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heart failure Flashcards

1
Q

What is heart failure?

A

Complex clinical syndrome resulting in insufficient blood supply/O2 to tissues and organs

**decreased CO –> decreased tissue perfusion
**EF

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2
Q

Two types of HF

A
  1. Heart failure with reduced ejection fraction
    -defect in ventricular systolic function/LV contraction
  2. Heart failure with preserved ejection fraction
    -defect in ventricular diastolic functioning/filling
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3
Q

Primary risk factors for HF

A

Hypertension and CAD!
-htn is modifiable and treatment for htn can reduce HF incidences by 50%

Other comorbidities
-DM
-metabolic syndrome
-age
-tobacco
-vascular disease

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4
Q

2 types of etiology of heart failure

A

Anything that messes with CO

  1. Primary causes –> directly damage the heart
  2. Precipitating causes –> increase workload of heart
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5
Q

Left sided HF

A

More common

Results from inability of LV to:
-empty adequately during systole or
-fill adequately during diastole
(or both)

Blood backs up into LA –> increased pulmonary hydrostatic pressure causes fluid leakage from pulmonary capillary bed into interstitium and then alveoli –> pulmonary congestion and edema

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6
Q

HFrEF

A

inability to pump blood effectively

Caused by
-impaired contractile function
-increased afterload
-mechanical abnormalities

Decreased LV ejection fraction (<40%)

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7
Q

HFpEF

A

inability of ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO

Main cause is HTN

Other causes= LV hypertrophy from HTN, old age, female, DM, obesity

Same end result as systolic failure

Diagnosis based on
-symptoms of HF
-normal LVEF
-LV diastolic dysfunction

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8
Q

Right sided HF

A

-RV doesn’t pump effectively
-fluid backs up in venous system
-fluid moves into tissues and organs
-left sided HF usually causes right sided HF

Other causes
-RV infarction, PE, and cor pulmonale

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9
Q

Biventricular failure

A

Both right and left ventricles are fucked up

Fluid build up and venous engorgement

decreased perfusion to vital organs

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10
Q

Compensatory mechanisms: RAAS

A

Homeostatic regulatory system
-goa is augmentation of preload and contractility to maintain CO
-Promotes sodium and water retention

Aldosterone, ADH, vasoconstriction

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11
Q

Compensatory mechanisms: SNS

A

Baroreceptors sense low arterial pressure

catecholamines are released

Stimulation of beta adrenergic receptors increae HR (chronotropy) and ventricular contractility (inotropy)

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12
Q

Endothelin

A

-vasoconstrictor peptide made by vascular endothelial cells
-usually stimulates contraction, but in the heart, acts as negative inotrope and decreases contraction

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13
Q

Proinflammatory cytokines

A

released in response to heart injury

TNG and IL-1 further depress heart function by causing myocyte hypertrophy and apoptosis

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14
Q

Compensatory mechanisms: dilation

A

Enlargement of heart chambers that occurs when pressure in LV is elevated over time

Initially Frank STarling Law

Eventually mechanism becomes inadequate and preload increases w/o subsequent increase in CO

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15
Q

Compensatory mechanisms: hypertrophy

A

Adaptive increase in muscle mass and heart wall thickness

Effective at first

Over time leads to poor contractility, increased O2 needs, poor coronary artery circulation, and risk for dysrhythmias

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16
Q

Compensatory mechanisms: remodeling

A

Continuous activation of neuro-hormonal responses (RAAS and SNS)

Hypertrophy of ventricular monocytes

Ventricles are larger, but less effective in pumping

Can cause life-threatening dysrhythmias and CD

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17
Q

Counterregulatory mechanisms: natriuretic peptides

A

ANP (atrial) and BNP (brain)
-released in response to increased blood volume and ventricular wall stretching
-causes diuresis, vasodilation, and lowered BP

Counteracts effects of SNS and RAAS

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18
Q

Counterregulatory mechanisms: NO and PG

A

released from vascular endothelium in response to compensatory mechanisms

Both relax arterial smooth muscle, resulting in vasodilation and decreased afterload

