Understanding Shock: Types, Diagnosis, and Management

Shock Overview

• Shock is defined as a state of circulatory insufficiency leading to an imbalance between tissue oxygen supply and demand, ultimately resulting in end-organ dysfunction.
• Initial approach is consistent across all types of shock
• Early recognition and rapid diagnosis are crucial.
• Identifying the underlying cause is important, but there may be multiple contributing factors
• Shock is not simply defined by hypotension or an isolated lab value. Systolic blood pressure <90 is a consideration.
• In the Emergency Department, 0.4-1.3% of presentations are shock related

Key Statistics and Mortality

• Septic shock has a mortality rate of around 26%.
• Cardiogenic shock has a mortality rate ranging from 39-48%.

Pathophysiology

• The body attempts to compensate for shock by prioritizing perfusion to vital organs.
• Baroreceptors trigger sympathetic nervous system activation, leading to arteriolar vasoconstriction and increased heart rate and contractility, aiming to raise cardiac output.
• Constriction of the venous system occurs to increase venous return.
• Release of epinephrine, norepinephrine, dopamine, and cortisol increases arteriolar and venous tone.
• ADH and RAAS are activated to increase water and sodium conservation.
• If shock persists, cellular death can occur, leading to hyperkalemia, hyponatremia, hyper/hypoglycemia, and lactic acidosis which may cause multi-organ dysfunction and coagulopathy.

Types of Shock

• There are four main types of shock: distributive, hypovolemic, cardiogenic, and obstructive.
• Distributive shock accounts for 33-50% of cases, is characterized by decreased preload and SVR, and is associated with sepsis, neurogenic shock, and anaphylaxis.
• Hypovolemic shock accounts for 31-36% of cases, involves decreased preload and cardiac output with increased SVR, and is caused by hemorrhage, capillary leak, GI losses, and burns.
• Cardiogenic shock accounts for 14-29% of cases, features increased preload, afterload, and SVR with decreased cardiac output, and is linked to myocardial infarction, dysrhythmias, heart failure, and valvular disease.
• Obstructive shock accounts for approximately 1% of cases, presents with decreased preload and increased SVR with decreased CO, and is associated with pulmonary embolism, pericardial tamponade, and tension pneumothorax.

Basic Hemodynamic Concepts

• Cardiac Output (CO) is equal to Stroke Volume multiplied by Heart Rate.
• Stroke Volume (SV) is dependent on preload, afterload, and contractility.
• Mean Arterial Pressure (MAP) depends on CO and Systemic Vascular Resistance (SVR); goal MAP is > 65 mm Hg, Spinal cord injury want MAP > 85.
• SVR is the resistance the heart pumps against in the arterial system.
• CO is dependent on inotropy, chronotropy, and lusitropy.

History and Presentation

• Clinical presentation of shock can be clear if there is an obvious underlying cause.
• Vague symptoms such as generalized weakness, lethargy, and altered mental status may be the earliest signs.
• Systemic hypotension is likely, though not always a reliable marker of global tissue hypoperfusion
• Tachycardia in a patient means understanding what's causing their heart rate to go up

Initial Assessment Considerations

• Patient monitoring should be appropriate for shock.
• Check for equipment malfunctions (arterial line issues etc)
• Ensure vasopressors are running through appropriate IV tubing, pumps are working, and medications are mixed correctly.
• Do mentation and clinical appearnace match the degree of hypotension?
• Consider if hidden sources of blood loss.
• The patient should be assessed for adequate volume resuscitation, pneumothorax post-central line placement, occult penetrating injury, ruptured spleen, large-vessel aneurysm, ectopic pregnancy, adrenal insufficiency, allergies, cardiac tamponade, acute myocardial infarction, aortic dissection, and pulmonary embolus.

