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AHI > CARE OF PATIENTS WITH HEART FAILURE > Flashcards

CARE OF PATIENTS WITH HEART FAILURE Flashcards

1
Q

Leading cause of hospital admissions for patients over 65 - affects many
Require lot follow-up care
Major cause of disability and death
Readmission an important quality measurement in acute care - readmitted often - core measure to provide edu
CMS core measure
Aka Pump failure-chronic inability of heart to work effectively as a pump
Heart not able to maintain adequate cardiac output to meet the metabolic needs of the body
Acute episodes lands them in hospital
Types
Most heart failure begins with failure of the left ventricle and progresses to failure of both ventricles; possible one fail by itself for short period of time

A

HF

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2
Q

Heart failure discharge education

A

CMS core measure

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3
Q

Left-sided heart failure
Right-sided heart failure
High-output failure

A

Types HF

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4
Q

Right ventricle can not empty/pump effectively
Causes:

A

Right sided HF

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5
Q

Left ventricular failure
Right ventricular MI (myocardial infarction)
Pulmonary hypertension
Chronic lung disease

A

Causes:- Right sided HF

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6
Q

Systemic Congestion
Jugular (neck vein) distention (JVD) - seen often
Enlarged liver and spleen
Anorexia and nausea
Dependent edema (legs and sacrum) - 4+ pitting edema in LE
Distended abdomen
Swollen hands and fingers
Polyuria at night
Weight gain - weigh daily; no more than 2 lb/daily or 5 lb/week: is an issue
Increased blood pressure (from excess volume)
Decreased blood pressure (from failure)

A

Symptoms of right sided HF

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7
Q

Decreased tissue perfusion from poor cardiac output and pulmonary congestion from increased pressure in pulmonary vessels
Systolic Heart Failure
Dystolic Heart Failure
Common Causes:

A

Left sided HF

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8
Q

Heart can not contract forcefully enough to eject adequate blood
HF with reduced EF: normally 50-70%; <40% = HF

A

Systolic Heart Failure - Left sided HF

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9
Q

Ventricle can not relax adequately during diastole preventing adequate filling of blood - not enough blood to be pumped out
HF with preserved LV func

A

Dystolic Heart Failure - Left sided HF

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10
Q

Hypertension
Coronary artery disease
Valvular disease

A

Common Causes:- Left sided HF

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11
Q

Pulmonary congestion - alveoli fill with fluid
Decreased cardiac output

A

Symptoms of left sided HF

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12
Q

Hacking cough, worse at night
Dyspnea - at rest, exertion, orthopnea
Crackles/wheezes in lungs
Pink, frothy sputum - lifethreating pulm edema; severe HF
Tachypnea
S3/S4 gallop: S3: increase in LV diastolic pressure and means not able to work as well - first sign of HF; S4: not sign of HF but sign decreased ventricular compliance

A

Pulmonary congestion - alveoli fill with fluid - Symptoms of left sided HF

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13
Q

Fatigue and weakness - affects ADLS
Oliguria during day (not much urine at night)/Nocturia at night
Angina
Confusion and restlessness
Dizziness - lack volume to body
Pallor and cool extremities
Weak peripheral pulses
Tachycardia

A

Decreased cardiac output - Symptoms of left sided HF

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14
Q

Not as common as right/left HF (CO remains below norm)
Occurs when cardiac output remains normal or above normal but there are increased metabolic needs or hyperkinetic conditions
Causes:
Not as common as the other two types

A

High output HF

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15
Q

Septicemia
High fever
Anemia
Hyperthyroidism

A

Causes: - High output HF

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16
Q

When cardiac output is insufficient to meet the demands of the body, are compensatory mechanisms that try work to improve cardiac output - might initially but do have damaging effect on heart
Initially increase cardiac output but eventually have a damaging effect of pump function
All the compensatory mechanisms contribute to increased oxygen needs of the myocardium
Eventually the heart can not keep up with the demands - damaging effect eventually
Then clinical manifestations of HF occur