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19
Q

Acute Decompensated Heart Failure

A

Increase (usually sudden) in symptoms of HF with decrease in functional status

-requires fast treatment and hospitalization

-pulmonary congestion and volume overload due to Na+ and fluid accumulation

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20
Q

Early vs late ADHF

A

early
-increased pulmonary venous pressure
-mild increase in respiratory rate
-decrease in PaO2

Late:
-interstitial edema
-tachypnea
-SOB

Further progression:
-alveolar edema == life threatening
-respiratory acidosis

Pulmonary edema results from left HF

21
Q

Pulmonary edema clinical manifestations

A

anxious, pale, cyanotic
dyspnea
orthopnea
tachypnea
paroxysmal nocturnal dyspnea
use of accessory muscles
cough w/ frothy, blood-tinged sputum
crackles and wheezes
tachycardia
hypo/hyper tension
S3 or S4

22
Q

4 categories of ADHF

A
  1. dry-warm
    2.Dry-cold
    3.wet-warm (most common)
  2. wet-cold

“wet” = volume overload
“warm” = adequate perfusion

23
Q

Chronic heart failure clinical manifestations

A

fatigue
dyspnea
orthopnea
paroxysmal noctunal dyspnea
cough
tachycardia
palpitations

Edema = peripheral, liver, abdomen, lungs –> may be pitting

Skin changes
neuro manifestations
mental status/behavior changes
sleep issues
chest pain
weight changes

24
Q

Heart failure complications

A

pleural effusion

Dysrhythmias and dyssynchronous contraction

Hepatomegaly

Cardiorenal syndrome

Anemia

25
Q

Diagnostic studies

A

Determine and treat underlying cuase

Echo: provides info on LVEF, heart valves, presence of effusion or thrombus

ECG, ambulatory heart monitors, chest xray, 6 min walk, MUGA scan, MRI, stress test, catheter/angiogram, EMB

BNP levels

26
Q

Goals of treatment for ADHF

A

Symptom relief
optimizing volume status
Supporting oxygenation and ventilation
identifying and addressing causes
avoiding complications
teaching related to exacerbations

27
Q

Interprofessional care for ADHF

A

Continuous monitoring and assessment –> VS (every 4 hrs), O2 sat, weight, mentation, ECGs, urinary output

High Fowlers

Hemodynamic monitoring if unstable

Supplemental O2, Bipap

Mech ventilation if unstable

28
Q

ADHF nonpharmacologic therapy

A

Ultrafiltration (aquapheresis) for patients with volume overload and resistance to diuretics

Mechanical cardiac assist devices for ppl w/ deterioriating HF (temporary)
-Intraaortic balloon pump
-ventricular assist devices

29
Q

ADHF drugs: diuretics and vasodilators

A

Diuretics
-decrease volume overload (preload)
-Loop diuretics = Furosemids

Vasodilators
-reduce circulating blood volume and improve coronary artery circulation
-IV: nitroglycerin, sodium nitroprusside, nesiritide
-help with preload, contractility, and afterload
-MONITOR BP

30
Q

Drug therapy: morphine and inotropes

A

Morphine:
-reduces preload and afterload by dilating blood vessels
-relieves dyspnea and anxiety

Positive inotropes
-Beta agonists (dopamine and NE) for contractility and dilation
-Phosphodiesterase inhibitors for same thing
-Digitalis = just an inotrope
-SHORT TERM ONLY
WATCH FOR ARHYTHMIAS

31
Q

Interprofessional care for chronic HF

A

Oxygen therapy
-relieves dyspnea and fatigue

Physical and emotiona lrest
-conserve energy and decrease O2 needs
-dependent on severity of HF

Structured exercise program
-cardiac rehab associated with better outcomes

32
Q

Drug therapy for chronic HF: RAAS inhibitors

A

ACE inhibitors - first for HFrEF (CAUTION RENAL)
Angiotensin II receptor blockers (if can’t have first line)
Neprilysin-angiotensin receptor inhibitors (stops RAAS and the degradation of BNP)
Aldosterone antagonists (CAUTION HYPERKALEMIA)

33
Q

Drugs for chronic HF: basic

A

Beta blockers
Vasodilators = nitrates
Combo therapy (vasodilator and isosorbide)
Positive inotropes (digitalis)

