Heart Failure Flashcards
Heart Failure
- An abnormal condition involving impaired cardiac pumping/filling
- Heart is unable to produce an adequate cardiac output (CO) to meet metabolic needs
- Progressive disease is characterized by myocardial cell dysfunction
- Inability of the heart to pump enough CO to meet the demands of the body
- Prevalence is high and it’s increasing; we’re living longer and are eating diets that’re full of unhealthy synthetic products & preservatives
Epidemiology - HF Risk Factors
- CAD
- HTN producing LVH
- DM, hyperlipidemia
- Sedentary lifestyle
- Obesity
- Excessive alcohol use, smoking, high sodium dietary intake
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Diastolic HF occurs as a result of __ __
filling failure
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Systolic HF occurs as a result of __ __
pump failure
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Refers to the inability of the ventricles to relax & thereby fill the chambers appropriately
Diastolic
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Refers to the action of contraction in the ventricles or the lower chambers (emptying)
Ventricles don’t have enough systemic vascular resistance (SVR) to exert sufficient pressure & eject the blood to the body in an optimal manner to perfuse the body effectively
Systolic
HF classification is based solely on measurement of ejection fraction (EF); is the % of blood that’s ejected from the ventricle w/each contraction
> Normal 55-70%; around 45% - indicates HF
HF - Pathophysiology
Characterized by
> Ventricular dysfunction
> Reduced exercise tolerance
> Diminished quality of life
> Shortened life expectancy
Compensatory Mechanisms
- SNS
- Renin-Angiotensin-Aldosterone
- Natriuretic peptides (BNP)
SNS is activated first; you see increased HR, contractility of the heart, & peripheral vasoconstriction (why we check pedal pulses & assess the heart)
Mechanisms then start to fail as heart cannot keep up w/workload & need for O2
Kidneys act by activating the __ __ __ __. Begins ok, but then retention of fluid to maintain volume & eventually strains the overworked heart w/volume & workload
renin-angiotensin-aldosterone system
A neurohormonal mechanism is the body’s release of ___
BNP (brain natriuretic peptide)
- Overstretching of the heart causes this peptide to be released in r/t inc pressure & volume
- Results in natural diuresis as well as dilation of veins & arteries
- These decrease __ and __ & therefore workload of the heart
preload; afterload
BNP
- Lab can draw BNP levels and if they’re elevated, then that’s a clear indication of HF
- Pts can be given a BNP rx that mimics the effects of the body’s natural BNP neurohormonal mechanism
___ can be released w/even a minor cardiac muscle stretch
ANP (so we look at BNP if there’s a question of HF)
Management
- Heavily dependent on hx & physical assessment as sx’s nonspecific
- Lab testing
> cardiac enzymes, serum electrolytes, CBC, UA, fasting lipid profile, LFT’s, - Rx’s
Complications
- Pulmonary edema
- Goals of HF management are manipulation of the critical components of CO (preload, afterload, contractility) and control of the compensatory mechanisms
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Is an acute complication of HF characterized by rapid accumulation of fluid in interstitial & alveolar spaces of the lung, resulting from elevated filling pressures within the heart
Pulmonary edema
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- Most common type
- Results from LVD
> HTN, CAD, cardiomyopathy
> Back up of blood into the left atrium & pulmonary veins - Pulmonary congestion
- Edema
Left HF
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Occurs as back up of blood into right atrium and venous systemic circulation
Right HF
HF: Where’s the backflow?
Right or Left?
- Backup of blood into the right atrium and venous systemic circulation
Right
Left - most common type
- Results from LVD (HTN, CAD, cardiomyopathy)
- Backup of blood into the left atrium and pulmonary veins
> Pulmonary congestion
> Edema
Remember: Left / Lungs (Left-sided HF classically is when the fluid is built up in the lungs)
HF Sx’s - ?
