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ADHF Flashcards

1
Q

ADHF

A
  • Occurs in patients with LV dysfxn history

- Evaluation reveals signs/sxs of pulmonary congestion, systemic congestion, and/or low CO

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2
Q

Physical Exam/Lab Findings

A
  • Increased lower extremity pitting edema
  • Hepatomegaly
  • JVD
  • (+) HJR
  • Rales/crackles
  • Tachycardia
  • Gallops
  • Elevated BNP (> 100) - higher = higher in hospital mortality risk
  • NT-proBNP > 450 for < 50 y.o. or >900 for > 50 y.o.
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3
Q

ADHF Epidemiology

A
  • After initial hospitalization, 50% readmitted within 6 months and 25-35% die within 12 months
  • Most costly CV syndrome
  • Mean LOS 5.3 days
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4
Q

Causes of ADHF

A
  • Non-adherence: medical, nutrition
  • ADE: NSAIDs, decongestants, Alka-seltzer, B-agonist
  • Undertreatment of HF: not on GDMT
  • Progression of disease
  • Acute MI: Check ECG and cardiac enzymes
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5
Q

CO

A
  • HR * SV
  • Amount of blood ejected from left ventricle
  • Normal: 4-8
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6
Q

CI

A
  • Cardiac Index
  • CO/BSA
  • Normal: 2.8-4.2
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7
Q

PP

A
  • Pulse Pressue
  • Difference between SBP and DBP (SBP-DBP)
  • <25% means SBP is inappropriately low/narrowed
  • Narrow PP in ADHF is indicative of decrease CO or perfusion
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8
Q

PAWP

A
  • Pulmonary Artery Wedge Pressure
  • Estimate of LV end-diastolic pressure (LVEDP)
  • LVEDP is equal to its volume (preload)
  • Normal PAWP < 12
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9
Q

SVR

A
  • Systemic Vascular Resistance
  • Pressure left ventricle must overcome to eject blood (afterload)
  • Normal: 900-1400
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10
Q

ADHF Treatment Goals

A
  1. Improve signs/sxs: decrease SOB, weight, and BNP and increase oxygenation
  2. Stabilize the hemodynamic condition: decrease PCWP and increase CO
  3. Decrease mortality
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11
Q

Comorbidity Identification

A
  • Class I recommendation to identify
    1. Acute coronary syndromes/coronary ischemia
    2. Severe HTN
    3. Atrial and ventricular arrhythmias
    4. Infections
    5. Pulmonary emboli
    6. Renal failure
    7. Medical or dietary nonadherence
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12
Q

Hemodynamic Subsets

A
  1. Warm (CI > 2.2) and dry (PCWP < 18): no signs of CHF
  2. Warm and Wet (PCWP > 18)
  3. Cold (CI < 2.2) and Dry: hypovolemic shock
  4. Cold and Wet: cardiogenic shock
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13
Q

Clinical Evidence of Congestion

A
  • Weight gain
  • Orthopnea
  • (+) JVP
  • Increasing S3
  • Loud P2
  • Edema
  • Ascites
  • Rales
  • (+) HUR
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14
Q

Clinical Evidence for Low Perfusion

A
  • Narrow pulse pressure
  • Cool forearms and legs
  • ACEI related hypotension
  • Declining serum Na
  • Worsening renal fxn
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15
Q

Warm/Dry Treatment

A
  • Goals: Initiate or titrate GDMT therapy
  • ACE or ARB or ARNI
  • BB
  • +/- aldosterone antagonist
  • +/- SGLT2-i
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16
Q

Warm and Wet Treatment

A
  • Goal: Relieve congestion
  • IV diuretics
  • +/- vasodilators
17
Q

Cold and Dry Treatment

A
  • Goal: Increase CO
  • Fluids
  • +/- IV inotropes
  • +/- mechanical assistance (IABP or LVAD)
18
Q

Cold and Wet Treatment

A
  • Goal: Increase CO and relieve congestion
  • Adequate BP (SBP >= 90): IV diuretics +/- vasodilators
  • Low BP (SBP < 90): IV inotropes + IV diuretics +/- mechanical assistance
19
Q