A

Compensatory mechanisms

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17
Q

Sympathetic nervous system stimulation
Renin-angiotensin-aldosterone system (RAAS) activated as well
Other chemical responses
Myocardial hypertrophy

A

When cardiac output is insufficient to meet the demands of the body, are compensatory mechanisms that try work to improve cardiac output - might initially but do have damaging effect on heart

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18
Q

Increases HR and blood pressure - increase blood flow
Results from tissue hypoxia - stimulation adrenergic receptors
CO initially increased but limited esp if heart poorly perfused because of aterosclerosis - may worsen because of this

A

Sympathetic nervous system stimulation

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19
Q

Causes vasoconstriction and retention of Na and water - fluid volume up - get blood out to body

A

Renin-angiotensin-aldosterone system (RAAS) activated as well

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20
Q

Immune response causes ventricular remodeling
Endothelin (secreted by endothelin cells as stretched and released because stretch on cardiac muscle) causes vasoconstriction - increases PVR and BP; HF worsens
Vasopressin causes vasocostriction - increase CO

A

Other chemical responses

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21
Q

Thicken of heart walls to increase muscle mass and lead to more forceful contractions
Helps as first; thicker - not as much stretch

A

Myocardial hypertrophy

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22
Q

Monitor diagnostics closely
Lab assessment
Imaging

A

Diagnostic assessment - HF

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23
Q

Electrolytes
BUN and creatinine
Hemoglobin and hematocrit
Urinalysis
ABG’s –
BNP (B-type natriuretic peptide)

A

Lab assessment

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24
Q

Abnormalities from complications of HF or side effects of drug therapy
Esp with diuretics

A

Electrolytes

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25
Q

Inadequate perfusion of kidneys can result in impairment and elevated levels
Monitor kidney func - blood not pumped effectively kidneys affected

A

BUN and creatinine

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26
Q

Could be result/low secondary to hemodilution
HF resulting from anemia?

A

Hemoglobin and hematocrit

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27
Q

Possible proteinuria and high specific gravity
Microalbuminuria - early indicator of decreased compliance of the heart and occurs before the BNP rises

A

Urinalysis

28
Q

Evaluates for hypoxemia
Decrease in gas exchange secondary due to fluid filled alveoli when left sided HF with dyspnea/exertion

A

ABG’s –

29
Q

Will be elevated and used for diagnosing HF (diastolic HF and acute dyspnea)
Response to left/right ventricular dysfunc
Higher levels - HF likely cause
BNP is produced and released by the ventricles when the patient has fluid overload becuase of HF (left/right sided ventricular dysfunc)
Natriuretic peptides are neurohormones that promote vasodilation and diuresis through sodium loss in the renal tubules
Therapy can lower levels
Patients with renal disease and age may also have elevated levels

A

BNP (B-type natriuretic peptide)

30
Q

Chest x-ray
Echocardiography (ultrasound of the heart)

A

Imaging

31
Q

Cardiomegaly (enlarged heart) may be present - hypertrophy of left side of heart
Look at for Pleural effusions with biventricular failure
Look at for LV failure

A

Chest x-ray

32
Q

Best tool in diagnosing HF
Measures chamber size, ejection fraction and flow
How advance, EF measurement; understanding how pat is
Noninvasive

A

Echocardiography (ultrasound of the heart)

33
Q

Start with ABCs
Impaired gas exchange related to ventilation/perfusion imbalance - want increase gas exchange
Decreased cardiac output related to altered contractility, preload, and afterload - want adequate perfusion
Fatigue related to hypoxemia - affects ADLs
Potential for pulmonary edema - not want develop (HF pats at high risk for this)

A

Priority probs - HF

34
Q

Oxygen
Monitor respirations and lung sounds - not labored/accessory muscles/abnormal sounds
If dyspnea present, high-Fowler’s position
Reposition, cough and deep breathe at least every 2 hours
Drug Therapy
Nutrition therapy
Fluid restriction
Weigh daily
Monitor and record intake and output closely
Provide periods of uninterrupted rest
Assess the patient’s response to increased activity - see if good activity and able get back to baseline prior to exacerbation of HF