- SOB, dyspnea, fatigue
- Crackles in lung auscultation
- Poor color, weak pulses, cool extremities
LEFT
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- Jugular vein distention (JVD)
- Generalized dependent edema
- Hepatomegaly
- Ascites
Right
- Left-sided HF can eventually cause right-sided HF & then sx’s can be less clear
- Severe exacerbations of HF, pt may present w/hypotension, cool extremities, decreased or no urine output, & poor or declining mentation
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If this is left untreated, treatment is delayed, or the HF progresses, it can rapidly decline into an acute decompensated state such as severe __ __
Pulmonary edema
- Other complications of HF can be pleural effusions, afib (which can cause thrombus/embolus formation & inc pts risk for stroke), fatal dysrhythmias, severe hepatomegaly, renal insufficiency or failure
- As pulmonary edema progresses, it inhibits O2 & CO2 exchange @ the alveolar-capillary interface
- Orthopnea
- Dyspnea, tachypnea
- Use of accessory muscles
- Cyanosis
- Cool & clammy skin
- Cough w/frothy, blood-tinged sputum
- Crackles, wheezes, rhonchi
- Tachycardia
- Hypo- or HTN
Flash Pulmonary Edema
! Fast & sudden
* Pt is usually anxious, pale, & possibly cyanotic
* Skin is clammy & cold from vasoconstriction caused by stimulation of SNS
Diagnostic Studies | Primary goal: Determine & treat underlying cause
- History & PE
- Cxr
- Lab studies (e.g., cardiac enzymes, BNP, electrolytes, CBC, UA, lipids)
- Hemodynamic assessment
- Echo
- Nuclear imaging/stress testing
- Cardiac cath
- Ejection fraction (MUGA scans)
BNP
Below __ pg/mL indicates no HF
Levels between __ and __ pg/mL suggest HF is present
Level above __ pg/mL indicates mild HF
100
100-300
300
Level above __ pg/mL indicates moderate HF
Level above __ pg/mL indicates severe HF
600
900
Electrolytes
- Assess K+ as diuretics might deplete
- Look at BUN as inadequate blood flow to the kidneys may impair kidney function
- H/H in anemia that could result in decreased CO
! Be aware of any National Hospital Quality Measures (6 core measures)
- Beta-blocker @ discharge
- Follow-up within 7 days >d/c
- Record of care transmitted to the next level of care within 7 days of d/c
- Documentation of advance care planning (adv dir) w/an HCP
- Documentation of adv dir within the medical record
- F/u d/c eval of pt status & treatment adherence within 72 hrs of d/c (can occur by phone, scheduled OV, or home visit)
Classification Systems
- New York Heart Association Functional Classification of HF: Classes I to IV
> Patients may progress up & back to any of the classifications @ any time during their dz, depending on treatment & response
- ACC/AHA Stages of HF: Stages A to D
> A pt can’t go backward in these stages
Class ?
No symptoms w/physical activity such as dyspnea or CP
Class I
Class ?
Marked limitation w/physical activity but comfortable @ rest
Class III
Class ?
Severe limitation & distress w/physical activity or at rest
Class IV
Class ?
Mild sx’s w/ordinary activities
Class II
Stage ?
Refractory HF eligible for heart transplant, inotropic and/or mechanical support
D
Stage ?
Asymptomatic w/LVH and/or impaired LV function
B
Stage ?
Pt’s w/risk factors but no LV impairment
A
Stage ?
Current or past sx’s of HF
C
Overall objective is to increase CO by effecting the SV (preload, afterload, & contractility)
“UNLOADFAST”
- Morphine is also used as it decreases preload & anxiety
“UNLOADFAST”
Improve Cardiac Output: Preload, Afterload, Contractility
Reduce ___
- Nutrition therapy
- Drug therapy
> Diuretics
> Venous vasodilators
Preload
Reduce Afterload
- Drugs
> __
> __
> __
ACE inhibitors
ARB
Human BNP
Drugs: Enhance Contractility
- Inotropic drugs
> ___ - Beta adrenergic blockers (usually short-term)
Digoxin
Treatments: Non-pharmacological
- Noninvasive ventilatory support (BIPAP)
- Cardiac resynchronization therapy (CRT) or biventricular pacing
- Cardiac transplantation
- Intra-aortic balloon pump (IABP) therapy
- Ventricular assist devices (VADs)
- AICD - automatic internal cardiac defibrillator
- Heart transplantation - depending on the cause
Nursing Management - HF
Nursing Diagnoses
* Activity intolerance
* Fluid volume excess
* Anxiety
* Deficient knowledge
Evaluation
* Respiratory status
* Fluid balance
* Activity tolerance
* Anxiety control
* Knowledge of disease process