ADHF General Management

A
  • Oxygen for hypoxemia
  • Check vital signs, weight, signs/sxs of perfusion and congestion
  • Daily electrolyes, BUN, SCr when using IV diuretics or active titration of HF meds
  • Low sodium (2gm/day) is recommended for most hospital patients
  • Fluid restriction (<2L/day) is recommended in moderate hyponatremia (<130) patients and should be considered in fluid overloaded patients
20
Q

Chronic Medications in ADHF

A
  • Continue GDMT treatment in absence of hemodynamic instability or CI
  • Hold/reduce BB should be considered if recently initiated or increased dose. Also consider in marked volume overload or low CI
  • If renal fxn significantly worsening, consider holding/reducing ACEI/ARBs/ARNIs/Aldosterone antagonists until improved
21
Q

Diuretics

A
  • Class I
  • Significant fluid overload => IV loop diuretics
  • If using loop diuretics, intial IV dose should equal or exceed chronic PO dose (2.5 * current oral dose)
  • Can be intermittent bolus or CI
  • Urine output and signs/sxs should be continually assessed
  • Titrate diuretic dose based on sxs and volume status
22
Q

Diuretic Monitoring/Goals

A

Monitor

  • K+ and Mg
  • BUN/Cr
  • BP
  • Is and Os
  • Daily weights
  • Volume status
  • CO: overdiuresis can decrease CO

Goals

  • Weight loss at least 1kg/day
  • Overdiuresis can reduce CO and worsen renal fxn
23
Q

Inadequate Diuresis

A
  • Can increase loop diuretic dose or add second diuretic (thiazide)
  • Sequential nephron blockage: Metolazone or Chlorothiazide with loop as well
24
Q

Vasodilators

A
  • If symptomatic hypotension is absent: IV nitroglycerin, nitroprusside, or nesiritide can be considered
  • Relieve dyspnea in ADHF patients
  • Used adjuvant with diuretics
25
Q

Nitroprusside/Nitroglycerin

A
  • Reduce preload and therefore PCWP
  • Nitroglycerin preferred when CO isn’t severely compromised or other inotropics are being administered
  • Nitroprusside preferred in increase SVR patients
  • Decrease glycerin doses if SBP decreases <90-100
  • Taper prusside to avoid rebound HTN
26
Q

Nitros AE/Monitoring

A

AE

  • Headache
  • Dizziness
  • Reflex tachycardia
  • Hypotension
  • Thiocyanate toxicity (prusside)

Monitoring

  • Vitals
  • HF sxs
27
Q

Nesiritide

A
  • Recombinant BNP
  • Promotes vasodilation, natiuresis, and diuresis
  • Reduces PCWP and SVR, increases CO
  • AE: Hypotension (CI: SBP < 90)
  • Monitor: vitals and renal fxn
  • Safe, but not very effective, limited role in ADHF
28
Q

IV Inotopes

A
  • Class IIb: may reasonable if patients present with severe systolic dusfxn, low BP, and significantly depressed CO to maintain perfusion
  • Class III: without the above presentations and if significantly depressed CO w/ or w/o congestion, the inotropes are potentially harmful
29
Q

Dobutamine

A
  • IV Inotrope
  • Potent B1/B2 agonist
  • Predominate effect is (+) inotropy/chronotropy to increase CO and vasodilation which decrease SVR
30
Q

Dopamine

A
  • IV Inotrope
  • Effects B, alpha, and DA receptors
  • Have to increase doses to get to B/alpha effects (medium = B and high =alpha)
31
Q

Milrinone

A
  • Inodilator
  • IV Inotrope
  • PDE3-i
  • Increases intracellular cAMP to increase intracellular calcium and increase contractility/CO
  • Slower onset than dopamine/dobutamine, requires loading dose
  • Longest high life, titration is difficult
32
Q

Inotrope Monitoring

A
  • Vitals
  • Urine output
  • K+
  • Telemetry (arrhythmias)
33
Q

Anticoagulation

A
  • Class I

- All ADHF patients should receive VTE prophylaxis as long as risk-benefit ratio is favorable

34
Q

BB Initiation

A
  • Class I to start after volume status optimization and D/C of diuretics, vasodilators, and inotropes
  • Start at low doses
  • Caution in those who required inotropes during their hospital stay
  • Recent evidence supports sacubitril/valsartan in ADHF patients if hemodynamically stable (SBP > 100 for 66 hours without interventions)

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