Management of Shock
Brian Haimerl
Cardiogenic shock
Background
- Pathophysiology: Primary insult (see etiologies) -> CO/CI decreased -> systemic hypoperfusion -> compensatory mechanisms including increased SVR and fluid retention -> further reduction of CO
- PA catheter findings: Typically, high PCWP >15mmHg (can be low/normal in right heart failure), low CO (CI <2.8 L/min/m2), high SVR (>1400 dynes/sec/cm5) and SvO2 <65%
- Etiologies: Acute MI, cardiomyopathy (LHF, RHF or biventricular), arrhythmia, mechanical such as 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
Distributive shock
Background
- Pathophysiology: Severe, peripheral vasodilation
- CO/CI increased, SVR decreased, PCWP and RAP normal to low, SvO2 >65%
- 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, associated bradycardia
- Adrenal insufficiency: History of chronic steroid use, 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. 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 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: IVF + pressors; trend H/H, BUN, and Ca; treat complications (necrotizing pancreatitis, abdominal compartment syndrome); address underlying etiology (see “Acute Pancreatitis” in GI section)
- Cardioversion If refractory to medical management
- Treatment of underlying cause if identifiable
- Ischemia, electrolyte disturbances, heart failure, drugs
Hypovolemic shock
Background
- Etiologies: Hemorrhagic and non-hemorrhagic
- Hemorrhagic: Common locations include the GI tract, retroperitoneal (*needs high index of suspicion), intra-abdominal, thighs, thorax
- Non-hemorrhagic: GI losses or decreased PO intake, severe burns, untreated Diabetes Insipidus
- POCUS with thin, collapsible IVC
Management – Hemorrhagic
- Ensure good access with two large-bore (at least 18G) IVs, ideally in AC or proximal versus Cordis or MAC CVC (can also use dialysis catheter, if necessary)
- Hyperacute bleed:
- 1:1:1 ratio FFP:Plt:RBC (balanced resuscitation), trauma blood is the fastest way to get RBCs
- Fast-pack (2 units pRBCs and 2u FFP) – can only order once
- If pt remains unstable -> massive transfusion protocol (MTP)
- Consider TEG to guide further transfusions if concerned for coagulopathy
- Monitor iCa and replete (citrated blood products will deplete Ca) - especially if 4 or more units of PRBCs given
- Minimize crystalloid products, if possible, w/primary use to prevent immediate hemodynamic collapse while waiting for blood products (contributes to coagulopathy, hypothermia, acidemia, trauma/surgery)
- For penetrating chest injuries/arterial bleeds: Consider permissive hypotension until source control/product transfusions (aggressive fluid resuscitation -> hypothermia, dilution of clotting factors and high MAP/SBP -> clot destabilization)
- Trend POC lactate/exam to guide decisions
- For acute traumatic arterial bleed or post-partum hemorrhage arriving within 3 hours of bleed, consider TXA (1-2g bolus)
- Reverse anticoagulation, if applicable
- Vasopressors: Generally, poorly effective. First line: Norepinephrine
- Source control: GI, IR, or EGS
- Variceal bleed: See GI Bleeding section for specific management
Management (Non-Hemorrhagic)
- Aggressive IVF resuscitation (balanced crystalloid); target MAP ≥65
- Can support BP during resuscitation with pressors (usually norepinephrine)
Obstructive Shock See dedicated section below
Obstructive Shock
Hannah Kieffer
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)
- Risk factors vary based on the underlying pathology:
- PE: Known DVT, prothrombotic conditions, malignancy, recent orthopedic surgery or prolonged travel; family history of clots/thrombophilia
- Pneumothorax: Recent chest trauma/thoracic procedures, mechanical ventilation, COPD/emphysema, endobronchial valve placement
- Tamponade: Recent cardiac procedure, ESRD, cancer, trauma, rheumatologic diseases
Approach in the hemodynamically unstable patient
Initial workup:
- Evaluate the patient at bedside and bring an ultrasound if available to perform POCUS
- Orders: STAT CBC, CMP, EKG, BNP, troponin, VBG, lactate, d-dimer, CXR
Supportive measures:
- Consider fluid administration, especially if concerned that patient is preload dependent (e.g. cardiac tamponade)
- Perform passive leg test (compare cardiac output/blood pressure between patient lying at 45 degrees and patient to lying back with both legs raised) or trial small fluid bolus to test for fluid responsiveness
- 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
- 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)
- 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 findings:
- PE: Distended IVC, RV dilation, McConnell’s sign, Septal D sign, underfilled LV
- Pneumothorax: Lack of lung sliding
- Cardiac tamponade: Diastolic collapse of the RV, large pericardial effusion
Further evaluation and management by most common etiologies
Pulmonary embolism
- Evaluation: STAT CTA PE
- Management:
- Supportive measures: vasopressors, supplemental O2
Start high-dose therapeutic heparin gtt if high suspicion even before clot has been identified/confirmed, with heparin bolus unless contraindicated (i.e., recent GI bleed)
NOTE: First line is LMWH due to faster onset of action and longer time in therapeutic range. At VUMC, we often start heparin gtt first because if pt is going for EKOS, they need to be able to turn off AC quickly. We recommend starting heparin gtt until decision for EKOS has been made. If no EKOS, switch to LMWH
- If massive PE, activate PERT (PE Response Team) for discussion regarding mechanical thrombectomy or chemical thrombolysis
- Call “1-1111” and state “that your pt has a massive PE”/”activate PERT”
- Look for the source for the embolism (four extremity dopplers)
- If no risk factors for VTE are identified, consider a benign hematology outpatient referral for a hypercoagulable work-up
- See “Pulmonary Embolism” in Cardiology section for more information
Cardiac tamponade
- Evaluation: Cardiac POCUS, follow up with formal echo
- Management:
- Supportive measures: Support preload; IV fluid bolus to temporarily improve cardiac output. AVOID diuretics, venodilators, and proning
- If un-stable, STAT consult cardiothoracic surgery for procedural management (pericardiocentesis vs drain)
- If stable, consult cardiology and/or cardiothoracic surgery
Tension pneumothorax
- Evaluation: Chest POCUS (look for lack of lung sliding), STAT CXR
- Management:
- If acutely unstable: Emergent needle decompression
- 14-16 gauge needle (7-8cm long) in 5th intercostal space at the mid-axillary line (5th ICS-MAL) vs 2nd intercostal space mid-clavicular line (2nd ICS-MCL)
- ATLS guidelines recommend 5th ICS-MAL since some studies suggest improved success rate and lower risk of complications (hitting major vessel) but data is not definitive
- Can consider 2nd ICS-MCL when left sided if small body habitus and c/f cardiac puncture
- If acutely unstable: Emergent needle decompression
- Otherwise, urgent chest tube placement with pulmonology (if at the VA overnight, ED attending can place one)
- Once stabilized, consult to pulmonology for chest tube placement is indicated in large, hemodynamically significant pneumothorax to ensure resolution.
- For more on chest tubes, see “Chest Tubes” in Pulmonary