Vital Signs and General Survey Findings

• Temperature: Hyperthermia or hypothermia may be present. Endogenous hypothermia must be distinguished.
• Heart rate is usually elevated; paradoxical bradycardia can occur due to hypoglycemia, beta-blocker use, or pre-existing cardiac disease.
• Systolic blood pressure: Initially may increase slightly, then falls as shock advances.
• Diastolic blood pressure: Correlates with arteriolar vasoconstriction, rising early then falling when compensation fails.
• Pulse pressure: Increases early, then decreases before systolic pressure.
• Mean arterial pressure: Often low, <65 mm Hg.
• CNS: Delirium, restlessness, disorientation, confusion, and coma may occur due to decreased cerebral perfusion.
• Skin/capillary refill: Pallor, pale, dusky, clammy, cyanosis, sweating, cool skin, and prolonged capillary refill (>2-3 seconds) are common.
• Cardiovascular: Neck vein distention/flattening, tachycardia, arrhythmias, S3 heart sound (high-output states), and signs of decreased coronary perfusion may be present.
• Respiratory: Tachypnea, increased minute ventilation, bronchospasm, and hyper- or hypocapnia leading to respiratory failure can occur.
• Splanchnic organs: Ileus, GI bleeding, pancreatitis, and mesenteric ischemia may occur.
• Renal: Reduced glomerular filtration rate leads to oliguria.
• Metabolic: Lactic acidosis, hyperglycemia, hypoglycemia, and hyperkalemia. Metabolic acidosis occurs.

Initial Diagnostics

• Key labs include CBC with differential, CMP, serum lactate, EKG and U/A with consideration for UTI.
• Additional diagnostics may include CXR, coagulation studies (PT/PTT, INR), ABG, LFTs, pan cultures, cortisol level, and pregnancy test.
• CT scans of the chest, abdomen, and pelvis should be considered to identify the source of shock.
• Point-of-care ultrasound (POCUS) can assess for free fluid in the abdomen, pleural effusion, and IVC volume status.

Treatment Priorities

• Airway: Ensure a patent airway. Consider intubation.
• Breathing: Control the work of breathing. Support ventilation.
• Circulation: Optimize circulation with fluids and/or vasopressors.
• Delivery: Ensure adequate oxygen delivery.
• Endpoints: Monitor resuscitation endpoints (lactate, acid/base status, urine output).

Airway and Breathing Management

• Definitive airway management often requires endotracheal intubation.
• Caution with sedatives during intubation as they can cause vasodilation and hypotension.
• Positive pressure ventilation can decrease preload and cardiac output (CV Collapse). Patients need to be resuscitated first.
• Significant work of breathing requires control, consider neuromuscular blockers for severe hypoxia/ARDS.

Ensuring Oxygen Delivery

• Control oxygen consumption to restore balance of supply/demand.
• Address hyperadrenergic states (stress, pain, cold treatment room, anxiety)
• Treat pain with analgesia, muscle relaxers, warm blankets, and anxiolytics
• Target oxygen saturation >92%.
• Maintain hemoglobin > 7 g/dL, higher if history of CAD.

Circulatory Optimization

• Initial rescue maneuvers include Trandelenberg and passive leg raise.
• Fluids: Isotonic crystalloids (Normal Saline, Lactated Ringers) 20-30ml/kg initial bolus
• Colloids when vessels can no longer hold fluids
• Blood transfusion, or Albumin
• Consider sodium bicarbonate for profound metabolic acidosis.
• Access via peripheral or central lines.

Crystalloid Fluids

• Normal plasma is roughly ~140 Na+ mEq/L ~100 Cl- mEq/L ~4 K+ mEq/L 2.4 Ca2+ mEq/L0.85 Glucose g/L.
• .9% saline (a.k.a. "normal saline" or NS) is 154 Na+ mEq/L and 154 Cl- mEq/L with no buffer, an osmolarity of 308, and is isotonic. It is typically used for resuscitation.
• 0.45% saline (a.k.a. ½ NS) is 77 Na+ mEq/L and 77 Cl- mEq/L, an osmolarity of 154, and is hypotonic. It is typically used for maintenance.
• 3% saline is 513 Na+ mEq/L and 513 Cl- mEq/L and is hypertonic. It is used for severe hyponatremia.
• D5 1/2NS + 20 meq KCL is 77 Na+ mEq/L, 97 Cl- mEq/L, 20 K+ mEq/L, and 50 Glucose g/L. It is hypertonic becoming hypotonic and is used for maintenance.
• D5W is is 50 Glucose g/L and is hypotonic.
• Lactated Ringer's (LR) / Hartmann's solution has 130 Na+ mEq/L, 109 Cl-mEq/L, 4 K+ mEq/L, 3 Ca2+ mEq/L and Lactate 28 mEq/L. It is isotonic and used for resuscitation.
• Avoid Lactated Ringers in Chronic Kidney Disease due to higher levels of potassium.

Hemodynamic Monitoring

• Hemodynamic monitoring is important to assess the severity of shock and response to treatment.
• Monitor pulse oximetry, telemetry, NiBP vs Arterial Line, EtCO2.
• Use a Foley to measure urine output.
• Arterial lines provide a second-to-second measurement of blood pressure.