A

Nursing interventions - HF

35
Q

Keep oxygen saturations 90% or greater - monitor O2 levels closely

A

Oxygen

36
Q

Maximizes chest expansion and improves oxygenation

A

If dyspnea present, high-Fowler’s position

37
Q

Up and moving
Improve oxygenation and prevent atelectasis

A

Reposition, cough and deep breathe at least every 2 hours

38
Q

Goal: To improve stroke volume
Will reduce afterload, reduce preload, and improve cardiac muscle contractility

A

Drug Therapy

39
Q

Encourage with pats
Goal to reduce sodium and water retention - not get edema
Reduce sodium intake (can be as low as 2 gram/day) - KEY

A

Nutrition therapy

40
Q

Range from 2 Liters to 3 Liters per day

A

Fluid restriction

41
Q

Encourage this; keep record
Most reliable indicator of fluid gain or loss
1 kg of weight gain or loss equals 1 liter of retained or lost fluid

A

Weigh daily

42
Q

Continuous positive airway pressure (CPAP) –
Cardiac resynchronization therapy (CRT) –
Gene Therapy -

A

Non surgical options: HF

43
Q

improves obstructive sleep apnea and supports cardiac output and ejection fraction - decreases afterload, preload, BP, dysrhythmias

A

Continuous positive airway pressure (CPAP) –

44
Q

uses a permanent pacemaker alone or in combination with an implantable cardioverter-defibrillator (ICD); aka biventricular pacemaker; more synchronous venous contractions - improves EF and CO causing contractility to improve

A

Cardiac resynchronization therapy (CRT) –

45
Q

end-stage HF who cannot have heart transplant; replaces norm genes with norm/modified genes by series of injections of growth factors into LV; improve exercise tolerance and repair cardiac cells

A

Gene Therapy -

46
Q

Heart transplantation
Ventricular Assistive Devices (VAD)

A

surgical options: HF

47
Q

Ultimate choice for end-stage HF

A

Heart transplantation

48
Q

Mechanical pump is implanted to work with patient’s heart to improve function
Debilitating end-stage HF and sent home on drug therapy and improves lives of pats and sent to hospice; short-term while waiting for transplant/long-term

A

Ventricular Assistive Devices (VAD)

49
Q

Arterial vasodilators reduce the resistance to left ventricular ejection (afterload) and improve cardiac output - reverse excessive vasoconstriction
Suppress RAAS
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin-receptor blockers (ARBs)
Human B-type Natriuretic Peptides (hBNPs)

A

Drugs to reduce afterload

50
Q

Enalapril (Vasotec)
Fisinopril (Monopril)
-pril

A

Angiotensin-converting enzyme (ACE) inhibitors

51
Q

Valsartan (Diovan)
Irbesartan (Avapro)
Losartan (Cozaar)
-sartan
Both more effective in Euro Americans/African Americans
Start slowly esp in volume depleted pats
ACE inhibitors are the first-line drug of choice
Monitor for:

A

Angiotensin-receptor blockers (ARBs)

52
Q

May cause dry cough - AE; nagging

A

ACE inhibitors are the first-line drug of choice

53
Q

Orthostatic hypotension
Acute confusion
Poor peripheral perfusion
Reduced urine output in patients with low systolic BP
Serum Potassium and creatinine levels - renal dysfunc?

