Management of Shock

Background

• Pathophysiology: Primary insult (see etiologies) -> cardiac output/cardiac index (CO/CI) decreased -> systemic hypoperfusion -> compensatory mechanisms including increased systemic vascular resistance (SVR) and fluid retention -> further reduction of CO/CI.
• PA catheter findings: high PCWP >15mmHg (can be low/normal in right heart failure), low CO (CI <1.8 L/min/m2 without hemodynamic support or <2.2 L/min/m2 with support), high SVR (>1400 dynes/sec/cm5) and SvO2 <65%.
• Etiologies: Acute MI, cardiomyopathy (LHF, RHF, or biventricular), arrhythmia, acute AR (ex: dissection) or MR (ex: ruptured papillary muscle), myocarditis, blunt cardiac trauma.

Presentation

• "Cold and wet" - cold and clammy skin/limbs, weak/nonpalpable distal pulses, edematous, elevated JVP; narrow pulse pressure; hypoxia w/crackles and pulmonary edema on CXR; POCUS with plump, non-collapsable IVC, reduced EF, and B-lines
• *Patients can be normotensive and still in cardiogenic shock w/ end-organ hypoperfusion*

Management

• See “cardiogenic shock” in the Cardiology section 

Background

• Pathophysiology: Severe, peripheral vasodilation, CO/CI increased, SVR decreased, PCWP and RAP normal to low, SvO2 >65%
• Etiologies and their Signs/Symptoms:
  • Sepsis (most common): 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 (including spine) trauma; focal neurologic deficits on exam, associated bradycardia.
  • Adrenal insufficiency: History of chronic steroid use or autoimmune diseases, often exacerbated during illness, may have GI symptoms, hyponatremia (common), hyperkalemia (rare), hypoglycemia, hypo/hyperthermia, NAGMA.
  • Pancreatitis: Abdominal pain with radiation to back, elevated lipase, evidence on CT scan.

Management

• Sepsis: See “Sepsis” in Infectious Disease
• Anaphylaxis: 0.3mg IM epinephrine (0.01mg/kg, max 0.5mg) ASAP to be repeated q5-15min x 3; IVF boluses for supportive treatment; after third IM epi, consider epi gtt (1-10 mcg/min) if persistent hypotension. EPINEPHRINE SAVES LIVES. Adjuncts: Include Albuterol nebs for bronchospasm, H1 and H2 blockers, glucocorticoids (methylprednisolone 1mg/kg). 
• Neurogenic: Caution with IVF resuscitation, can worsen cerebral and spinal cord edema; preferred pressor is norepinephrine; for neurogenic shock 2/2 spinal cord pathology, consider higher MAP goal 85-90 mmHg for 7 days to improve spinal cord perfusion.
• Adrenal insufficiency: Stress dose steroids with hydrocortisone – initial dose of 100mg IV followed by 50mg q6h. IVF resuscitation.
  • NOTE: Adrenal crisis NEVER comes out of nowhere; look for precipitating factor (missed medication, infection, trauma, surgery, or stressors).
• Pancreatitis: See “Acute Pancreatitis” in GI section.

Background

• Etiologies and their 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 IVCs, untreated Diabetes Insipidus
• POCUS with thin, collapsible IVC

Management (Non-Hemorrhagic)

• Aggressive IVF resuscitation (balanced crystalloid); target MAP ≥65 mmHg
• Can support BP during resuscitation with pressors (usually norepinephrine)

Management (Hemorrhagic)

• Ensure good access with two large-bore (at least 18G) peripheral IVs; Cordis or MAC CVC
• Hyperacute bleed:
  • RESUSCITATION:
    • 1:1:1 ratio FFP:Plt:RBC (balanced resuscitation) or TEG-driven resuscitation (see below)
    • Sourcing Product: call blood blank for fast pack cooler (2RBC, 2FFP) vs initiating massive transfusion protocol (MTP) - can only do fast pack cooler one time per patient episode
  • Replete Ca (1g CaCl or 3g CaGluc for every 3-4 units of blood product), monitor iCa
    • 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
  • SOURCE CONTROL -> GI, IR, or EGS
  • Consider TXA (1-2g bolus) ifConsider TXA (1-2g bolus) if acute traumatic arterial bleed or post-partum hemorrhage
  • Reverse anticoagulation 

TEG Directed Therapy for Bleeding Patient Image Source

Thromboelastogram (TEG):

Background

• Obstructive shock occurs when there is increased resistance to forward blood flow. This can occur due to:
  • Resistance in the pulmonary/cardiovascular circuit (i.e., pulmonary embolism, intracardiac mass).
  • Extrinsic compression on the heart and decreased diastolic filling (i.e., pericardial tamponade, tension pneumothorax, dynamic hyperinflation (auto-PEEP).

Approach in the hemodynamically unstable patient

Supportive measures:

• Consider fluid administration, especially if concerned that patient is preload dependent (e.g. cardiac tamponade).
• Try to avoid vasopressors since increasing afterload could aggravate obstructive shock. However, if vital, can consider norepinephrine vs vasopressin to maintain lowest necessary MAP (both thought to have lesser effect on pulmonary vasculature).
• If ventilated, aim for low volume and low PEEP settings to minimize afterload on the right ventricle.

Clinical signs/symptoms

• General: Hypotension, tachycardia, hypoxemia, elevated JVP, cold extremities.
• Tension pneumothorax: Unilateral breath sounds, asymmetrical chest rise, CXR with one lung collapsed, tracheal deviation/mediastinal shift away from the pneumothorax. POCUS shows lack of lung sliding.
• Pulmonary embolism: Chest pain, hypoxia, sense of impending doom. On EKG: Most common is sinus tachycardia but look for right heart strain (right axis deviation, S1Q3T3, ST depressions in inferior leads/precordial leads, new RBBB). POCUS may show distended IVC, RV dilation, McConnell’s sign, Septal D sign, underfilled LV.
• Cardiac tamponade: Beck’s Triad (distant heart sounds, JVD, and hypotension), electrical alternans, low amplitude on EKG, pulsus paradoxus (drop in systolic blood pressure by >10 mmHg during inspiration). POCUS with diastolic collapse of the RV, large pericardial effusion.

Further evaluation and management by most common etiologies

Pulmonary embolism

• Evaluation: STAT CTA PE
• Management: See "Pulmonary Embolism" in Cardiology section.

Cardiac tamponade

• Evaluation: Cardiac POCUS or TTE
• Management:
  • Supportive measures: Support preload; IV fluid bolus to temporarily improve cardiac output.
  • If unstable, STAT consult cardiology for procedural management (pericardiocentesis vs drain).

Tension pneumothorax

• Evaluation: Chest POCUS (look for lack of lung sliding), STAT CXR.
• Management:
  • If acutely unstable: Emergent needle decompression (2nd Intercostal space at the midclavicular line).
  • Otherwise, urgent chest tube placement with pulmonology (if at the VA overnight, ED attending can place one).
• For more on chest tubes, see “Chest Tubes” in Pulmonary.