34
Q

Drugs for chronic HF: Inhibitors of cardiac Sinus Node

A

Ivabradine (Corlanor)

Must be in sinus rhythm with resting HR of greater than 70 bpm and taking optimal doses of other meds
-inhibits sinus node
-reduces HR
-decreases hospitalization for patients with HFrEF

35
Q

Drugs for chronic HF: diuretics

A

-reduce edema, pulmonary venous pressure, and preload
-promote sodium and water excretion
-loop or thiazide diuretics (thiazidide prevent Na absorption)
-monitor for hypokalemia

36
Q

Devices for chronic HF

A

ICD
CRT (cardiac resynchronization therapy)
Pulmonary artery sensor

All can be monitored remotely

37
Q

Nutrition for chronic HF

A

Low sodium
-individualize based on cultural background
-try to stay under 2 g/ day

Fluid restriction for stage “D” HF patients
-take weights –> bad if 3 lb in 2 days or 3-5 lb in a week

38
Q

Basic principles of care for chronic HF

A

-it’s progressive
-treatment plans are established w/ QOL goals
-symptom management depends on adherence to self-management protocols
-precipitating factors, etiologies, and comorbid conditions must be addressed
-complex care needs often require multiple settings –> increased fragmented care
-support systems are essential to success

39
Q

Nursing intervention for chronic HF

A

-monitor respiration
-give O2
-semi-fowler’s position
-monitor hemodynamics
-daily weights
-I and O
-administer prescribed drugs
-monitor edema

-alternate rest with activity
-give diversionary activities
-monitor response to activity
-colab w/ OT/PT
-reduce anxiety
-evaluate support system
-patient teaching

40
Q

ambulatory care for chronic HF

A

Transitional care programs should include
-comprehensive discharge planning
-collaboration among providers
-planned, timely follow up with HCP

41
Q

Patient teaching chronic HF

A

Signs and symptoms of worsening HF
-teleheatlh and device remote monitoring tech
-therapeutic interventions to avoid re-hospitalization

Teach ab drugs
-basic action of each one
-signs of toxicity
-how to take pulse (full min)
-home BP monitoring
-signs of hypo- or hyper- kalemia

Exercise
-individualize
-emphasize importance of rest periods
-energy conserving behaviors
-PT/OT
-Enviro- changes

42
Q

Therapeutic options for stage D chronic HF

A

-chronic inotropy therapy
-mechanical circulatory support devices (IABP, ECMO, LVAD)
-paliative care/ hospice
-heart transplant

43
Q

End of life care HF

A

estimated 5 year survival rate

End of life care discussions and care emphasizes
-advanced directives
-advanced HF therapies
-palliative care and hospice

44
Q

Expected outcomes for treatment of chronic HF

A

-maintain adequate O2/CO2 exchange to meet O2 needs of body

maintain adequate blood pumped by heart to maintain metabolic demands

reduction or absence of edema and stable baseline weight

achieve a realistic program of activity that balances with energy conserving activities

45
Q

Heart Transplantation:
stats
who’s chosen

A

Gold standard therapysuitable for patients in end stage HF
-3000 on list - average 2000 available
-survival is 85-90% at 1 yr; 70% at 3 yrs

Selection process favors those who’d benefit most

Candidates undergo physical, diagnostic, and psychologic evaluation

46
Q

Heart transplant:
when on the list

A

stable patients wait at home and continue with med care

unstable patients need hospitalization for intensive therapy

overall waiting period is long –> lots of ppl die while waiting

47
Q

Steps of heart transplant

A
  1. retrieve heart
  2. remove recipient’s heart except portions of atria (2 dif approaches) and venous connections
  3. connect donor’s heart
48
Q

Post heart transplant monitoring

A

acute rejection
infection
risk for cancer related to immunosuppressive therpy
cardiac vaculopathy

Immunosuppressive therapy

49
Q

Checking for rejection

A

Endomyocardial biopsy (EMB) to check for rejection
-done from right ventricle
-weekly for first month
-monthly for 6 months; then yearly

Patho (44 decks)

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