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646 Test 2 > HF > Flashcards

HF Flashcards

1
Q

What is HF?

A

A complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood

A chronic, progressive condition where the heart isn’t able to pump enough blood to meet the body’s needs for blood and oxygen

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2
Q

What is cardiac output?

A

CO = SV x HR

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3
Q

What factors impact CO?

A

Contractility
Preload
Afterload

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4
Q

What is contractility?

A

The heart’s ability to squeeze - “force of contraction”

When it is inadequate, it is called systolic failure

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5
Q

What makes the contractility bad?

A
  • Dead tissue doesn’t move…post MI, cardiotoxic drugs (Adriamycin)
  • Abnormal heart cells (muscular dystrophy)
  • Excessive wall stress (dilation of ventricle, neurohormonal activation)
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6
Q

What is preload?

A

The amount of blood filling the ventricle

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7
Q

What is afterload?

A

The resistance the heart must pump against to empty the ventricle
Elevated afterload in HTN and aortic stenosis

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8
Q

Why do people get HF?

A
  • Impaired contractility (systolic failure)
  • Increased afterload (heart can’t overcome resistance)
  • Impaired filling/inability to relax (diastolic failure)
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9
Q

What are causes of HFrEF (systolic failure)?

A

Impaired contractility 2/2:

  • MI
  • Chronic volume overload from mitral regurgitation or aortic regurgitation (causes too much blood in the LV –> dilation –> decreased function)
  • Dilated cardiomyopathy (no evident cause)

Increased afterload 2/2:

  • Aortic stenosis
  • HTN
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10
Q

What is normal EF?

A

55-70%?

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11
Q

What are causes of HFpEF (diastolic failure)?

A

Impaired relaxation 2/2:

  • LVH (cavity is smaller due to thicker ventricle, decreased blood fill)
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy (muscle or pericardium is so stiff that heart can’t relax)
  • MI

Insufficient preload 2/2:

  • Mitral stenosis
  • Pericardial constriction
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12
Q

What are the symptoms of HF?

A
  • Dyspnea
  • Ankle edema
  • Pulmonary edema
  • Fatigue
  • Exercise intolerance
  • Orthopnea
  • Paroxysmal nocturnal dyspnea (sleeping on many pillows?)
  • Weight loss and cachexia (because heart is working extra hard and cannot get adequate calories…late stage)
  • Cough
  • Nocturia
  • Palpitations
  • Depression
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13
Q

What are the signs of HF?

A
  • Elevated venous pressure
  • Positive hepatojugular reflux
  • Tachycardia
  • Pulmonary rales
  • Tachypnea
  • Third/fourth heart sound
  • Hepatomegaly
  • Ankle edema
  • Cardiomegaly
  • Splenomegaly (2/2 increased venous pressure)
  • Hypotension (inadequate blood pumped from heart)
  • Pulsus alternans (alternating strong and weak beats, almost always indicates systolic HF)
  • Extrasystoles (beat outside of normal rhythm)
  • A fib
  • Weight loss
  • Ascites
  • Pleural effusion
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14
Q

What are signs and symptoms of left-sided HF?

A
  • Dyspnea and orthopnea (pulmonary edema)
  • Paroxysmal nocturnal dyspnea (PND)
  • Fatigue, decreased exercise tolerance
  • Tachycardia, tachypnea
  • Pulmonary rales
  • S3/S4 gallop

Can lead to right-sided HF

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15
Q

What are signs and symptoms of right-sided HF?

A
  • Peripheral edema
  • Hepatomegaly (pain?)
  • JVD (with hepatojugular reflux - rises at least 3 cm and is sustained throughout entire time pressure is exerted on liver)
  • Fatigue, decreased exercise tolerance
  • S3/S4 gallop
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16
Q

What is S4?

A

Atrial gallop that occurs during the active filling of the ventricle (atrial contraction)
Often a sign of diastolic HF
TEN-nes-see

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17
Q

What is S3?

A

Ventricular gallop that occurs during passive filling of the ventricle
ken-tu-CKY

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18
Q

What are the NYHA Classes of HF?

A

Class I (Mild) = no limitation of physical activity. Ordinary physical activity does NOT cause undue fatigue, palpitation, or dyspnea (SOB)

Class II (Mild) = slight limitation of physical activity. Comfortable at rest, but ordinary physical activity DOES result in fatigue, palpitation, or dyspnea

Class III (Moderate) = MARKED LIMITATION of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea

Class IV (Severe) = Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency AT REST. If any physical activity is undertaken, discomfort increases

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19
Q

What are guideline suggestions for managing a “Stage A” patient (at high risk for HF but without structural heart disease or sx of HF)?

