Acute Heart Failure

Question 1

Etiology / Pathophysiology

Answer 1

• Includes patients with both HFrEF and HFpEF
• Acute worsening of chronic HF accounts for ~ 70% of cases
   Patients become refractory due to a relatively mild insult
• New or “acute”HF accounts for ~ 25% of cases
• Progressive worsening of CO in chronic heart failure accounts for ~ 5% of cases
• Cardiogenic shock: hypotension (SBP < 90 mmHg or MAP < 70 mmHg) with low CO

Question 2

Diagnostic Tools

Answer 2

• Non-Invasive Testing
   Detailed physical examination
   Laboratory assessment
• Routine testing: Cr, K, Na
• BNP and NTproBNP: BNP > 400 is closely associated with acute HF
• Invasive hemodynamic monitoring
   Routine use is discouraged
   Flow directed PA catheters (Swan-Ganz catheters)

Question 3

Clinical Presentation of ADHF

Answer 3

• Patients can be categorized on basis of fluid status and cardiac function
• Warm or cold…
   Describes cardiac function or ability to perfuse tissues
• Wet or dry…
   Describes volume status
  I: normal - warm and dry
  II: pulmonary congestion - warm and wet
  III: hypoperfusion - cool and dry
  IV: hypoperfusion and pulmonary congestion - cool and wet

Question 4

Maintaining Chronic Therapy while Hospitalized

Answer 4

• GDMT should be continued in the absence of hemodynamic instability or contraindications….hypotension/cardiogenic shock
• Caution with aggressive diuresis and RAASi/SGLT2i
   Caution with increases and up-titration
   Increases in SeCr (~20%) do not worsen outcomes
   Significant worsening may warrant reduction or temp D/C

Question 5

Maintaining Chronic Therapy while Hospitalized: beta blockers

Answer 5

 Do not stop unless recent initiation or up-titration resulted in current
decompensation
 Consider holding if dobutamine needed or hemodynamically unstable
 Do not add or up titrate until optimization of volume status and successful D/C of IV diuretics, VDs and inotropes
 Start at low doses and use special caution if inotropes used in hospital

Question 6

Maintaining Chronic Therapy while Hospitalized: digoxin

Answer 6

 Continue at dose to achieve SDC 0.5-0.9 ng/mL
 Avoid D/C unless compelling reason
 Caution with regard to renal function

Question 7

Management of Decompensation Episodes

Answer 7

• Diuretics, inotropes, vasodilators, vasopressors
• No therapy shown conclusively to reduce mortality
• Treatments…reduce symptoms, restoring perfusion, and minimizing cardiac damage and A/Es

Question 8

Drug therapy for I - warm and dry

Answer 8

optimize chronic therapy

Question 9

Drug therapy for II - warm and wet

Answer 9

IV diuretics +/- IV venous vasodilator

Question 10

Drug therapy for III - cold and dry

Answer 10

if PCWP <15: IV fluids until PCWP 15-18
if PCWP >/= 15: SBP < 90: IV inotrope
if PCWP >/= 15, SBP >/= 90: IV inotrope or arterial vasodilator

Question 11

Drug therapy for IV - cold and wet

Answer 11

IV diuretics + if SBP < 90: IV inotrope, if SBP >/= 90: IV arterial vasodilator

Question 12

Diuretics in Hospitalized Patients

Answer 12

• Used primarily to treat systemic/pulmonary congestion in Subset II or IV, first line agents with fluid overload
• No difference in efficacy between intermittent dosing and continuous infusion
• Initial IV dose should equal or exceed the chronic daily dose and given as intermittent bolus
• Loops most widely used, THZ used as add-on if refractory
• If resistance:
   Sodium and water restriction
   Increase dose, rather than frequency, to ceiling
   Combination therapy (thiazides + loops)
• PO: MTZ 2.5-5 mg/day; HCTZ 12.5-25 mg/day; IV: CTZ 250-500 mg/day
   Ultrafiltration

Question 13

Diuretics in Hospitalized Patients: dosing and monitoring

Answer 13

• Dosing:
   Increase dose patient was receiving at home, Remember
  furosemide bioavailability
   Ceiling effect? 160-200 mg IV furosemide (depends on renal function)
   If Continuous Infusion: F 0.1 mg/Kg/hr doubled q2-4h; max 0.4
• Monitoring
   urine output and S/S of congestion, should be serially assessed
   Ins/Outs, body weight, vital signs, S/S perfusion and congestion.
  Serum electrolytes, BUN, and creatinine daily
   Desire 1-2 L/day above input early

Question 14

Vasodilator Therapy

Answer 14

• Used (in combination with diuretics) to reduce pulmonary congestion in wet, Stage II and IV, HF
   Venodilators increase venous capacitance and reduce preload and reduce myocardial stress
• Rapid symptomatic relief
• NTG is venodilator of choice
   Arterial vasodilators are useful in patients with elevated SVR
• Patients with symptomatic hypotension should not receive vasodilators
• Should be considered over inotropes
• Frequent BP monitoring is needed

Question 15

Vasodilators

Answer 15

nitroprusside, nitroglycerin, nesiritide, morphine, enalaprilat, hydralazine
for warm and wet

Question 16

Nitroprusside

Answer 16

balanced vasodilator
used for HTN crisis
AEs: cyanide and thiocyanate toxicity (usually > 3 days use)

Question 17

Nitroglycerin

Answer 17

venous > arterial VD
for ACS and HTN crisis

Question 18

Nesiritide

Answer 18

balanced vasodilation

Question 19

Positive Inotropes

Answer 19

beta agonists: dobutamine, dopamine - stimulate cAMP and stimulate Ca2+ to enter cell and cause increase in contraction
PDE 3 inhibitors: milrinone, amrinone - decrease degradation of cAMP by inhibiting PDE, increase cAMP, increase Ca2+, increase force of contraction
use less than 72-96 hours due to - downregulate receptor and cause desensitization if used long term

Question 20

Dobutamine

Answer 20

MOA: simulates AC to increase cAMP
requires beta receptor

Question 21

Milrinone

Answer 21

increase cAMP in myocardium (inc CO) and vascularture (dec SVR)
clinical effects: positive inotrope, venous > arterial VD

Question 22

Dopamine

Answer 22

Typically plays secondary role to dobutamine/milrinone. Sometimes referred to as a vasopressor

Question 23

ADHF: Positive Inotrope Therapy

Answer 23

• Primarily to manage hypoperfusion or cold HF patients
• Reasonable to consider vasodilators before inotropes when adequate BP
• Useful for symptom relief in hypotension (SBP <90 mm Hg)
• Useful in patients with end organ dysfunction (AKI, altered mental status, systemic hypoperfusion, hypotension, CV collapse)
• Useful when disease is refractory to other HF therapies
   Need for mechanical circulatory support, transplant, palliative care
• Choice of dobutamine vs. milrinone is individualized - milrinone is better choice b/c it’s a vasodilator
   High SVR
   Beta-blocker use

Question 24

Cool and Dry (Subset III)

Answer 24

• These patients will have symptoms of low output (Cool) but not congestion (Dry). i.e. inadequate perfusion with no congestion
• The primary goal of therapy is to increase output and perfusion with positive inotropes +/- intravenous fluids
   Initial therapy - fluids until BP maximized: Must be cautious replacement
   Therapy following fluids: If patients still remains “Cool”, inotropic or arterial vasodilator therapy maybe required