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Year 3 - Clinical > 21 - Heart Failure > Flashcards

21 - Heart Failure Flashcards

1
Q

What is heart failure and what are the primary manifestations?

A
  • Progressive clinical syndrome that can result from any changes in cardiac structure or function that impair ability of ventricle to fill or eject blood
  • Primary manifestations = dyspnea, fatigue, fluid retention
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2
Q

Cause of HF

A
  • Abnormality in systolic function, diastolic function, or both
  • Leading causes = coronary artery disease & HTN
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3
Q

Major cause of death in people w/ HF?

A
  • Sudden cardiac death (ventricular arrhythmia)

- Stable px are at risk across all stages of disease

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4
Q

What is CO? What determines it?

A
  • Amount of blood pumped out of left ventricle in 1 minute

- HR * SV

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5
Q

What affects HR?

A
  • Autonomic innervation
  • Hormones
  • Fitness levels
  • Age
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6
Q

What affects SV?

A
  • Heart size
  • Fitness levels
  • Gender
  • Contractility
  • Duration of contraction
  • Preload and afterload
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7
Q

What is SV? What determines it?

A
  • Volume ejected from ventricles in each beat
  • EDV - ESV
  • EDV = end diastolic volume
  • ESV = end systolic volume
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8
Q

What is preload? When is it increased?

A
  • Volume of blood in ventricles at end of diastole (EDV)

- Increased in hypervolemia, regurgitation of cardiac valves, HF

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9
Q

What is afterload? When is it increased?

A
  • Resistance left ventricle must overcome to circulate blood

- Increased in HTN & vasoconstriction

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10
Q

What is BP? What determines it?

A
  • Measure of force being exerted on walls of arteries as blood is pumped out of heart
  • SVR * CO
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11
Q

What is SVR?

A
  • Systemic vascular resistance

- Squeeze of the blood vessels outside the heart resisting blood flow

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12
Q

What are the compensatory mechanisms in HF?

A
  • Increased HR (symp activation) – one of the “first responders” to reduced CO
  • Increased preload using RAAS (Na & H2O retention)
  • Peripheral vasoconstriction
  • Ventricular hypertrophy & remodeling (this is what really causes progression of the disease)
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13
Q

Describe the Frank-Starling mechanism

A

Force of heart contraction is directly proportional to initial length of muscle fiber (w/in physiological limits); greater the stretch of the ventricular muscle, the more powerful the contraction is

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14
Q

What are the neurohormonal factors involved in HF and what does each do?

A
  • Angiotensin 2 – vasoconstriction, activates SNS, sodium retention, aldosterone release
  • Norepi – tachycardia, vasoconstriction, increased contractility
  • Aldosterone – RAAS sodium & water retention, contributes to ventricular remodeling
  • Natriuretic peptides (atrial ANP, brain BNP) – BNP most important; both ANP & BNP increased in HF
  • Arginine vasopressin (aka antidiuretic hormone ADH) – increases water retention, vasoconstriction, & contributes to ventricular remodeling
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15
Q

What is the difference between myocardial and non-myocardial heart disease?

A
  • Myocardial = ischemia, inflammation, dilated cardiomyopathy, familial; can be systolic and/or diastolic
  • Non-myocardial = vascular (HTN), valvular (mitral/aortic insufficiency or stenosis), electric (A. fib, heart block), pericardial (tamponade, constriction)
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16
Q

What are some precipitating factors that lead to acute decompensation?

