Shock

Gordon R. Bernard, M.D.

Division of Allergy, Pulmonary, and Critical Care Medicine

Vanderbilt University

Overall Objectives

• Understand the pathophysiology of shock

• Know the types of shock and how they differ

• Understand the therapeutic approaches to shock

Definition

• (Gross, 1882) “A manifestation of the rude unhinging of the machinery of life.”

• (Guyton, 1966) “An abnormal state of the circulation in which cardiac output is reduced enough that the tissues of the body are damaged from lack of blood flow.”

Types of Shock

• Hypovolemic• Loss of blood or plasma

• Cardiogenic• Myocardial infarction• Cardiac trauma

• Distributive• e.g., septic shock

• Obstructive• Pulmonary embolism

Arterial Resistance

• Controlled by:

• a) Arteriolar tone

• b) Precapillary sphincter» Control capillary hydrostatic pressure

• c) Postcapillary sphincter

Blood Pressure = SVR X C.O.

Factors Causing Reduced Cardiac Output

• A. Reduced venous return• Hypovolemic shock• Endotoxic shock• Anaphylactic shock• Obstruction to venous return

• B. Reduced pumping ability• Cardiogenic shock

Hemorrhagic shock

• Due to volume loss:

• Blood

• Plasma

• Fluid/electrolyte

• 10% of blood volume can be lost with minimal hemodynamic effects.

• 20% loss followed by initiation of BP reduction.

• Sympathetic activity increases.

• Vasoconstriction occurs (cerebral and coronary circulation protected).

CORRELATION OF MAGNITUDE OF VOLUME DEFICIT AND CLINICAL PRESENTATION

Approximatedeficit

Decrease in BloodVolume Degree Signs

ml %

0 – 500 0 – 10 None None

500 – 1200 10 - 25 Mild(Compromised)

Slight tachycardiaPostural blood pressure changesMild peripheral vasoconstriction

1200 – 1600 25 – 15 Moderate Thready pulse, 100-120 beats/minBlood pressure 90-100 mmHg systolicMarked vasocontrictionDiaphoresisAnxiety, restlessnessDecreased urinary output

1600-2500 16 – 60 Severe Thready pulse > 120 beats/minBlood pressure <60 mmHg systolicMarked vasocontrictionObtundationNo urinary output

Shock

Clinical Features• Sensorium

Anxiety to obtundation• Weakness or prostration• Pallor• Sweating• Tachycardia• Thready pulse• Hypotension• Tachypnea

Hypovolemic Shock

First signs are postural drop in pressure(10 mm) or increase in heart rate

Laboratory Changes

• Hematocrit - No change until dilution occurs• Blood Gas Studies:

Indicate degree of acid-base disturbance and lactic acidosis (anaerobic metabolism)

• Electrolytes and Renal Function Tests:Important baseline information

• Blood - Type and crossmatch• Urine Output - Monitor continuously

Initial:

Time Required for Blood Typing Procedures

Blood Bank Activity Time Required

Release O-negative blood (no 1 minutetesting)

Issue type specific blood (group 15 minutesand type recipient’s blood)

Carry out saline and albumin 30 minutes cross-matches

Finish complete crossmatch (regroup, 45 minutes retype, carry out saline, Coombs, and albumin crossmatches, screen recipient’s blood)

Compensatory Mechanisms

• To maintain perfusion pressure

• Sympathetic discharge• Catecholamines increase• Heart rate and contractility increased• Afferent arterioles in vascular beds constrict• Peripheral resistance• Venous capacitance vessels constricted• Increase in venous return

• Aim is to effectively perfuse coronary and carotid arteries.

• Catecholamines produce greater contraction of precapillary sphincter than postcapillary sphincter.

• Therefore, cappilary hydrostatic pressure is reduced.

• In early stages of shock this is important in pulling fluid into the intravascular space and increasing blood volume (Hct reduced).

Overall Effect:

• Constriction of arterioles and venules

• Increase in central blood volume

• Increase in cardiac output (circulates the available blood more rapidly)

• Draws interstitial fluid into intravascular space

Sympathetic Discharge

• Negative effects if sustained• Sludging of blood• Disseminated intravascular coagulation• Profound acidosis• Tissue hypoxia-cell death

• Acidosis, metabolites and hypoxia relax precapillary sphincter more than post capillary sphincter.

Late Shock

• Postcapillary sphincter resistance greater than precapillary

• Therefore, hydrostatic pressure increased

• Interstitial edema produced

Capillary Injury

• Important part of the shock process

• Maybe due to:• Increased platelet adhesiveness• Release of vasoactive materials

• Leads to further loss of plasma volume.

• Also, if in pulmonary bed may contribute to shock lung.

Shock Lung (ARDS)

• Pulmonary edema

• Alveolar hemorrhage

• Pulmonary vascular congestion

• Loss of surfactant

• Increased lymph flow

Hypovolemic Shock

• Control bleeding

• Establish and maintain airway + O2

• Assist ventilation (if necessary)

• Replace volume

• Acid-base correction

Therapy

Fluids

• Any fluid can improve perfusion, at least temporarily

• Only RBC’s carry oxygen

Two generalizations:

Fluids

• Crystalloids (electrolyte solutions)

• Colloids (large molecular weight)

• Red blood cells

Object is to refill the vascular compartment.