Endpoints of Resuscitation

• Use hemodynamic and physiologic values to maximize survival and minimize morbidity.
• MAP > 65 mmHg
• CVP 8-12 mmHg
• PaO2 > 70% (ABG)
• Urine output > 0.5-1 ml/kg/h
• Labs: CBC, ABG, Lactate, BMP/CMP- ensure adequate source control.

Hypovolemic Shock

• Hypovolemic shock is characterized by decreased intravascular fluid or blood volume.
• Etiologies include hemorrhage, GI losses, and burns.
• Leads to a drop in preload, stroke volume, and cardiac output and may see increased systemic vascular resistance (SVR)

Hemorrhagic Shock

• Mortality is 30-40%
• Restore circulating volume ASAP to allow O2 carrying capacity (tissue perfusion) AND prevent/correct derangements in coagulation
• Trauma Triad for Hemorrhagic Shock is Acidosis/Coagulopathy/Hypothermia
• Dependent on factors.
• Patients may present as tachycardic or hypotensive and can have poor peripheral perfusion, narrow pulse pressure and AMS
• Athletes, elderly, those on beta blockers, and pregnant patients may not present with typical signs and symptoms.

Diagnosis- Hemorrhagic Shock (ED Mgmt)

• Initial H/H is unreliable
• Restore intravascular volume
• Maintain O2 carrying capacity
• Limit ongoing blood loss
• Prevent Coagulopathy and Hypothermia
• Initial CBC H/H unreliable, Lactate, Coags, BMP; Renal function, Glucose think DKA, Trend LYTES including Ca+
• Type and Cross
• Large bore IV Access
• CXR/Pelvis/Long Bones for Primary Survey
• Monitor/EKG
• POCUS for primary survey
• Consider Trop if mechanism unclear. ABG if intubated
• IF STABLE then CT
• Oxygenate/Ventilate, Control Bleeding, Protect Spinal Cord
• In hemorrhagic shock, the Goal is permissive hypotension.

Treatment of Hemorrhagic Shock

• Isotonic fluids such as LR or NS should be administered as crystalloids. However, most will not remain intravascular due to low oncotic pressure.
• For NON Hemorrhagic a LOTS of fluids with Vasopressors

Blood products:

• EARLY PRBC
• Transfuse Hgb < 7 unless unstable VS or if CAD/CVD/PVD and Hgb <10 O negative universal
• Fresh Frozen Plasma (FFP); Coagulation factors, AB+ universal
• PLT 4-6 units random pooled platelet-ideally raise PLT count by 50k

Massive Transfusion Protocol

• Defined as requirement for > 10 units of PRBC within first 24hrs of injury and may consider TXA for massive hemorrhage situations.
• Give blood.
• Bleeding should be controlled/stopped.
• Consists of 10% military and 3-5% civilian. NOT a replacement for surgical hemostasis.
• 4 values (>2 = sensitivity for MTP 76-90%- Penetrating Trauma, Positive FAST SBP <90 and HR > 120

Distributive Shock

• Relative intravascular volume depletion due to marked systemic vasodilation
• Septic shock is the most common cause.
• Etiologies include Sepsis MCC. Anaphylaxis, Adrenal Insufficiency and Neurogenic
• Physiology: SVR is down
• CO and HR are up (trying to compensate)

Sepsis

• Sepsis is characterized by widespread inflammation and organ distress.
• Multiple organisms may be involved and often caused by gram positive bacteria.
• 300-1000k/100,000 per year in US.
• Leading cause of hospital death- 15-20%.
• Impaired perfusion, O2 delivery, direct cellular damage due to inflammation multi-system organ failure DEATH
• May not include blood stream infection
• Fungal sources may be the cause for immunocompromised patients.
• MRSA, Vancomycin-resistant enterococcus (VRE), MDROS

Sepsis Definitions

• Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.
• Proven or suspected infection AND evidence of organ failure (score>2) A) AMS B) RR>22 C) SBP <100
• Septic Shock as of 2016-is sepsis requiring vasopressors and elevated lactate

Presentation of Sepsis

• Can be subtle, early in course.
• AMS
• 40% of pt's in ED with unclear hypotension Sepsis
• Look at VS: Fever, Hypotension and/or Tachycardia
• No clear source with profound leukocytosis get imaging!
• CBC, CMP, Lactate, Coags, Pan cultures consider imaging