A
  • Increased circulating volume (increased preload) – high salt intake, noncompliance w/ fluid restriction or diuretics, NSAIDs, renal failure
  • Conditions that increase afterload – uncontrolled HTN
  • Conditions that impair contractility – MI, negative inotropic medications (diltiazem, verapamil)
  • Increased metabolic demand – infection, pregnancy, anemia, hyperthyroidism, tachyarrhythmias
  • Non-compliance w/ medications
  • Bradyarrhythmias
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17
Q

Describe ejection fraction

A
  • % of blood ejected from heart w/ each contraction
  • Normal ~ 60%
  • EF < 40% referred to as HR w/ reduced left ventricular function (HRrEF) – systolic dysfunction
  • EF >/ 40% referred to as HR w/ preserved left ventricular function (HFpEF) – diastolic dysfunction
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18
Q

Signs and sx of HF

A
  • Vasoconstriction -> decreased CO
  • Increased HR -> increased oxygen utilization
  • Increased preload -> peripheral & pulmonary edema
  • Decreased exercise tolerance
  • Pulmonary congestion (left sided) – exertional dyspnea, orthopnea (SOB when you lie down), paroxysmal nocturnal dyspnea, pulmonary edema
  • Systemic congestion (right sided) – peripheral edema, jugular vein distention, organomegaly
  • Low CO findings – fatigue, poor appetite, cold, pale clammy skin, altered mental status, resting tachycardia
19
Q

What is the difference between right sided and left sided HF?

A
  • Right sided = blood backed up in abdominal organs & periphery
  • Left sided = blood backed up in lungs
  • Often occur simultaneously, or progresses to both left & right HF
20
Q

Describe the NYHA functional classes of HF

A
  • Class 1 = able to perform ordinary physical activity
  • Class 2 = ordinary physical activity results in sx
  • Class 3 = less than ordinary physical activity results in sx
  • Class 4 = sx may be present at rest
21
Q

What are some tests used to diagnose HF?

A
  • EKG (electrocardiogram) may be normal or show numerous abnormalities (acute ST-T wave changes)
  • Serum creatinine may be increased due to hypoperfusion
  • Complete blood count used to see if HF due to reduced O2-carrying capacity
  • Chest x-ray for detection of cardiac enlargement, pulmonary edema, & pleural effusions
  • Echocardiogram to assess LV size, valve function, pericardial effusion, wall motion abnormalities, & EF
  • Hyponatremia may indicate worsening volume overload and/or disease progression
22
Q

Goals of therapy for HF

A
  • Minimize disabling sx
  • Decrease hospitalization
  • Improve QOL
  • Minimize disease complications
  • Slow progression of disease
  • Improve survival
23
Q

Causes of decompensation/ exacerbation

A
  • Cardiac events – MI, HTN
  • Non-cardiac events – ex: pulmonary infections
  • Non-adherence to meds or fluid/diet restriction
  • Certain drugs – NSAIDs, DPP 4 inhibitor saxagliptin, thiazolidinediones (rosiglitazone, pioglitazone)
24
Q

Tx of HFrEF

A
  • Must take off a CCB
  • Triple therapy – ACEi/ARB, beta blocker & MRA to improve survival & reduce morbidity while improving functional capacity
  • Reasses sx
    • If NYHA1 – continue triple therapy
    • If NYHA 2-4 and HR >/ 70 bpm – add ivabradine & swtich ACEi/ARB to ARNI for eligible px
    • If NYHA 2-4 and HR < 70 bpm – switch ACEi/ARB to ARNI for eligible px
  • Reassess sx & LVEF
    • If NYHA 1 or LVEF > 35% – continue present management
    • If NYHA 1-3 & LVEF /< 35% – refer to ICD/CRT algorithm
    • If NYHA 4 – consider hydralazine/nitrates, referral to advanced HF therapy, or palliative care
25
Q

What are some characteristics of HFpEF

A
  • Diastolic HF
  • Normal contractility & heart size
  • Impaired LV filling during diastole
  • LV stiffness & inability to relax during diastole
  • Results in increased resting pressure w/in ventricle
  • Increased pressure impedes ventricular filling, therefore reducing stroke volume (EF preserved)
  • Focus on decreasing sx & addressing risk factors (ex: HTN, smoking)
  • Treat comorbid conditions by controlling HR & BP, alleviating causes of myocardial ischemia, reducing volume, & restoring/maintaining sinus rhythm
26
Q

