Internal Medicine/Critical Care Medicine Shock Jose Emmanuel M Palo, MD Internal Medicine/Critical Care Medicine

In critical illness, heart and lung must be considered as one organ system. Adapted from Weibel ER: The Pathway for Oxygen: Structure and Function in the Mammalian Respiratory System. Cambridge, MA, Harvard University Press, 1984

Mechanical events always preceded by electrical events. Cardiac Cycle Mechanical events always preceded by electrical events.

Shock clinical syndrome of organ dysfunction due to cellular hypoxia from hypoperfusion

Definitions unrelated to “emotional shock” or the acute stress reaction

Inflammatory mediators Hypoperfusion Cellular injury Microvascular/ endothelial dysfunction Cellular Death Inflammatory mediators

Multiple organ failure Cellular Death Multiple organ failure Death

Determinants of Effective Tissue Perfusion Cardiovascular Performance Cardiac Function Venous Return Vascular Performance Oxygen Transport Cardiopulmonary level Cellular level Microvascular Function Cellular Energy Metabolism Determinants of Effective Tissue Perfusion in Shock   1) Cardiovascular Performance (total systemic perfusion/cardiac output) Cardiac Function Preload Afterload Contractility Heart rate Venous Return Right atrial pressure (dependent on cardiac function) Mean circulatory pressure Stressed vascular volume Mean vascular compliance Venous vascular resistance Distribution of blood flow 2) Distribution of Cardiac Output Intrinsic regulatory systems (local tissue factors) Extrinsic regulatory systems (sympathetic/adrenal activity) Anatomic vascular disease Exogenous vasoactive agents (inotropes, vasopressors, vasodilators) 3) Microvascular Function Pre- and postcapillary sphincter function Capillary endothelial integrity Microvascular obstruction (fibrin, platelets, WBC, RBC) 4) Local Oxygen Unloading and Diffusion Oxyhemoglobin Affinity RBC 2,3 DPG Blood pH Temperature 5) Cellular Energy Generation/Utilization Capability Citric acid (Kreb's) cycle Oxidative phosphorylation pathway Other energy metabolism pathways (e.g. ATP utilization)

Cardiovascular Function In humans, most critical organ perfusion is auto-regulated at MAP between 60-100 mmHg

Cardiovascular Function Perfusion pressure ~ MAP

SV x HR MAP = CO x SVR SNS and PNS balance catecholamine levels/responsiveness ACTH and cortisol R-A-A Vasopressin prostacycline Nitric Oxide Adenosine Drugs Preload Afterload Contractility SV x HR MAP = CO x SVR

amount of oxygen leaving Oxygen Transport DO2 = 1.39 x CO x Hb x saO2 amount of oxygen leaving the heart per unit time

amount of oxygen being consumed per unit time Oxygen Transport VO2 = 1.39 x CO x Hb x (saO2-svO2) amount of oxygen being consumed per unit time

Physiologic Oxygen Supply Dependency Critical Delivery Threshold Lactic Acidosis VO2 DO2 Mizock BA. Crit Care Med. 1992;20:80-93.

Pathologic Oxygen Supply Dependency Physiologic VO2 DO2 Mizock BA. Crit Care Med. 1992;20:80-93.

Arterial Desaturation Compensation VO2 = 1.39 x CO x Hb x (saO2-svO2) Arterial Desaturation

Compensation VO2 = 1.39 x CO x Hb x (saO2-svO2) Anemia

Compensation VO2 = 1.39 x CO x Hb x (saO2-svO2) Decreased CO

Oxygen Unloading Association Segment

Oxygen Unloading Dissociation Segment

Oxygen Unloading

Shock Types Hypovolemic Distributive Cardiogenic Obstructive afterload preload

Hypovolemic Shock decreased effective blood volume decreased end- diastolic filling pressures trauma, diarrheal illness relative hypovolemic state in septic shock volume is key

Stages of Hypovolemic Shock Mild (<20% EBV) Moderate (20-40%) Severe (>40%) cool ext inc capillary refill time diaphoresis collapsed veins anxiety (plus) tachycardia tachypnea oliguria postural changes marked tachycardia hypotension coma

Distributive Shock decreased SVR due to loss of vasomotor control frequently, need volume to unmask a distributive shock state sepsis, anaphylaxis, anaphylactoid reactions, neurogenic shock, hypoadrenalism

Distributive Shock Anaphylactoid shock Anaphylactic shock insect envenomations antibiotics (beta-lactams, vancomycin, sulfonamides) heterologous serum (anti-toxin, anti-sera) blood transfusion immunoglobulins (esp IgA deficient) Egg-based vaccines latex Anaphylactoid shock ionic contrast media protamine opiates polysaccharide volume expanders (dextran, hydroxyethyl starch) muscle relaxants anesthetics