Choice:

Selection of Replacement Fluid

• Electrolyte solutions (crystalloids)

• Rapidly escape from intravascular space into the interstitium. Therefore, short-lived volume expansion.

Colloids (large molecules)

• Increase plasma onocotic pressure• Draw fluid into plasma space• Remain in circulation longer than crystalloids

• Raise interstitial onocotic pressure• May cause pulmonary edema

e.g. Dextran, Albumin, Hetastarch, P.P.F.

But

When they escape from circulation, e.g., through damaged capillaries:

Colloid vs Crystalloid Controversy

Choi PTL, et al. Critical Care Med 1999;27:200-10. Schierhout G, et al. BMJ 1998;316:961-4.

Lowe 1977 0.68Lucas 1978 0.07Butros 1979 2.22Virgillo 1979 1.07Moss 1981 2.43Goodwin 1983 0.27Modic 1983 1.08Rackow 1983 1.23Shires 1983 1.0Metildi 1984 0.82Sade 1985 1.83Karanko 1987 2.37Davidson 1991 1.0London 1992 0.22Pocka 1994 0.90

Overall 0.97

1 100.10.01 100

FavorsCrystalloid

FavorsColloid

Cardiogenic Shock

• Myocardial infarction

• Rhythm disturbance

Due to impaired cardiac pumping due to:

CVP Increased

Pulmonary Capillary Wedge increased

Cardiogenic Shock

• Systolic BP < 80 mm

• Cardiac Index < 2.1 liters/min/m2

• Urinary output < 20 ml/hr

• Reduced cerebral perfusion (Confusion Obtundation)

Cardiogenic Shock

• Incidence 15% of M.I.

• Mortality 70-90%

• Usually > 40% of left ventricle infarcted

Potentially Repairable Lesions

• Ruptured chordae tendinae

• Intraventricular septal defects

Cardiogenic Shock

PCWP < 18 mmHg PCWP > 18 mmHg

Expand Blood Volume Inotropic drug

Diuretic

Vasodilator

Mechanical Asst.

Dobutamine

• ß1 Stimulant

• Mainly inotropic effects

• Probably drug of choice in cardiogenic shock

Septic Shock

• Endotoxin or other mediator release• Activation of vasoactive kinins• Activation of intrinsic coagulation system

• Increasing capillary permeability• Decreased peripheral vascular resistance• Disseminated intravascular coagulation

• Mortality 40-50%

Causing

Hemodynamics:

• Peripheral resistance fails

• C.O. and HR rise (but not enough)

• BP falls

Therapy for Septic Shock

• General supportive measures

• Specific antibacterial therapy

• Corticosteroids?

• Activated protein C

Recent Randomized Studies Suggest:

High-dose steroids produce short-term improvement but no long-term effects on survival.

Treatment of Shock

Remember: problem is flow, not simply blood pressure

Aim:

To increase flow through the microcirculation

Vasoconstrictors

• Phenylephrine• Vasoconstricts• Elevates blood pressure but increases

myocardial work• Decrease cardiac output• Decrease tissue perfusion• Rarely used except in anesthesia for

management of drug induced vasodilation

1-Agonists

Dopamine

Effects Effects Dopaminergic

Low doses(1-2g/kg/min)

- - +++

Intermediate doses(2-10g/kg/min)

- ++ +++

High doses +++ +++ +++

Vasopressin in Septic Shock

• Redistributes blood flow– Away from muscle, skin, gut – To brain and heart

• High dose: coronary vasoconstriction

• Antidiuretic effect

• Inexpensive

• No proven effect on ultimate outcome

BP and Vasopressin Levels After AVP for Septic Shock

0

40

80

120

160

Baseline AVP 0.04U/min

AVP Off AVP 0.01U/min

Landry DW, et al. Circulation 1997;95:1122-5. Landry DW, et al. Crit Care Med 1997;25:1279-82.

SBP

N=10

SB

P (

mm

Hg

) o

r A

VP

leve

l (pg

/mL

)

TNFTNFIL-1, 6, 8IL-1, 6, 8

Nitric oxideNitric oxideOxidantsOxidants

BradykininBradykininThromboxaneThromboxane

ProstaglandinsProstaglandinsLeukotrienesLeukotrienes

EnzymesEnzymesComplementComplement

TNFsr IL-TNFsr IL-1ra1ra

PGE2 PGE2 IL-6 IL-IL-6 IL-

1010

Tissue FactorTissue Factor

TNFTNFIL-1IL-1IL-6IL-6IL-8IL-8

TNFTNFIL-1IL-1IL-6IL-6IL-8IL-8

VIIIaVIIIa

VaVa

TAFITAFI

PAI-1PAI-1

Inhibition of Inhibition of FibrinolysisFibrinolysis

ThrombinThrombin

APCAPC

APCAPC

APCAPC

APCAPC

APCAPC

APCAPC

APCAPC

Primary Analysis: Primary Analysis: 28-Day All-Cause Mortality28-Day All-Cause Mortality

24.7

30.8

0

5

10

15

20

25

30

35

Placebo Drotrecogin Alfa (Activated)

Mo

rtal

ity

2-sided P value 0.005Relative risk reduction 19.4%Increase in odds of survival 38.1%

N=840 N=850

Bernard GR, et al. N Engl J Med 2001;344:699-709.