SHOCK syndromes:

an Overview

Dr. R.Padhi, MD, DipCard, FCCP

Asst Prof Internal Medicine &
Critical Care,
SOA University, Bhubaneswar.
 DEFINITION

Shock is a multifactorial
syndrome leading to systemic and
localized tissue hypoperfusion
resulting in cellular hypoxia and
multiorgan failure.
 Description
Perfusion may be decreased with obvious signs
such as hypotention
Perfusion may be decreased because of
maldistribution (septic shock) in which global
perfusion is normal or even elevated.
Prognosis of shock depend on the degree and
duration of hypoperfusion, the number of organs
affected, and the presence of prior organ
dysfunction
 Hinshaw and Cox etiologic
classification of shock
The four categories of shock are
(a) hypovolemic,
(b) obstructive,
(c) cardiogenic,
and (d) distributive.
 PATHOPHYSIOLOGY
The result of shock is decreased tissue
perfusion and cellular hypoxia & ischemia.
Ischemic cells are primed by alterations in
calcium and cAMP and formation of superoxide
radicals
Endothelial cells in hypoxic states have
enhanced vascular permeability and
dysregulated membrane transport functions and
altered NO systhesis
Reperfusion leads to enhanced oxygen radicals
with detremental effects
PATHOPHYSIOLOGY cont..

Hypoxia as well as Reperfusion leads to

1.activation of neutrophils
2.release of proinflammatory cytokines
3.cellular injury
4.organ dysfunction
5. and frequently death.
Arterial and venous oxygen saturations in
various vascular regions.
 Hemodynamic Monitoring

MAP = [SBP + 2(DBP)]/3

Mean Pulmonary Arterial Pressure (MPAP) =
[PAS + 2(PAD)]/3
Preload, by the Frank-Starling Law, is
defined in terms of myocardial fibril length at
end-diastole - Pulmonary Artery Occlusion
and Central Venous Pressure are direct
measurements usuing Swan-Ganz catheters
 CI is the total blood flow from the heart (in
liters per minute) divided by BSA. SVI is
the volume of blood ejected from the heart
per beat, divided by BSA:
• CI = cardiac output/BSA
• SVI = CI/heart rate
Systemic Vascular Resistance Index

Resistance = voltage difference/current

Vascular resistance = pressure
change/total blood flow
SVRI = change in pressure across the
systemic circuit (mm Hg)/total blood flow
(L/min/m2)
SVRI (in dynes / sec / cm-5) = (MAP -
CVP) (79.9) / CI
 The constant, 79.9, is used to convert mm Hg/ L/
minute f dynes / sec /cm-5.

Increased SVRI is commonly seen

1. Obstructive
2. Hypovolemic
3. Late septic
4. Cardiogenic shock
5. nonshock – pheochromocytoma, infusions
of noradrenaline, dopamine, vasopressin
and other vasopressors
 Decreased SVRI
1. Distributive shock states (neurogenic or
early septic shock).
2. Vasodilators, such as sodium
nitroprusside, nitroglycerin
Hemodynamic parameters
Normal values
Hemodynamic parameters in
shock states
 Arterial Lactate

The by-products of glycolysis are

hydrogen ion, pyruvate, and lactate
hydrogen ion and lactate accumulate,
resulting in acidosis, injury, and cellular
death
Elevated lactate concentrations predict an
increased mortality rate
 Base Deficit
Base deficit is the amount of base, in
millimoles per liter, required to titrate whole
blood to normal pH at normal physiologic
values of temperature, arterial co2 tension,
and arterialoxygen tension. The normal
range for base deficit is +3 to -3 mmol per L.
The presence of an elevated base deficit
correlates with the presence and severity of
shock
 Oxygen Transport