Purpose of using ACE inhibitors for HF

A
  • For HFrEF – improve survival, slow disease progression, reduce hospitalizations & improve QOL (most benefit at target doses)
  • Hemodynamic effects – increase CO, decrease preload, systemic vascular resistance, & BP
  • Hormonal effects (inhibit RAAS) – decrease angiotensin 2, aldosterone, & slow ventricular remodelling
  • Indicated for all px w/ HFrEF along w/ BB & MRA
  • Clinical pearl – introduce in graduated doses when pt is normovolemic or hypervolemic to avoid unnecessary hypotension or renal dysfunction
27
Q

ACE inhibitors – adverse effects

A
  • Hypotension – risk factors = stimulated RAAS, hyponatremia, diuretics, intravascular volume depletion
  • Renal impairment
  • Hyperkalemia (concurrent use w/ K+ sparing diuretics, MRAs, or K+ supplements)
  • Cough
  • Rash (more common w/ captopril)
  • Taste alterations
  • Angioedema (swelling of face, lips, tongue, larynx) – immediately d/c & don’t retry
28
Q

ACE inhibitors – contraindications

A
  • Hx of angioedema due to prior ACEi use
  • Renal failure (creatinine > 220 umol/L)
  • Bilateral renal artery stenosis
  • High potassium (K+ > 5.5)
  • Hypotension (cutoff is 80/50)
  • Pregnancy
29
Q

ACE inhibitors – monitoring

A
  • Efficacy
  • Right & left sided sx
  • Exercise tolerance
  • Weight/fluid balance
  • Side effects
  • Check renal function & electrolytes at baseline
  • Monitor blood chemistry 1-2 weeks after dose initiation & 1-2 weeks after final dose titration, then monitor every 3-4 months thereafter
30
Q

Effects of ARBs for HF

A
  • Blocks AT1 receptor in vascular cardiac, brain, kidney, & adrenal gland tissue
  • Candesartan shown to reduce CV mortality; valsartan shown to improve hospitalization rate due to HF
  • Alternative if ACEi cough
  • Combination w/ ACEi no longer recommended
  • ADEs = similar to ACEi, less cough
31
Q

Effects of beta blockers for HF

A
  • Long term symp activation may contribute to disease progression, augmented activation of RAAS, peripheral vasoconstriction, & remodeling of cardiac myocytes
  • Decrease all-cause mortality, sudden cardiac death, death due to worsening HF compared to placebo
  • First line in addition to ACEi & MRA
  • Indicated for all HFrEF (carvedilol, metoprolol, & bisoprolol)
  • Start low, go slow to target doses (increase 50-100% every 2-4 weeks)
  • Watch for fluid retention (weight gain) & monitor HR, BP, & EKG
32
Q

Beta blockers – contraindications

A
  • Acute decompensated HR/pulmonary congestion

- Significant hypotension or bradycardia

33
Q

Beta blockers – side effects

A
  • Fatigue (improves after 3-6 weeks)
  • Postural hypotension
  • Fluid retention
  • Cold extremities
34
Q

Describe MRAs (mineralocorticoid receptor antagonist) for HF

A
  • Reduce mortality in HFrEF (NYHA class 2-4 sx)
  • Decrease risk of hospitalization in HFpEF
  • Monitor potassium & renal function
  • Should be considered as adjunctive therapy (ie already on ACEi & BB) in px w/ mild or moderate to severe HF (NYHA class 2-4)
  • Rationale – aldosterone contributes to sodium/water retention, symp activation, myocardial & vascular fibrosis & other pathophysiologic effects seen in HF
  • Spironolactone = aldosterone receptor antagonist, but also binds to androgen & progesterone receptors
  • Eplerenone = selective aldosterone receptor antagonist; has greater selectivity for aldosterone receptor than spironolactone & therefore doesn’t lead to gynecomastia
35
Q

Caution MRA use w/:

A
  • Hyperkalemia (risk increases w/ concurrent use of ACEi or renal impairment)
  • CI for px w/ sCr > 220 umol/L and/or K+ > 5 mmol/L
  • Concurrent digoxin use (hyperkalemia may precipitate digoxin toxicity)
36
Q

