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

ShockJose Emmanuel M Palo, MD

Internal Medicine/Critical Care Medicine

Adapted from Weibel ER: The Pathway for Oxygen: Structure and Function in the Mammalian Respiratory System. Cambridge, MA, Harvard University Press, 1984

In critical illness, heart and lung must be considered

as one organ system.

Shock

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

Definitions

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

Cellular Death

Hypoperfusion

Cellular injury

Inflammatory mediators

Microvascular/endothelialdysfunction

Cellular Death

Multiple organ failure

Death

Cardiovascular Performance•Cardiac Function•Venous Return

•Vascular Performance

Oxygen Transport•Cardiopulmonary level•Cellular level

Microvascular FunctionCellular Energy Metabolism

Cardiovascular Performance•Cardiac Function•Venous Return

•Vascular Performance

Oxygen Transport•Cardiopulmonary level•Cellular level

Microvascular FunctionCellular Energy Metabolism

Determinants of Effective Determinants of Effective Tissue PerfusionTissue Perfusion

Cardiovascular Function

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

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

Cardiovascular Function

Perfusion pressure ~ MAP Perfusion pressure ~ MAP

MAP = CO x SVR MAP = CO x SVR

•SNS and PNS balance

•catecholamine levels/responsiveness

•ACTH and cortisol

•R-A-A•Vasopressin•prostacycline

•Nitric Oxide•Adenosine•Drugs

SV x HR SV x HR

PreloadAfterloadContractility

Oxygen Transport

DO2 =DO2 =1.39 x CO x Hb x saO21.39 x CO x Hb x saO2

amount of oxygen leavingthe heart per unit time

amount of oxygen leavingthe heart per unit time

Oxygen Transport

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

amount of oxygen being consumed per

unit time

amount of oxygen being consumed per

unit time

Mizock BA. Crit Care Med. 1992;20:80-93.

VO

2

DO2

Critical DeliveryThreshold

Lactic

Acidosi

s

Physiologic Oxygen Physiologic Oxygen Supply DependencySupply Dependency

Compensation

Arterial DesaturationArterial Desaturation


Compensation

AnemiaAnemia


Compensation

Decreased CODecreased CO


Oxygen UnloadingAssociationSegment

Oxygen Unloading

Dissociation Segment

Oxygen Unloading

Shock TypesHypovolemicHypovolemic

DistributiveDistributive

CardiogenicCardiogenic

ObstructiveObstructive

afterloadafterload

preloadpreload

• decreased effective blood volume

• decreased end-diastolic filling pressures

• trauma, diarrheal illness

• relative hypovolemic state in septic shock

• volume is key

• decreased effective blood volume

• decreased end-diastolic filling pressures

• trauma, diarrheal illness

• relative hypovolemic state in septic shock

• volume is key

Hypovolemic Shock

Stages of Hypovolemic Shock

Mild (<20% EBV)

Moderate(20-40%)

Severe(>40%)

-cool extcool ext-inc inc

capillary capillary refill timerefill time

-diaphoresisdiaphoresis-collapsed collapsed

veinsveins-anxietyanxiety

-(plus)(plus)-tachycarditachycardi

aa-tachypneatachypnea-oliguriaoliguria-postural postural

changeschanges

-(plus)(plus)-marked marked

tachycarditachycardiaa

-hypotensiohypotensionn

-comacoma

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 ShockDistributive 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

• 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

CO SVR PWP CO SVR PWP EDVEDV

HypovolemicHypovolemic

DistributiveDistributive

CardiogenicCardiogenic

ObstructiveObstructive

afterloadafterload

preloadpreload

Hemodynamics of Shock Types

Management Principles

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

• 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

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

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

Clinical SignsClinical Signs

Proximal (CVP)

CO Thermistor

Balloon port

Distal (PCWP)

Sup Vena Cava

R Atrium

R Ventricle

Pulmo Artery

The Swan-Ganz Catheter

Diagnosis and EvaluationDiagnosis and Evaluation

Arterial pressure catheter

CVP monitoring

Pulmonary artery catheter (+/- RVEF, oximetry)

MVO2

DO2 and VO222

Invasive Monitoring

• CVP

• PCWP

• Straight leg raising

• Intrathoracic fluid index

• Pulse pressure variability

• Pre-ejection period variability

• Pulse contour analysis

Static and dynamic volume

assessment

SV

RAP

Advanced Concepts: PPVar

PEEP

Advanced Concepts: Straight

Leg Raising

Michard, 2008

Advanced Concepts:

Microvascular Function

Advanced

Concepts:

Cellular Energeti

cs

Initial Therapeutic StepsInitial Therapeutic Steps

A Clinical Approach to Shock A Clinical Approach to Shock Diagnosis and ManagementDiagnosis and Management

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

When Diagnosis Remains Undefined orWhen Diagnosis Remains Undefined orInitial Management FailsInitial Management Fails


Pulmonary Artery Catheterization• Cardiac output• Oxygen delivery• Filling pressures

• EchocardiographyPericardial fluid

Cardiac function

Valve or shunt abnormalities

Immediate Goals in ShockImmediate 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.


MAP = CO x SVR MAP = CO x SVR

•SNS and PNS balance

•catecholamine levels/responsiveness

•ACTH and cortisol

•R-A-A•Vasopressin•prostacycline

•Nitric Oxide•Adenosine•Drugs

SV x HR SV x HR

PreloadAfterloadContractility

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)

•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)


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)


•)

•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)


•)

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

•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

Documents

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