Case 1 65 year old female nursing home resident with a hx CAD, PUD, recent hip fracture Transferred to ED with decreased mental status BP in ED 80/50
Case 1 65 year old female nursing home resident with a hx CAD, PUD, recent hip fracture Transferred to ED with decreased mental status BP in ED 80/50 This case demonstrates some common risk factors for causes of shock (ACS from CAD?, bleeding from a peptic ulcer?, PE from immobility?) and common manifestations of shock (altered mental status, hypotension)
Shock Definition Physiology of shock Types of shock Stages of shock Clinical presentation of shock A bit on vasopressors, inotropes
Definition Inadequate perfusion of tissues which is insufficient to meet cellular metabolic needs There is no set blood pressure, cardiac output, CVP, urine output, or etc that defines shock.
Mechanisms of Hypotension MAP mean arterial pressure SVR Cardiac Output Stroke Volume Heart Rate Preload Contractility Dr. Kreit circa 2010
Mechanisms of Hypotension Hypotension SVR Cardiac Output Stroke Volume Heart Rate Preload Contractility Dr. Kreit circa 2010
Compensatory Mechanisms that maintain MAP SVR + + LV Preload + Stroke Volume + Cardiac Output + Arterial Pressure + + Baroreceptors Sympathetic activity Renin Na and H 2 O Retention Arterial constriction Venous constriction Vasopressin Heart Rate Contractility Angiotensin II Aldosterone Adapted from Dr. Kreit circa 2010
Systemic O2 Delivery Regulation of O2 delivery (DO2) Normally, via cardiac output (CO) and tissue extraction There is no normal cardiac output Only adequate or inadequate cardiac output for given metabolic conditions Pinsky Chest 2007; 132: 2020
Shock Physiology Imbalance of O2 delivery and consumption Shock results in inadequate O2 delivery Cellular hypoxia anaerobic metabolism ATP generation ion pumps, membrane function Initially, damage is reversible eventually there is irreversible injury Cell death, organ failure, MOSF, death
Types of Shock 4 major categories Hinshaw and Cox Volume, pump, container Hypovolemic- volume Fluid losses (fistulas, burns), hemorrhage Cardiogenic- pump Myopathic, arrhythmic, mechanical, thyroid Distributive- container Sepsis/SIRS, anaphylaxis, neurogenic, adrenal Obstructive PE, Aortic stenosis, tamponade, tension pneumo
Types of Shock Shock Type CO Cardiac output PCWP pulmonary capillary wedge pressure SVR systemic vascular resistance Hypovolemic Cardiogenic Obstructive NL or Distributive or NL
Septic shock SIRS HR, WBC (, ), RR (PaCO2), Temp (, ) Sepsis SIRS with culture+ infection or identified infection Severe Sepsis Sepsis with organ hypoperfusion or dysfunction Septic Shock Severe sepsis with hypotension after volume Refractory Septic Shock Shock requiring high dose pressors after resuscitation
Stages of Shock Pre-shock ( compensated shock ) Homeostatic mechanisms are sufficient You may see: HR peripheral vasoconstriction BP remains nearly normal Shock Homeostatic mechanisms are overwhelmed Organ dysfunction first appears End organ dysfunction
Case 2 You are call by a nurse: Mrs. Jones is hypotensive Step #1?
Case 2 You are call by a nurse: Mrs. Jones is hypotensive Step #1 Go See Patient Assess and Treat simultaneously ABCs IV access, crystalloid volume early Pulse ox, UOP, central venous and arterial lines H&P clues Comorbidities, localizing sxs, etc. Bleeding, cardiac exam, JVP, infection, etc
Clinical Presentation of Shock Signs and symptoms Anxiousness, altered mental status Tachycardia, tachypnea Cool extremities (±in early distributive shock) Weak pulses urine output, acidemia (lactate) eventually you will see SBP (a late sign)
Shock Management Improve DO2 to adequate level There are no static values It requires a knowledge of CO, vascular tone Are they fluid (pre-load) responsive? Can assess with: Traditional parameters/methods: CVP/Fluid challenge) - not always reliable Pulse Pressure Variation, Passive leg raising If pre-load optimized is CO adequate? Assess SvO2 for tissue oxygenation
Early Goal Directed Therapy Functional Hemodynamic Monitoring - early aggressive resuscitation - end point of improved tissue oxygenation - multicenter trials ongoing Rivers et al. NEJM 2001; 345:1368
A bit on vasopressors and inotropes:
Adrenergic receptors ADRENOCEPTORS α1 α2 β1 β2 - Vasoconstriction - Increased peripheral resistance - Inhibition of norepinephrine release - Tachycardia - Increased myocardial contractility - Vasodilation - Decreased peripheral resistance - Increased blood pressure - Bronchodialation
Vasopressor parmacology Dopamine α1 β1 β2 DA MAP PCWP CO SVR HR <3 mcg/kg/min 0 + 0 ++++ 3-10 mcg/kg/min 0/+ ++++ ++ ++++ >10 mcg/kg/min +++ ++++ + 0 Norepinephrine 0.01-3 mcg/kg/min +++++ ++ 0 0 Phenylephrine 0.5-9 mcg/kg/min +++++ 0 0 0 NA Vasopressin <0.04 U/min V1 (vascular smooth muscle) V2 (renal collecting duct) Circulation 2008;118;1047-1056
Inotrope pharmacology Dopamine α1 β1 β2 MAP PAP CO SVR HR MOC 3-10 mcg/kg/min 0/+ ++++ ++ >10 mcg/kg/min +++ ++++ + Dobutamine 2-20 mcg/kg/min + ++++ +++ Epinephrine 0.01-0.1 mcg/kg/min +++++ ++++ +++ Milrinone 0.125-0.75 mcg/kg/min MOC; myocardial oxygen consumption PDE-3 inhibitor Circulation 2008;118:1047-56 Crit Care Med 2008;36:S106-11
What pressor to chose? De Backer D. NEJM 2010
More adverse events with dopamine De Backer D. NEJM 2010
Vasopressors and Inotropes Clinical considerations with pressors Ensure fluid replete Treating people with pressors who are hypovolemic can cause digital and organ ischemia ph 7.0 to 7.1 Pressor-receptor interaction is poor with acidosis. May need to give buffer to get ph up. Central line preferable
Take Home Messages Shock = inadequate tissue oxygen delivery Cardiogenic, hypovolemic, distributive, obstructive Treat patient at the bedside Treat underlying cause, make sure volume replete, and use pressors judiciously