Cardiogenic Shock loss of cardiac pump function (intrinsic) due to myocardial damage, loss of contractility Special: valvular dysfunction characterized by elevations of both diastolic volumes and pressures

Extra-Cardiac Obstructive due to obstruction of flow in the cardiovascular circuit preload obstruction: cardiac tamponade, constrictive pericarditis, other intrathoracic processes afterload obstruction: pulmonary embolism

Hemodynamics of Shock Types CO SVR PWP EDV Hypovolemic Distributive Cardiogenic Obstructive afterload preload

Management Principles frequently reversible in early stages early recognition and emergent intervention are key clinical signs and symptoms may be due to the primary shock state, compensatory mechanisms or end- organ effects

Clinical Signs Primary diagnosis - tachycardia, tachypnea, oliguria, encephalopathy (confusion), peripheral hypoperfusion (mottled, poor capillary refill vs. hyperemic and warm), hypotension Differential DX: JVP - hypovolemic vs. cardiogenic Left S3, S4, new murmurs - cardiogenic Right heart failure - PE, tamponade Pulsus paradoxus, Kussmaul’s sign - tamponade Fever, rigors, infection focus - septic

The Swan-Ganz Catheter Proximal (CVP) CO Thermistor Balloon port Distal (PCWP) Pulmo Artery Sup Vena Cava R Atrium R Ventricle

Diagnosis and Evaluation Invasive Monitoring Arterial pressure catheter CVP monitoring Pulmonary artery catheter (+/- RVEF, oximetry) MVO2 DO2 and VO2 2 2

Static and dynamic volume assessment CVP PCWP Straight leg raising Intrathoracic fluid index Pulse pressure variability Pre-ejection period variability Pulse contour analysis

Advanced Concepts: PPVar resp fluctuations during positive pressure ventilation cause decreased R-sided preload and increased R-sided afterload during inspiration, leading to decreased CO on the R, followed by decreased CO on the L a few beats later. This shows up as a decrease in pulse pressure. Wide variation in pulse pressure due to positive pressure ventilation denotes preload dependence. PEEP moves it to the L. Spec 100%, sensitivity 68%. SV PEEP RAP

Advanced Concepts: Straight Leg Raising concept is that of a reversible fluid load. Michard, 2008

Advanced Concepts: Microvascular Function sublingual sidestream darkfield imaging

Advanced Concepts: Cellular Energetics

A Clinical Approach to Shock Diagnosis and Management Initial Therapeutic Steps Admit to ICU Venous access (1 or 2 wide-bore catheters) Central venous catheter Arterial catheter ECG monitoring Pulse oximetry Hemodynamic support (MAP < 60 mmHg) Fluid challenge Vasopressors for severe shock unresponsive to fluids

A Clinical Approach to Shock Diagnosis and Management When Diagnosis Remains Undefined or Initial Management Fails Pulmonary Artery Catheterization Cardiac output Oxygen delivery Filling pressures Echocardiography Pericardial fluid Cardiac function Valve or shunt abnormalities

A Clinical Approach to Shock Diagnosis and Management Immediate Goals in Shock Hemodynamic support MAP > 60mmHg PAOP = 12 - 18 mmHg Cardiac Index > 2.2 L/min/m2 Maintain oxygen delivery Hemoglobin > 9 g/dL Arterial saturation > 92% Supplemental oxygen/mechanical ventilation Reversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L) Maintain urine output Reverse encephalopathy Improving renal, liver fxn tests MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.

SV x HR MAP = CO x SVR SNS and PNS balance catecholamine levels/responsiveness ACTH and cortisol R-A-A Vasopressin prostacycline Nitric Oxide Adenosine Drugs Preload Afterload Contractility SV x HR MAP = CO x SVR

Case #1 90/M inpatient for cholecystitis, treated now for 11 days with antibiotics and fluid Pacemaker 2 yrs ago for symptomatic bradycardia PAC placed for peri-operative management BP 189/86 PAWP 23 (6-12) HR 80 CO 3 L/min (4-8) SVR 6600 (700-1300) lactate 5 mmol/L (<2.2)

Case #2 50/M brought to ER unresponsive, arrested and had ACLS/CPR for 12 minutes Comatose now and on norepinephrine Urine output 0 BP 55/40 HR 45 PACW 8 (6-12) RA 0 (2-6) CO 3.6 (4-8) SVR 1000 (700-1300) lactate 12 mmol/L (<2.2) )

Case #3 59/M 2 days after STEMI, not on mechanical ventilator BP 55/40 HR 110 RR 26 PA 35/18 CVP 18 PPV 8%

End(points) shock is common and life-threatening differentiating diagnoses frequently requires invasive procedures management is time dependent use therapy with the highest physiologic benefit at the lowest physiologic cost