Sepsis Clinical Diagnosis

• Do NOT WITHOLD ABX/Source ASAP
• VANC AND ZOSYN-control

Sepsis Sequela

• Hepatic injury, AKI, and hypoperfusion are possible sequelae.
• Watch meds/IV Contrast
• Hematologic Neutropenia, Thrombocytopenia DIC

Severe Sepsis/Shock Management

• Surviving Sepsis Campaign: The goal is 1 hour from triage
• Obtain Lactate. If elevated >2, trend <6 hours
• Initial IVF 30ml/kg crystalloid for hypotension or lactate >4
• Labs/cultures prior to Abx
• Early Abx therapy targeted to source vs empiric
• Initiate vasopressors, MAP>65; I st Line: Norepinephrine (Levophed)

Neurogenic Shock

• Seen in < 20% of SCI
• Loss of peripheral sympathetic innervation-> extreme vasodilation secondary to loss of sympathetic tone; Blood pools in distal circulation-> systemic HYPOtension
• T1-T4 nerve roots affected -> Cardiac innervation affected; Bradycardic
• Presentation- Warm, peripherial vasodilation, HYPOtension, Bradycardic
• MORE TO COME IN NEURO TRAUMA!

Anaphylaxis

• Multiple causes, known/unknown etiology; Lifetime risk 1-3%; Likely underdiagnosed
• Occurs from activation of mast cells and basophils
• Anaphylaxis includes histamines and Prostaglandin D2; bronchoconstrictor and is a peripheral vasodilator

ED Presentation-Anaphylaxis

• Often sudden, <60min prior to exposure
• Pruritis, Flushing, Urticaria; Fullness in throat; Anxiety; SOB; Resp Distress and Shock/HD Collapse

Diagnosis of Anaphylaxis

• Clinical Diagnosis where2 or more body systems are involved with +/- HYPOtension and +/- Airway compromise

Treatment for Anaphylaxis

• Epinephrine Im being 1st line
• Airway stabilization
• Support with IV Crystalloids 1-2L
• Corticosteroids being 2nd line
• Followed by Benadryl and then H2 Blocker
• Albuterol for Bronchospasm

Obstructive Shock

• Rare, about 1%; Etiology: Cardiac Tamponade PE and Tension PTX
• Decrease venous return or cardiac compliance to increased LVOT

Cardiogenic Shock

• Patient has a pump that isn't working correctly/efficiently with normal circulating volume.
• Etiology: MCC-MI/Cardiomyopathy/Arrythmia
• Risk Factors- Elderly and Female/ Acute or prior ischemic event for Impaired Ef/Extensive Infarct and Prox LAD
• LV doesn't deliver O2 blood to periphery in preload, afterload, contractility, RV Function

Presentation-Cardiogenic Shock

• Physical Exam: Hypotension, Sinus tach. Tachypnea/Pulm Edema(LV Failure) and Pale/Cyanotic/Cool or Mottled skin and Low Urine Output

Diagnostics and Treatment-Cardiogenic Shock

• Diagnostics- CBC/BMP/TROP/BNP and EKG with Arterial Line
• Continuous Monitor/Maintain Secure Airway
• Reperfusion if STEMI-ASA being the NO Alpha/Betablockers/Initially 250cc bolus IVF
• Give Vasopressors; Ist Line: Norepi (Levophed)
• 2nd line: Dopamine

Vasopressor Therapy

• Utilized when there has been inadequate response to volume resuscitation or contraindication to volumewas or
• Work best when the “tank is full” vs when depleted
• Utilized when there has been inadequate response to volume resuscitation or contraindication to volume
• Work on α-adrenergic, β-adrenergic, vasopressin, and dopaminergic receptors

Vasopressor information

• Dobutamine; 2.0-20.0 mcg/kg/min
• Side effects Inotrope causes tachydysrhythmias
• Dopamine; 0.5-20 mcg/kg/min
• Side effects include a cerebral, mesenteric,coronary, and vasodilator
• Epinephrine; 2-10 mcg/min
• Side effects include causes tachydysrhythmia
• Phenylephrine; 10-200 mcg/min
• Side effects include- Headache, restlessness, excitability.
• Vasopressin; 0.01-0.04 units/min
• Side effects include- Directs stimulates

Other Information

• Goal of MAP is a minimum of 65
• In hypovolemix patient, crystalloids are preferred
• Hearts low during neurogenic is also indicative of hemorrhage or hypovolemia