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
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.
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
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
5
Q
CO
A
- HR * SV
- Amount of blood ejected from left ventricle
- Normal: 4-8
6
Q
CI
A
- Cardiac Index
- CO/BSA
- Normal: 2.8-4.2
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
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
9
Q
SVR
A
- Systemic Vascular Resistance
- Pressure left ventricle must overcome to eject blood (afterload)
- Normal: 900-1400
10
Q
ADHF Treatment Goals
A
- Improve signs/sxs: decrease SOB, weight, and BNP and increase oxygenation
- Stabilize the hemodynamic condition: decrease PCWP and increase CO
- Decrease mortality
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
12
Q
Hemodynamic Subsets
A
- Warm (CI > 2.2) and dry (PCWP < 18): no signs of CHF
- Warm and Wet (PCWP > 18)
- Cold (CI < 2.2) and Dry: hypovolemic shock
- Cold and Wet: cardiogenic shock
13
Q
Clinical Evidence of Congestion
A
- Weight gain
- Orthopnea
- (+) JVP
- Increasing S3
- Loud P2
- Edema
- Ascites
- Rales
- (+) HUR
14
Q
Clinical Evidence for Low Perfusion
A
- Narrow pulse pressure
- Cool forearms and legs
- ACEI related hypotension
- Declining serum Na
- Worsening renal fxn
15
Q
Warm/Dry Treatment
A
- Goals: Initiate or titrate GDMT therapy
- ACE or ARB or ARNI
- BB
- +/- aldosterone antagonist
- +/- SGLT2-i
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
Nitroprusside/Nitroglycerin
- 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
Nitros AE/Monitoring
AE
- Headache
- Dizziness
- Reflex tachycardia
- Hypotension
- Thiocyanate toxicity (prusside)
Monitoring
- Vitals
- HF sxs
27
Nesiritide
- 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
IV Inotopes
- 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
Dobutamine
- IV Inotrope
- Potent B1/B2 agonist
- Predominate effect is (+) inotropy/chronotropy to increase CO and vasodilation which decrease SVR
30
Dopamine
- IV Inotrope
- Effects B, alpha, and DA receptors
- Have to increase doses to get to B/alpha effects (medium = B and high =alpha)
31
Milrinone
- 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
Inotrope Monitoring
- Vitals
- Urine output
- K+
- Telemetry (arrhythmias)
33
Anticoagulation
- Class I
| - All ADHF patients should receive VTE prophylaxis as long as risk-benefit ratio is favorable
34
BB Initiation
- 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)