A

These are patients with HTN, atherosclerotic disease, DM, obesity, or metabolic syndrome
OR patients using cardiotoxins or with family history of cardiomyopathy

Goals: heart healthy lifestyle, prevent vascular coronary disease, prevent LV structural abnormalities

Drugs:

  • ACEs or ARBs in appropriate patients for vascular disease or DM
  • Statins as appropriate
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20
Q

What are guideline suggestions for managing a “Stage B” patient (NYHA Class I: structural heart disease but without sx of HF)?

A

These are patients with previous MI, LV remodeling (LVH and low EF), or asymptomatic valvular disease

Goals: Prevent HF sx, prevent further cardiac remodeling

Drugs:

  • ACEs or ARBs as appropriate
  • BBs as appropriate

In select patients, ICD or revascularization or valvular surgery

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21
Q

What are guideline suggestions for managing a “Stage C” patient with HFpEF (NYHA Class II-III: structural heart disease with prior or current sx of HF)?

A

These are patients with known structural heart disease and HF s/sx

Goals: control sx, improve HRQOL, prevent hospitalization and mortality, identify comorbidities

Treatment:

  • Diuresis to relieve sx of congestion
  • Follow guideline indications for comorbidities (HTN, AF, CAD, DM, etc.)
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22
Q

What are guideline suggestions for managing a “Stage C” patient with HFrEF (NYHA Class II-III: structural heart disease with prior or current sx of HF)?

A

These are patients with known structural heart disease and HF s/sx

Goals: control sx, patient education, prevent hospitalizations and mortality

Drugs:

  • Diuretics for fluid retention
  • ACEs or ARBs
  • BBs
  • Aldosterone antagonists
  • In some patients: hydralazine/isosorbide dinitrate; ACE and ARB; digitalis

In select patients: CRT; ICD; revascularization or valvular surgery

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23
Q

What are guideline suggestions for managing a “Stage D” patient (NYHA Class IV: refractory HF with sx at rest despite GDMT)?

A

These are patients with marked HF symptoms at rest and/or recurrent hospitalizations despite GDMT

Goals: control sx, improve HRQOL, reduce hospital readmissions, establish patient’s EOL goals

Options:

  • Advanced care measures
  • Heart transplant
  • Chronic inotropes
  • Temporary or permanent MCS
  • Experimental surgery or drugs
  • Palliative care and hospice
  • ICD deactivation
24
Q

What are the body’s compensatory mechanisms?

A 
Frank-Starling mechanism
Neurohormonal alterations (like RAAS)
Ventricular hypertrophy and remodeling
25
Q

What is the Frank-Starling Mechanism?

A

The ability of the heart to change its force of contraction and (therefore) stroke volume in response to changes in venous return
In the failing heart, these factors that normally help increase cardiac output during exercise are chronically active and cause increased preload and ventricular end-diastolic pressures (especially in a noncompliant, dilated ventricle), with the threat of edema formation.

26
Q

What are adrenergic nervous system alterations?

A

Baroreceptors cause an increase in HR, augment contractility, and vasoconstrict through alpha receptors

27
Q

What are the RAAS alterations?

A

RAAS (Renin Angiotensin Aldosterone System)

Renin release causes vasoconstriction, increased thirst, and augments sodium reabsorption in the kidneys

28
Q

What are natriuretic peptide alterations?

A

Natriuretic peptides are released when the ventricular myocardium is subjected to hemodynamic stress (stretch)
Causes excretion of sodium and water, vasodilation, and inhibit the RAAS, adrenergic nervous system, and ADH actions to try to decrease resistance, make you pee, etc.

29
Q

What are precipitating and reversible causes of HF?

A
  • Increased metabolic demands (infection, anemia, hyperthyroidism)
  • Increased preload (excessive sodium, excessive fluid intake/administration, renal failure)
  • Increased afterload (PNA, uncontrolled HTN, PE)
  • Impaired contractility (negative inotropic medications, MI, alcohol)
  • Medication non-adherence
30
Q

What are diagnostic studies for HF?

A
  • *Echo - shows how heart is squeezing and relaxing
  • CBC, CMP, BNP
  • TSH, Urinalysis
  • EKG
  • CXR - cardiomegaly and effusions?
31
Q

What is B-type “brain” natriuretic peptide?