Measured variables units Normal range

Arterial oxygen tension mmHg 70 to 100
(Pao2)
Arterial carbon dioxide mmHg 35 to 50
tension (PaCO2)
Arterial oxygen Fraction 0.93 to 0.98
saturation (Sao2 or Spo2)
Mixed venous oxygen Fraction 0.70 to 0.78
saturation (S[v with bar
above]o2)
Mixed venous oxygen mmHg 36 to 42
tension (Pvo2)
Hemoglobin (Hgb) g/dL 13 to 17
Calculated variables
Oxygen delivery index mL/min/m2 500 to650
([D with dot above]o2)
Oxygen consumption mL/min/m2 110 to 150
index ([V with dot
above]o2)
Arterial oxygen content mL o2/dL blood 16 to 22
(Cao2)
Mixed venous oxygen mL o2/dL blood 12 to 17
content (Cvo2)
Arterial-venous oxygen mL o2/dL blood 3.5 to 5.5
content difference (Ca-
vo2)
Oxygen utilization Fraction 0.22 to 0.30
coefficient (OUC)
Respiratory quotient Fraction 0.7 to 1
(RQ)
Intrapulmonary shunt Fraction 0.03 to 0.08
(Qs/Qt)
 OXYGEN TRANSPORT
ASSESSMENT
Shock is a disease of hypoperfusion & hence
oxygen delivery to tissues is inadequate to
meet cellular demands
Oxygen delivery index (DO2): is the arterial
oxygen content x CI
Arterial oxygen content is % saturated Hb x
the binding coefficient (1.34) + oxygen
dissolved in plasma (insignificant)
CaO2=(1.34xHgb xSaO2) + (PaO2x0.003)
Relationship between oxygen consumption
(˙VO2 ) and oxygen transport (DO2 ).
 Mixed venous oxygen content can be
calculated as:
Cvo2 = mixed venous oxygen content as
blood returns to the heart
= oxygen bound to venous hemoglobin
(1.34 x Hgb x Svo2
O2 consumption index(vO2)
=(1.34xHgbx SaO2-SvO2) x CI x 10
OER =VO2/DO2 is approx 25%
DO2 can be increased by increasing Hgb or by increasing
CI.
One of the most important determinants of tissue [D 02] is
Hgb concentration. The optimal Hgb concentration to
maximize tissue o2 has traditionally been thought to be 10
to 13 g per dL. Several recent studies, however, have
suggested that transfusion to such levels in critically ill
patients provides no survival benefit in the absence of
recent acute myocardial infarction, unstable angina, or
acute blood loss. These studies have advocated
maintenance of a Hgb concentration of 7 to 9 g per dL in
the critically ill patient.
 Diagnosis
Vital signs : HR,BP,RR,SPO2,TEMP and UO
are traditional measures to determine shock
however 50 to 85% of patients with shock
have normal vital signs
HR: Tachycardia is an early sign; brady in
late shock, young and those on
betaBlockers
BP: hypotension and narrowed pulse
pressure : MAP is a better guide
Temperature: Hypo, normo or hyperthermia:
but hypothermia in severe septic and
hypovolumic shock
UO: hypovlemia guide and end organ
perfusion (kidneys): delayed sign as already 1
to 2 hours lost before recognizing
Pulse oximetry: early indicator of hypoxia but
not of value in hypothermia; low perfusion
Overview of Management
Overview of Management cont.
PA catheter: CI; PCWP
 Resucitation Endpoints
1.Lactic Acid Production: Cells in hypoxia
will switch to anaerobic metabolism the by
product of which is Lactic acid (normal <
4mmol/L)
The rate of clearance is a better marker
than absolute levels
2. Base deficit: easily obtained by ABG; the
correction of BD - a guide to resuscitation.
Resucitation Endpoints cont..
Intramucosal pH monitoring: the
mesenteric organs have the earliest &
greatest hypoperfusion in shock.
Gastric Tonometry: measures
intramuscular pH (stomach) – reduction in
pH is correlates with mortality.
 Vasoactive Agent Receptor Activity

Agent a1 a2 b1 b2 Dopa

Dobutamine + + ++++ ++ 0

Dopamine ++/+++ ? ++++ ++ ++++

Epinephrine ++++ ++++ ++++ +++ 0

Norepinephrine +++ +++ +/++ 0 0

Phenylephrine ++/+++ + ? 0 0
 CARDIOGENIC SHOCK
CS is a state of end-organ hypoperfusion due to
cardiac failure.
The definition of CS includes hemodynamic parameters:
1.Persistent hypotension (SBP <90 mm Hg)
2.Severe reduction in cardiac index (<1.8 L /min/m2)
3.Adequate or elevated filling pressure (LV/RV EDP)
PCWP > 18 mm Hg (PAOP)or
CVP >10 to15 mm Hg (CVP)
Pathophysiology
Pathophysiology cont..
MANAGEMENT
 Changes in Cardiac Performance During Acute &
Recovery Phases of Septic Shock
Parillo, JE. Pathogenetic Mechanisms of Septic Shock NEJM 328(20):1471-1477.

Acute Phase (Hypotension and Reduced SVR)

MAP 40 mm Hg
CVP 2 mm Hg
Cardiac Output 11.25 L/min
Heart Rate 150 beats/min
SVR 270 dyn*sec*cm-5
EF 225ml-50ml =33%
LVEDV 225 ml LVESV 150 ml 225ml

Recovery Phase (Normotension)

MAP 75 mm Hg
CVP 5 mm Hg
Cardiac Output 5.25 L/min
HR 70 beats/min
Stroke Volume 75 ml
SVR 1067 dyn*sec*cm-5
EF 125 ml- 50 ml =60%
LVEDV 125 ml LVESV 50 ml
125 ml
 Hemodynamic Patterns with Prognostic
Value


A lower heart rate at the onset of disease is predictive of
survival.

Normalization within 24 hours of either tachycardia or elevated
cardiac index is associated with survival. Persistence of
hyperdynamic state increases likelihood of death.
Parker et al. Serial Cardiovascular Variables in Survivors and Nonsurvivors; HR as an Early Predictor
of Prognosis
Crit Care Med 1987(15): 927-9.


A low ejection fraction and ventricular dilatation are also
associated with survival. This perhabs reflects Frank-Starling
compensation of sepsis induced myocardial depression.
Parrilo, JE. Pathogenetic Mechanisms of Septic Shock, NEJM 1993; 328(20): 1471-77.