Inpatient / Cardiology

Cardiogenic Shock

Last Updated: 1/17/2023

# Cardiogenic Shock 2/2 ***

-- ABCs: 
to ICU if SBP <90 for 30 minutes or need for pressor/inotrope with monitoring of CVP, a-line, or PA catheter
-- Chart Check: *** "dry weight", prior echo, cath reports, heart failure, ischemic heart disease
-- HPI Intake: *** weight gain, salt intake, medication adherence/access, new medications
-- Can't Miss: *** new MI
-- Admission Orders: *** EKG and trop,
-- Initial Treatment to Consider: ***  if pulm edema, can trial BIPAP; if HTN or normotensive focus on afterload reduction; if hypotensive trial 500cc bolus vs passive leg raise (~200-300cc) and assess response, if persists start levo and consider need for inotrope (usually dobutamine if hypotensive); if wet and cold and SBP >90, can trial diuresis;

-- History: *** "dry weight", prior echo, cath reports, heart failure, ischemic heart disease; recent weight gain, salt intake, medication adherence/access, new medications
-- Clinical: *** AMS, oliguria and UOP
-- Exam: *** hypotension, general appearance, AMS, cold vs warm extremities, cap refill, volume assessment (LE edema, JVP, IVC, mucous membranes), murmurs, crackles; POCUS (b-lines, heart - large chambers and poor contractility)
-- Data: *** EKG, Echo, lactate, CMP (liver and renal funtion), cath (Index, PCWP)
-- Etiology/DDx: *** MI, heart failure, myocarditis, aortic stenosis, acute MR/TR, trauma/contusion; Obstructive shock (tamponade, PE)

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

-- Continuous telemetry and pulse ox with goal >92%
-- f/u echo
-- trend VBG/lactate q ***
-- RHC can help determine filling pressures

-- Lungs: *** if resp distress trial BIPAP, thoracentesis for effusions
-- Afterload: *** hydral 37.5mg q6-8, nitroprusside 20mg q6-8 (goal to reduce wall stress with MAP >60 and SVR <800-1200)
-- Pressor: *** start with levo prior to RHC which can further tailor therapy
-- Preload: *** bolus vs diuretics or UF with dialysis (goal PCWP 14-18, CVP 8-12)
-- Contractility: *** dobutamine 0.5-1mcg/kg/min or milrinone 0.125mcg/kg/min (will drop afterload, renall cleared) with goal CI >2.2, central sat >65%
-- Etiology: *** cardiovert new arrythmia, pace if bradycardic, ACS pathway and cath lab for ischemia, valve repair/replacement
-- MCS: *** IABP (0.5L/min), Impella (2.5-5L/min), VA-ECMO (4-10L/min), VAD (10L/min) - usually as bridge to recovery or transplant
-- Avoid NSAIDs, ACE/ARB and consider holding CHF and HTN medications based on hemodynamic status

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If You Remember Nothing Else

Cardiogenic shock is not always easy to spot. Rely on your exam (those was the most worrisome cardiogenic shock will be ill-appearing, cold and wet on exam, with reduced UOP) and look for evidence of poor end-organ perfusion via labs such as LFTs, creatinine, and lactate. In undifferentiated shock, levo is first pressor which is okay in cardiogenic shock. Next you will often add an inodilator such as dobutamine or milrinone. Management of cardiogenic shock is a complicated balance of managing volume, afterload, and contractility. You will often need q8 hemos (from PA catheter) to help guide these decisions on a day-to-day basis. Normal RHC tracing - “rule of 5s”  RA 5, RV 25/5, PA 25/10, PCWP 10, LV 125/10. Mechanocirculatory support (MCS) is often used as a bridge to more definitive treatment or procedures, but LVADs can be considered a destination in certain circumstances.

Clinical Pearls

  • Revascularization for MI is the only proven way to improve mortality in patients with cardiogenic shock so don’t miss it!
  • Cardiogenic shock can be sneaky, especially in younger otherwise healthy patients who are able to compensate - may just have sinus tachycardia! So don't just slam them with beta blockers to try to treat the tachycardia because it may be compensatory
  • Urine output (goal >0.5ml/kg/hr) is a great way to assess end-organ perfusion and organ failure
  • When not sure what type of shock or patient’s volume status can trial (in order) - POCUS --> fluid challenge with 500cc vs passive leg raise --> place central and get a MVO2 --> get RHC
  • Fluids or diuresis won't fix the heart. A common mistake is to note that a patient with CHF is overloaded and diurese them without noting that they are also cold. This will help with their edema and perhaps oxygenation, but will worsen their end-organ perfusion and possibly lead to renal failure. On the flip side, in those with AKI, if you give aggressive fluid and do not note that they are overloaded, you will fill up their lungs and cause pulmonary edema and respiratory failure.
  • Passive Leg Raise which can equate to a bolus of 150-300cc - raise 45 degrees for 1 minute and assess response of HR, BP, CVP (via POCUS)
  • Mixed Venous Saturation >65% suggests increased CO, <65% suggests reduced CO
  • Normal RHC tracing - “rule of 5s”  RA 5, RV 25/5, PA 25/10, PCWP 10, LV 125/10
  • Normal Cardiac Index is 2.6-4.2; Normal SVR is 700-1200
  • Cardiac Index accounts for the patients body surface area (BSA)
  • Cardiogenic shock RHC - increased CVP, increased PCWP, low CO/CI, increased SVR
  • On RHC, (wet) cardiogenic shock will show CI <2.2 and PCWP >15
  • Dobutamime and milrinone are inodilators (increase production or decrease breakdown of cAMP which leads to more squeeze) and both can cause some hypotension - milrinone has less chronotropy and fewer arrhythmic side effects; dobutamine not great for those taking BB’s (its a beta agonist)
  • Mechanical Circulatory Support (MCS) augments CO without increasing oxygen demand whereas inotropes increase CO but via increased squeeze which requires O2; Intra-Arotic Balloon Pump (IABP) - inflates during diastole to increase coronary perfusion and decreased afterload, does not require AC at 1:1, does not allow mobility; Impella - partial LV or RV support, requires AC and allows mobility, complications include bleeding and thrombocytopenia, clotting, arrhythmias; Durable VAD - bridge to transplant vs destination therapy, allows mobility and can be long-term option for years
  • Cardiac Output (CO) and thus CI is either measured via thermodilution (rarely) or calculated via the Fick equation (which needs a central sat and Hgb as part of the calculation so they are not perfect); further, O2 consumption is based on calculation from body surface area but in reality it varies based on the body’s metabolism at that time

Trials and Literature

  • ESCAPE Trial - no mortaltity benefit for PA catheter to guide heart failure treatment in patients not on an inotrope; but SHOULD get if cardiogenic/mixed shock or those with MCS (JAMA, 2005)
  • IABP-SHOCK II Trial - IABP do not decrease mortality in cardiogenic shock (NEJM, 2012)
  • ISAR-SHOCK Trial - Impella improved CO compared to IABP but did not improve mortality at 30 days (secondary endpoint); these are very difficult trials to enroll for based on how sick the patients are (J Am Coll Cardiol, 2008)

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