A
  • n-terminal-pro-BNP (nt-pro-BNP) - the inactive fragment when pro-BNP is cleaved into BNP and nt-pro-BNP
  • BNP is synthesized and secreted by the ventricular myocardium in response to increased volume or pressure
  • Renally ecxreted
  • Okay fur the use in the evaluation of dyspnea, but generally not recommended for serial measurement
  • Tells the body to excrete more volume (increased pee)
  • Many things can cause elevations in BNP, so it is not a very specific measurement
32
Q

What does the general/overall treatment of HF look like?

A
  • Good primary care!! HTN and HLD tx
  • Treat underlying condition: valve repair/replacement, coronary artery revascularization, anti-HTN, alcohol cessation, rhythm reestablishment
  • Eliminate acute precipitating cause - infection, arrhythmia, salt intake, medication changes, thyroid, etc.
  • Treat HF sx: diuretics, vasodilators, positive inotropic drugs
  • Modulate neurohormonal response

A lot of palliative care since you are not treating to cure, you are treating sx

33
Q

What are patient education recommendations?

A

Diet: sodium restriction (<1500 mg/day), alcohol cessation, caffeine avoidance
Smoking cessation!!
Exercise: may be monitored (cardiac rehab, stress test), mild-moderate intensity to ~60% of maximal HR. Should try to get within 10% of ideal weight if obese
Daily weights: same scale, first thing in the morning after peeing. Contact provider w/ 2lb weight gain in one day or 5lb in one week. Can teach “sliding scale” to titrate diuretic dosing
Medications: do NOT miss doses or prescriptions; avoid NSAIDs, CCBs, and thiazolidinediones
Vaccines!

34
Q

Why are diuretics used in HF?

A

They decrease the preload so that the hydrostatic pressure no longer causes pulmonary/venous congestion
This decreased preload should not impact CO since the Frank-Starling curve has “flattened”

[In HF, the Frank–Starling curve is moved down (flattened) so that more venous return and filling pressure is required to increase contractility and stroke volume. This change in the Frank–Starling curve helps to explain why increasing fluid retention occurs as cardiac dysfunction worsens in HF. More and more preload is required to increase stroke volume as inotropy decreases. Eventually, in end-stage HF, stroke volume becomes much more afterload-dependent, so that reductions in afterload have a more pronounced effect on cardiac output than they do in normal hearts.]

35
Q

What are the most effective diuretics?

A

Loop diuretics!
1st Line: Furosemide (Lasix)
Also, bumetanide, torsemide, ethacrinic acid

36
Q

Furosemide dosing

A

Start with 20 to 40 mg QD or BID

Increase by 20 mg; with a maximum of 600 mg/day

37
Q

What are side effects and monitoring parameters for diuretics?

A

SE: hypokalemia, hypomagnesemia, orthostatic hypotension, lethargy/drowsiness
Monitor kidney function and electrolytes

38
Q

What are the vasodilators?

A

Nitrates = venous vasodilators
Hydralazine = arteriole vasodilator
ACEs, ARBs, hydralazine+isosorbide dinatrate = “balanced” vasodilators
Nesiritide = recombinant BNP (IV drip)

39
Q

What are the benefits of ACEs?

A
  • Help break the cycle of RAAS
  • Decrease afterload (anti-hypertensive)
  • Renal protective
  • Indicated POST MI

[end in -pril]

40
Q

What are the SE of ACEs?

A
  • Hypotension
  • AKI
  • Hyperkalemia
  • Cough
  • Angioedema

Contraindicated in pregnancy

41
Q

What are the benefits of ARBs?

A
  • Help to break the cycle of RAAS
  • Decrease afterload (anti-hypertensive)
  • Renal protective
  • Indicated POST MI

[end in -sartan]

42
Q

What are the SE of ARBs?

A
  • Cough (3 vs. 9%)
  • Angioedema
  • Hypotension

Contraindicated in pregnancy

43
Q

What are aldosterone antagonists?

A

Spironolactone and Epleronone

You must monitor kidney function and potassium because of risk of hyperkalemia (potassium-sparing)

44
Q

What’s the deal with Beta-Adrenergic Blockers?

A
  • They were initially contraindicated because they decrease HR…but that allows the heart to rest and improves outcomes
  • Only carvedilol, bisoprolol, and sustained release metoprolol have been studied and approved for HF
  • Improve indices of LV function, delay progression of myocardial dysfunction, and improve survival
  • Must monitor BP and HR (they blockade sympathetic nervous system)
45
Q

What are the only approved and studied beta blockers to use in HF?

