heart failure Flashcards
What is heart failure?
Complex clinical syndrome resulting in insufficient blood supply/O2 to tissues and organs
**decreased CO –> decreased tissue perfusion
**EF
Two types of HF
- Heart failure with reduced ejection fraction
-defect in ventricular systolic function/LV contraction - Heart failure with preserved ejection fraction
-defect in ventricular diastolic functioning/filling
Primary risk factors for HF
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
2 types of etiology of heart failure
Anything that messes with CO
- Primary causes –> directly damage the heart
- Precipitating causes –> increase workload of heart
Left sided HF
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
HFrEF
inability to pump blood effectively
Caused by
-impaired contractile function
-increased afterload
-mechanical abnormalities
Decreased LV ejection fraction (<40%)
HFpEF
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
Right sided HF
-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
Biventricular failure
Both right and left ventricles are fucked up
Fluid build up and venous engorgement
decreased perfusion to vital organs
Compensatory mechanisms: RAAS
Homeostatic regulatory system
-goa is augmentation of preload and contractility to maintain CO
-Promotes sodium and water retention
Aldosterone, ADH, vasoconstriction
Compensatory mechanisms: SNS
Baroreceptors sense low arterial pressure
catecholamines are released
Stimulation of beta adrenergic receptors increae HR (chronotropy) and ventricular contractility (inotropy)
Endothelin
-vasoconstrictor peptide made by vascular endothelial cells
-usually stimulates contraction, but in the heart, acts as negative inotrope and decreases contraction
Proinflammatory cytokines
released in response to heart injury
TNG and IL-1 further depress heart function by causing myocyte hypertrophy and apoptosis
Compensatory mechanisms: dilation
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
Compensatory mechanisms: hypertrophy
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
Compensatory mechanisms: remodeling
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
Counterregulatory mechanisms: natriuretic peptides
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
Counterregulatory mechanisms: NO and PG
released from vascular endothelium in response to compensatory mechanisms
Both relax arterial smooth muscle, resulting in vasodilation and decreased afterload
Acute Decompensated Heart Failure
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
Early vs late ADHF
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
Pulmonary edema clinical manifestations
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
4 categories of ADHF
- dry-warm
2.Dry-cold
3.wet-warm (most common) - wet-cold
“wet” = volume overload
“warm” = adequate perfusion
Chronic heart failure clinical manifestations
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
Heart failure complications
pleural effusion
Dysrhythmias and dyssynchronous contraction
Hepatomegaly
Cardiorenal syndrome
Anemia
Diagnostic studies
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
Goals of treatment for ADHF
Symptom relief
optimizing volume status
Supporting oxygenation and ventilation
identifying and addressing causes
avoiding complications
teaching related to exacerbations
Interprofessional care for ADHF
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
ADHF nonpharmacologic therapy
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
ADHF drugs: diuretics and vasodilators
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
Drug therapy: morphine and inotropes
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
Interprofessional care for chronic HF
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
Drug therapy for chronic HF: RAAS inhibitors
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)
Drugs for chronic HF: basic
Beta blockers
Vasodilators = nitrates
Combo therapy (vasodilator and isosorbide)
Positive inotropes (digitalis)
Drugs for chronic HF: Inhibitors of cardiac Sinus Node
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
Drugs for chronic HF: diuretics
-reduce edema, pulmonary venous pressure, and preload
-promote sodium and water excretion
-loop or thiazide diuretics (thiazidide prevent Na absorption)
-monitor for hypokalemia
Devices for chronic HF
ICD
CRT (cardiac resynchronization therapy)
Pulmonary artery sensor
All can be monitored remotely
Nutrition for chronic HF
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
Basic principles of care for chronic HF
-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
Nursing intervention for chronic HF
-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
ambulatory care for chronic HF
Transitional care programs should include
-comprehensive discharge planning
-collaboration among providers
-planned, timely follow up with HCP
Patient teaching chronic HF
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
Therapeutic options for stage D chronic HF
-chronic inotropy therapy
-mechanical circulatory support devices (IABP, ECMO, LVAD)
-paliative care/ hospice
-heart transplant
End of life care HF
estimated 5 year survival rate
End of life care discussions and care emphasizes
-advanced directives
-advanced HF therapies
-palliative care and hospice
Expected outcomes for treatment of chronic HF
-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
Heart Transplantation:
stats
who’s chosen
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
Heart transplant:
when on the list
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
Steps of heart transplant
- retrieve heart
- remove recipient’s heart except portions of atria (2 dif approaches) and venous connections
- connect donor’s heart
Post heart transplant monitoring
acute rejection
infection
risk for cancer related to immunosuppressive therpy
cardiac vaculopathy
Immunosuppressive therapy
Checking for rejection
Endomyocardial biopsy (EMB) to check for rejection
-done from right ventricle
-weekly for first month
-monthly for 6 months; then yearly