A

Monitor for: - ACE, ARBs

54
Q

Used to treat acute HF
Drug Causes loss of sodium and vasodilation
Nesiritide (Natrecor)
Monitor BP and pulse - sig decreases in BP
Serum BNP will increase after administration - expected
Bolus followed by continuous infusion up to 48 hrs
Give in dedicated line - not compatible with most meds

A

Human B-type Natriuretic Peptides (hBNPs)

55
Q

Reduce preload by decreasing volume and pressure in the left ventricle, increasing ventricular muscle stretch and contraction
Diuretics
Venous vasodilators (nitrates)
Morphine sulfate

A

Drugs to reduce preload

56
Q

First-line drug of choice in older adults with HF and fluid overloaded pats
Enhance renal excretion of sodium and water
Monitor for dehydration - get rid fluid
Monitor potassium levels - often on K replacement protocol
If creatinine level is greater than 1.8 mg/dL, notify health care provider before administering supplemental potassium - eye on labwork
Loop excretes K
Loop - Furosemide (Lasix)
Loop - Torsemide (Demadex)
Loop - Bumetanide (Bumex)
Thiazide – Hydrochlorothiazide (HCTZ); Metolazone (Zaroxolyn); not excrete K; not want get too high
Potassium-sparing – Spironolactone (Aldactone); not excrete K; not want get too high

A

Diuretics

57
Q

For HF patients that have persistent dyspnea
Returns venous vasculature to more norm capacity; decrease volume blood returning to heart and improve LV func
May be administered IV, orally, topically - acute HF pats
Monitor BP when starting/increasing because vasodilation can cause
Headache is common but the patient will develop a tolerance to this side effect - go away/diminish

A

Venous vasodilators (nitrates)

58
Q

Reduces venous return
Given in acute heart failure to reduce anxiety
Decreases preload and afterload
Slows respirations and reduces the pain associated with a myocardial infarction (MI)

A

Morphine sulfate

59
Q

Digoxin (Lanoxin)
Inotropic drugs
Beta-adrenergic blockers

A

Drugs to improve contractility

60
Q

Provides symptomatic benefits for patients in chronic HF: Reduce HR; Increase contractility; slows conduction through AV node - decreases dyspnea and improves func activity in pats
Added to ACEs/ARBs/diuretics does reduce exacerbations HF and hospitalizations
Inconsistent absorption in GI tract - drugs interfere with absorption (including antacids)
Eliminated by renal excretion - if have renal disease consider
Maintain lower dose for older pats
Monitor for digoxin toxicity (s/s: anorexia, fatigue, blurred vision, changes in mental status, dysrhythmias: PVCs); hypokolemia can potentiate toxicity and closely monitor older pats
HR and rhythm for no changes

A

Digoxin (Lanoxin)

61
Q

IV route and continuous drips
Increase force cardiac contraction
Dobutamine (Dobutrex): used for short-term treatment of acute episodes of HF
Milrinone (Primacor) - vasodilator; acute episodes HF; can go if adv HF; go home with central line
Levosimendan (Simdax) - HF pats at risk MI; short half-life; never pause these influces

A

Inotropic drugs

62
Q

Start slowly
Not used in patients with acute HF
Blocks the sympathetic stimulation
Monitor closely so not have bradycardia, hypotension; benefits mild to mod disease pats: EF, decrease hospitalizations, decreases orthopnea, increases activity tolerance
Increase contracility
-lol
Carvedilol (Coreg)
Metoprolol succinate (Toprol XL)
Bisoprolol (Zebeta)

A

Beta-adrenergic blockers

63
Q

Diet
Activity schedule
Drug therapy - afford meds, AE, requirements what take before
Discharge instructions
Resources and equipment needs
VERY IMPORTANT TO DECREASE READMISSIONS need appt before leaving; home support; pamphlets, books; support groups; any activity assistance: walker/canes

A

Patient teaching for HF

64
Q

Sodium restriction and fluid restriction
Why imp

A

Diet

65
Q

Notify any of the following symptoms to health care provider - know when notify HCP

A

Discharge instructions

66
Q

Rapid weight gain (3 lbs in a week or 1-2 lb overnight) - weigh daily
Decrease in exercise tolerance lasting 2 to 3 days
Cold symptoms (cough) lasting more than 3-5 days
Excessive awakening at night to urinate
Development of dyspnea or angina at rest or worsening angina
Increased swelling in the feet, ankles, or hands

A

Notify any of the following symptoms to health care provider - know when notify HCP

AHI (77 decks)

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