
- usually afterload reduction: ACE/ARB
41
what is the phar treatment target and what meds are used for heart failure preserved ejection fraction
- treatment: associated conditions and symptoms (hypertension & edema) - A.fib is common: Beta blockers, calcium channel blockers - myocardial ischemia: beta blockers, nitrates - volume overload: diuretics
42
what meds are used for heart failure reduced ejection fraction? include mechanisms (3)
ACE/ARB - inhibit RAAS - block conversion of AT1 to AT2, lowering arteriolar resistance - prevents release of aldosterone - afterload reduction Beta blockers - competitive antagonists blocking SNS catecholamine receptors - B1 blockers are cardioselective - reduce HR, allow prolonged diastolic filling time MRA - mineralocorticoid receptor antagonist (aldosterone receptor) - regulates Na reabsorption and fluid balance
43
what does neprilysin inhibitor - sacubitril do
- decrease BP, sympathetic tone - decrease aldosterone levels - decreases myocardial fibrosis and hypertrophy - increases natriuresis and diuresis
44
what does angiotensin receptor neprilysin inhibitors do - ex. sacubitril/valsartan - entresto
- decrease Na and H2O retention - decrease vasoconstriction, increase vasodilation - decrease hypertrophy - decrease fibrosis - increase natriuresis and diuresis - increase aldosterone suppression
45
what does ivabradine -lancora do
- Acts on the If channel which is highly expressed in the sinoatrial node - Reduces pacemaker rate selectively and allows more time for relaxation/end diastole. - There is reduced HR without loss of contractility. - There are NO BP LOWERING EFFECTS. - Therapy is added IN ADDITION TO routine therapy (I.e. Beta-blockade).
46
what does glucose cotransporter 2 (SGLT2) inhibitor - Dapaglifozin do
- may be used in persistently symptomatic patient who already optimized other therapies - reduces absorption of filtered glucose from tubular lumen and lowers renal threshold for glucose -> increase urinary excretion of glucose, therefore reducing plasma glucose [ ] - reduces Na reabsorption and increases Na delivery to distal tubule, decreasing cardiac pre/afterload - improves myocardial metabolism and improve cardiac efficiency - has vascular effects promoting vasodilation and reduce afterload
47
pharmacological management: diuretics (types, mechanisms, considerations)
thiazide diuretics - inhibits Na reabsorption in distal tubule loop diuretics - promotes Na, Cl, and H2O excretion - consider onset and duration of action - set targets (weight loss, symptom resolution) - is pt on Lasix - patients should be on Lasix with stable symptoms/weight for 24h prior to leaving hospital
48
pharmacological management: vasodilators (types, mechanisms, considerations)
nitroglycerin - vasodilation, reduction of preload and afterload - renal impairment: consider hydralazine and nitrates
49
pharmacological management: digoxin (mechanism)
- inhibits Na-K-ATPase pump - decreases HR - increased myocyte contractile performance and improves overall LV systolic function
50
what is the management of venous thromboembolism prophylaxis
anticoagulation - low dose unfractionated heparin or low molecular weight heparin (if not already anticoagulated and have no contraindications) - not used for pt with heart failure -history of atrial fibrillation - EF <35%
51
what are the 3 devices to manage HF
- cardiac resynchronization therapy - implantable cardioverter-defibrillator - circulation mechanical circulatory assist devices
52
what are the surgical interventions of HF
- heart transplant - valvular replacement - coronary revascularization procedures (coronary artery bypass graft, Percutaneous Coronary Intervention)
53
what are some follow up care considerations of HF
- serial follow up appointments - evaluate clinical status - support HF self-management (pt and family understanding, self-assessment, proper med use) - evaluate therapy response - assess for potential management changes - assess ability to perform ADL, use of drugs, alternative therapies, diet and sodium intake - so further testing - community support group
54
exacerbation management (4)
1. recognize a change - increase weight >2-3lb above baseline overnight or 5lb in a week - increase orthopnea, PND - dyspnea, edema worsening 2. evaluate the change - are symptoms worse? is there a reason they are worse? 3. implement a treatment strategy - increase diuretics - remove cause of exacerbation 4. evaluate effectiveness - weight and symptoms back to normal - contact health care professional if symptoms are not back to normal
55
what are the 5 identifications of precipitating factors in an acute event?
1. diet 2. medication adherence 3. volume status 4. drug interactions 5. cardiac vs noncardiac
56
palliation and symptom control of HF (goals, common symptoms)
- goals are individualized - no cure for HF - primary aim is symptom management and relief of suffering - optimize medications is fundamental to symptom management - dyspnea, pain and fatigue are common symptoms

NURS305 (6 decks)

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