Management of Shock¶

Alex Toporex, Soibhan Kelley

Cardiogenic Shock¶

Pathophysiology: CO/CI decreased, SVR increased, PCWP and RAP elevated (left heart failure) or PCWP low/normal and RAP elevated (right heart failure)
Etiologies: Cardiomyopathy (LHF, RHF or biventricular), arrhythmia, mechanical such as acute AR (ex: dissection) or MR (ex: ruptured papillary muscle)

Edematous, elevated JVP, “cold and wet”; hypoxia w/crackles and pulm edema on CXR; mixed venous sat < 50-60%; POCUS with plump, non-compressible IVC, reduced EF, and B-lines

Pathophysiology: severe, peripheral vasodilation
- CO/CI increased, SVR decreased, PCWP and RAP normal to low
Etiologies: sepsis (most common), anaphylaxis, neurogenic, adrenal insufficiency, pancreatitis
Signs/symptoms:
- Sepsis: localizing signs of infection; tachycardia, tachypnea, may be hypo/hyperthermic; POCUS with hyperdynamic cardiac function
- Anaphylaxis: history of anaphylaxis; urticaria, edema, diarrhea, wheezing on exam
- Neurogenic: history of CNS trauma; focal neurologic deficits on exam
- Adrenal insufficiency: hx chronic steroid use, may have GI symptoms, hyponatremia (common), hyperkalemia (rare), hypoglycemia, hypo/hyperthermia, NAGMA
- Pancreatitis: abdominal pain, elevated lipase, evidence on CT scan

Sepsis: see sepsis section
Anaphylaxis: 0.3mg IM epinephrine ASAP to be repeated q5-15min x 3; after third IM epi, consider IVF and epi gtt if persistent hypotension. Adjuncts: albuterol nebs for bronchospasm, H1 and H2 blockers, ± glucocorticoids (methylprednisolone 1mg/kg). EPINEPHRINE SAVES LIVES.
Neurogenic: caution with IVF resuscitation, can worsen cerebral and spinal cord edema; preferred pressors are norepinephrine and phenylephrine; for neurogenic shock 2/2 spinal cord pathology, consider higher MAP goal 85-90 mmHg
Adrenal insufficiency: stress dose steroids with hydrocortisone 100mg IV q8h or 50mg q6h
Pancreatitis: IVF + pressors; trend H/H and Ca; treat complications (necrotizing pancreatitis, abdominal compartment syndrome); address underlying etiology (see GI section)

Etiologies: Hemorrhagic and non-hemorrhagic
Signs/symptoms:
- Hemorrhagic: Common sources include GI, retroperitoneal (*needs high index of suspicion), traumatic, intraabdominal, thighs, thorax.
- Non-hemorrhagic: 2/2 GI losses or decreased PO intake
- POCUS with thin, collapsible IVC

Ensure good access with two large-bore (at least 18G) IVs ideally in AC or above; Cordis or MAC CVC (can also use dialysis catheter, if necessary)
Hyperacute bleed:
- 1:1:1 ratio FFP:Plt:RBC (balanced resuscitation), trauma blood (fastest way to get RBCs); massive transfusion protocol (MTP)
- Monitor iCa and replete (citrated blood products will deplete Ca)
- Minimize crystalloid if possible, w/primary use to prevent immediate hemodynamic collapse (contributes to coagulopathy, hypothermia, acidemia, trauma/surgery)
- Permissive hypotension until source control/transfusions with arterial bleeds (high MAP/SBP -> clot destabilization); trend POC lactate/exam to guide
- Acute traumatic arterial bleed or post-partum hemorrhage consider TXA (1-2g bolus)
- Reverse anticoagulation, if applicable
- Vasopressors -> generally poorly effective, would start with norepinephrine
- Source control -> GI, IR, or EGS
Variceal bleed: See GI Bleeding section for specific management