Post on 02-Jan-2016
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
VO2 =VO2 =1.39 x CO x Hb x (saO2-svO2)1.39 x CO x Hb x (saO2-svO2)
Compensation
AnemiaAnemia
VO2 =VO2 =1.39 x CO x Hb x (saO2-svO2)1.39 x CO x Hb x (saO2-svO2)
Compensation
Decreased CODecreased CO
VO2 =VO2 =1.39 x CO x Hb x (saO2-svO2)1.39 x CO x Hb x (saO2-svO2)
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
A Clinical Approach to Shock A Clinical Approach to Shock Diagnosis and ManagementDiagnosis and Management
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.
A Clinical Approach to Shock A Clinical Approach to Shock Diagnosis and ManagementDiagnosis and Management
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)
•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)
•)
•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
•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