A

Carvedilol
Bisoprolol
Sustained release Metoprolol

46
Q

What is the deal with hydralazine and isosorbide dinitrate (BiDil)?

A
  • Recommended for AA patients with NYHA class III-IV who are receiving optimal therapy with ACEs and beta blockers
  • Can be useful in pts who cannot be given ACE or ARB because of drug intolerance, hypotension, or renal insufficiency
  • Vasodilates arteriole and venous
47
Q

What’s the deal with neprilysin inhibitors? (Sacubitril)

A
  • Comparable benefits to ACEs with regard to decreasing HF progression, hospitalizations, mortality
  • Inhibit neprilysin from breaking down natriuretic (and other vasoactive) peptides
  • Use in patients with mild-moderate HF with BNP>150 or nt-proBNP>600; or BNP>100 and prior hospitalization w/in past 12 months
  • Used in patients who have already tolerated target doses of ACE/ARB
48
Q

What’s the deal with the ARNI Entresto?

A
  • Combination of Sacubitril and Valsartan
  • Should not be administered concomitantly with ACE or w/in 36 hours of last ACE dose
  • Should not be administered to patients with history of angioedema
  • Should not be administered to pts who cannot afford it ($400+/month)
49
Q

What’s the MOA of Corlanor (Ivabradine)?

A
  • Blocks the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel that is responsible for the cardiac pacemaker current that regulates HR
  • Selective inhibitor of the SA pacemaker modulating “f-current”, slows the sinus rate by prolonging the slow depolarization phase
  • Decreases HR, but does NOT affect contractility
  • In patients with HFrEF, the reduced HR gives clinical benefit
50
Q

Who should take Corlanor (Ivabradine)?

A

Patients with symptomatic chronic stable HF with LV EF <35%, in sinus rhythm with resting HR >70 bpm who are either on max-tolerated dose of BB or have contraindication to BB use
Concurrent tx should include ARB or ACE and mineralocorticoid receptor blocker (e.g., spironolactone)

51
Q

What are the contraindications to using Corlanor (Ivabradine)?

A
  • Acute decompensated HF
  • BP <90/50
  • Sick sinus syndrome, SA block or 3rd degree AV block, unless functioning demand pacemaker is present
  • Pacemaker dependence (HR maintained exclusively by pacemaker)
  • Severe hepatic impairment
  • In combo with strong CYP3A4 inhibitors
  • Cannot afford to pay for it
52
Q

What are the various positive inotropes?

A
  • Dobutamine or Dopamine (Beta-Adrenergic)
  • Phosphodiesterase Inhibitors = Amrinone/Milrinone
  • Digitalis
53
Q

What’s the deal with digitalis (positive inotrope)?

A

Must monitor the blood level; goal: 0.5-0.8 ng/mL
Treat pts in Class II-IV despite optimal therapy
Provides symptomatic relief, but no morbidity/mortality benefit
Indicated for A fib

54
Q

What are additional considerations for patients with HF?

A
  • Iron therapy, sleep study (OSA)
  • Cardiac Resynchronization Therapy (CRT)
  • Internal Cardiac Defibrillator (ICD)
  • Anticoagulation
  • Cardiac Assist Device
  • Cardiac transplant
55
Q

What constitutes a diagnosis of HF?

A

2 major criteria or 1 major and 2 minor criteria…

Major:

  • Paroxysmal nocturnal dyspnea
  • Orthopnea
  • Elevated JVP
  • Pulmonary rales
  • 3rd heart sound
  • Cardiomegaly on CXR
  • Pulmonary edema on CXR
  • Weight loss >4.5 kg in 5 days in response to tx of presumed HF

Minor:

  • B/L leg edema
  • Nocturnal cough
  • Dyspnea on ordinary exertion
  • Hepatomegaly
  • Pleural effusion
  • Tachycardia (>120bpm)
  • Weight loss >4.5 kg in 5 days
56
Q

What is included in the initial evaluation of a patient with HF?

A
  • Complete history and physical
  • History of alcohol, illicit drugs, standard or “alternative” therapies, and chemo drugs
  • Ability to perform routine and desired ADLs
  • Assessment of volume status, orthostatic BP changes, height and weight, and BMI
  • CBC, urinalysis, CMP, glucose (A1C?), lipid profile, thyroid panel
  • EKG and CXR
  • Echo
  • Cardiac cath if concerned for ischemia

646 Test 2 (8 decks)

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