Describe use of diuretics for HF

A
  • Sx control (peripheral edema or pulmonary congestion)
  • Don’t improve survival
  • Many px will need chronic diuretic therapy to maintain euvolemia after fluid overload is resolved
  • Overdiuresis can lead to reduction in CO, renal perfusion, & sx of volume depletion
  • Loop diuretics = more “efficient” diuresis
  • Start w/ low dose & adjust to achieve daily body weight reduction of 0.75-1 kg until euvolemia
  • Aim to maintain px on dry weight w/ lowest possible dose
37
Q

Important notes about loop diuretics for HF

A
  • Possible diuretic resistance (no weight loss despite increasing furosemide dose)
    • Add metolazone (usually given 30 min prior to furosemide); only used if at 120 mg furosemide
    • Try furosemide IV
  • Metolazone – usual dose 2.5-10 mg/day; not used long-term, only for exacerbations
38
Q

Diuretics – adverse effects & monitoring

A
  • Volume depletion – leads to dehydration & reduction in BP & CO
  • Check for signs of hypovolemia, symptomatic hypotension
  • Loss of K+ & Mg (can induce or potentiate digoxin toxicity; aim to keep K+ over 4 mmol/L)
  • Renal impairment (check sCr & BUN)
39
Q

Describe hydralazine/ nitrate use for HF

A
  • Significant reduction in mortality & improvement in exercise
  • Most often used in px that can’t tolerate ACEi
  • Sometimes used in combination w/ ACEi in black px b/c have less sensitivity to RAAS inhibition
  • Rationale – vasodilation decreases cardiac work by overcoming detrimental effects of compensatory mechanisms; achieved through reduction of preload (nitrates) & afterload (hydralazine)
  • Standard add-on for individuals of African descent
  • All px can consider if ongoing sx w/ ACEi & BB or unable to tolerate neither ACEi nor ARB
40
Q

Digoxin use for HF?

A
  • Symptomatic benefits for HFrEF
  • Improve QOL & reduce hospitalizations in px w/ symptomatic HF
  • No mortality benefit
  • Not first line (use after ACEi, BB, & MRA)
  • Slows AV node conduction in A. fib & atrial flutter
  • Increases vagal stimulation to SA node resulting in bradycardia
  • Increases force & velocity of contraction through inhibition of Na/K/ATPase
  • Factors affecting activity/toxicity – electrolyte disturbances (hypo & hyperkalemia) and renal function
41
Q

What is entresto? What is it shown to improve? When is it used? Contraindications?

A
  • ARNI (angiotensin 2 receptor blocker & neprilysin inhibitor) – combination necessary as inhibition of neprilysin leads to RAAS activation
  • 1 trial showed reduction in all-cause mortality, CV mortality, & HF hospitalization rate; but higher reports of symptomatic hypotension & angioedema than enalapril alone
  • May be considered as replacement for ACEi in px w/ HFrEF who remain symptomatic despite optimal tx w/ ACEi, BB, & MRA
  • CI = hx of angioedema, hypotension, eGFR < 30 mL/min, K > 5.2 mmol/L
42
Q

Describe lancora

A
  • Generic = ivabradine
  • Blocks I-f current in SA node that is responsible for controlling HR, which slows depolarization of sinus node & slows HR
  • Doesn’t affect BP, myocardial contractility, or AV conduction
  • Common SE = bradycardia, atrial fibrillation, visual disturbances
  • CCS 2017 HF guideline = should be considered in px w/ HFrEF, who remain symptomatic despite tx w/ appropriate doses of GDMT w/ resting HR > 70 bpm & previous hospitalization w/in 12 months
43
Q

Non-pharms for HF

A
  • Exercise training
  • Restriction of dietary sodium (< 2 g/day)
  • Fluid restriction (< 1.5-2 L/day)
  • Daily AM weights (w/o clothes & after voiding)
  • Limit alcohol
  • Quit smoking
  • Look for & treat depression

Year 3 - Clinical (30 decks)

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