“In name, there are many doctors,

but in reality only a few…”

SHOCK
 HISTORICAL ASPECT
Concept of shock has evolved for centuries
Appearance of a patient in shock or pre-terminal
stage have since been referred to as Hippocratic
facies
1743 - First medical use of the term “shock”
by Henri Francois Le Dran’s “
1785 - “Shock”- used by English surgeon, George

James Guthrie to mean “physiologic

instability”
 DEFINITION
Inadequate delivery of oxygen and nutrients
to maintain normal tissue and cellular
function
“inadequate tissue perfusion”

Results from dysfunction of:

Heart
Blood volume
Arteriolar resistance (afterload)
Venous capacitance (preload)
 DEFINITION
Results into LOW FLOW STATE
Decreased circulating volume
Loss of autonomic vascular control
Impaired cardiac output

Events: Hypovolemia ^ peripheral

vascular resistance^ CR to maintain CO
^CO ^ O2 consumption blood shunted
 PATHOPHYSIOLOGY
Initial insult activates neuroendocrine
and inflammatory mediator response
Persistent hypoperfusion will result in
hemodynamic derrangement, end-organ
dysfunction, cell death, and death of
patient.
 PATHOPHYSIOLOGY
“shock is not a single pathologic entity”

Basic common anomalies:

Inadequate O2 transport
inadequate O2 utilization

Common in all forms of shock:

Decreased CO
Decreased venous return
Increased peripheral resistance
(Decreased blood pressure)
Mechanisms to Correct Shock
Increase contractility and peripheral
vascular tone
Hormonal response to preserve salt and
intravascular volume
Changes in mirocirculation to regulate
regional blood flow
 Phases of Shock
Compensated phase
Shock corrected with neuroendocrine response
Minimal blood loss
Decompensated phase
There is continued uncorrected hypoperfusion
Cell death and tissue injury are ongoing
Reversible
Irreversible phase
Cardiac decompensation
Sufficient tissue injury and cell death have occured
CLINICAL MANIFESTATIONS
S/Sx
Restlessness
anxiety
thirst
hypotension (sys BP < 80-90 mm Hg)
tachycardia (rapid, thready, imperceptible)
diaphoresis (cold, clammy skin…becoz of sweating)
tachypnea
^ depth of respiration
oliguria/anuria
NEUROENDOCRINE RESPONSE
GOAL: to maintain perfusion to the heart
and brain, above other organs
Peripheral vasoconstriction, fluid
conservation
Mechanisms:
1. ANS control of peripheral vascular tone, cardiac
contractility
2. Hormonal response to stress and hypovolemia
3. Organ specific local microcirculatory
mechanisms regulation of regional blood flow
NEUROENDOCRINE RESPONSE
Afferent signals:
Afferent impulses
Barroreceptor impulses
Chemoreceptor impulses
NEUROENDOCRINE RESPONSE
Afferent signals:
Stimuli: hypovolemia, pain, hypoxemia,
hypercarbia, acidosis, infection,
changes in temperature, emotional
arousal, hypoglycemia
Pain signalsspinothalamic
tractshypothalamushypothalamic-
pituitary-adrenal axis ANS
sympathetic stimulation of adrenal
medulla catecholamines
NEUROENDOCRINE RESPONSE
Baroreceptor signals
Hypovolemia baroreceptors in atria/carotid
decrease pressureANS activation
sympathetic stimulation peripheral
vasoconstriction
NEUROENDOCRINE RESPONSE
Chemoreceptor signals
Decrease O2 tension, ^ H ion concentration, ^
CO2 levels chemoreceptors in aorta and
carotid vasodilatation of coronary arteries,
bradycardia, vasoconstriction of splanchnic
and skeletal circulation
 Cardiovascular Response
Betaadrenergic receptors to the heart
increase heart rate and contractility
Sympathetic stimulation of the peripheral
circulation via the alpha adrenergic
receptors causes vasoconstriction
Release of catecholamines from increase
sympathetic output
 HORMONAL RESPONSES
Predominant response: increase sympathetic
activity
• Cold, clammy perspiration, ^CR, ^ peripheral resistance,
decrease renal flow
^ catecholamines ^ CR, contractility
Decreased insulin ^ glucose, AA, fat stores
Decreased capillary hydrostatic pressure,
mobilization of fluids from interstitial to
intravascular space
HORMONAL RESPONSES
Activation of hypothalamic-pituitary-adrenal
axis
CRH > ACTH > increase in Cortisol
• Induces catabolic state
• Stimulates gluconeogenesis and insulin
resistance
• Stimulates lipolysis
• Causes retention of sodium and water
HORMONAL RESPONSES
Activation of hypothalamic-pituitary-adrenal
axis
Renin-angiotensin is activated
• Angiotensin II causes vasoconstriction of
both splanchnic and peripheral beds
• Stimulates secretion of aldosterone,ADH,and
ACTH
Pituitary system
• Releases ADH
 CVS RESPONSE
Preload
At rest: majority of blood volume within
venous system
Venous returnventricular end-
diastolic wall tension= determines CO
Decr arterial pressure ^ contraction of
venous muscle, passive elastic
recoil^ venous return
 CVS RESPONSE
Ventricular contraction
Frank-Starling Curve
• Force of ventricular contraction= function of
preload
• Contraction based on initial muscle
strength
Cardiac disease  decr cardiac
performance
Burns, hemorrhage, trauma, septic
shock cardiac dysfunction
 CVS RESPONSE
Afterload
Force that resists myocardial
contraction
Det. by arterial pressure and per.
resistance and viscosity
(N): ^ afterload ^ preload ^SV
Shock: decr volumedecr
preloaddecr CO
 CVS RESPONSE
Cellular effects
Decr O2 decr oxydative phosphorylation, ATP
productionanaerobic glycolysispyruvate
lactate ^lactic acidmetabolic acidosis
Decr pHchanges in gene expression, impaired
metabolic pathway, impaired cell membrane ion
exchange cell injury cell death
Decr ATP
• ^ Na^H2O influxswellingrupture of lysosomes,
cell membrane necrosis
Textbook of Surgery, Sabiston
EVALUATION/MONITORING
GUIDELINES:
1. intelligent monitoring =
clinical observation + laboratories

2. repeated measurements and

observation are essential

3. multidisciplinary approach =
optimum results
EVALUATION/MONITORING
Depend on hospital resources
Locally : BP, CR, CVP, UO, Hgb, Hct,
ECG, ABG, +/-arterial lactate levels,
stroke index, LV stroke work, O2
consumption, plasma/urine osmolality
EVALUATION/MONITORING
BP (120/80)
Diastolic- peripheral resistance,
vasoconstriction
Pulse P- stiffness of aorta, ^ w/ age, low
in shock
As long as other factors are favorable, a
relatively low BP is compatible with
adequate tissue perfusion!
EVALUATION/MONITORING
CR (70-75/min)
^ in hypovolemic, neurogenic, septic
Variable in cardiogenic shock
Compensatory mechanism
CVP ( 5 +/- 2 cm)
Measured in the SVC, close to R atrium
Reflects R ventricular filling pressure/preload
(better measured by Swan-Ganz catheter)
In shock, safe to infuse fluids up to 15 cm
Good correlation between CVP and PCWP
EVALUATION/MONITORING
CVP
Variability affected by:
1. Cardiac distensibility and contractibility
2. Venomotor state of central veins
3. Intrathoracic pressure
4. Vasoconstrictors
Hgb/Hct (12-14 gm%, 35-45 vol%)
• Reflects the efficacy of transcapillary
refill phenomenon
EVALUATION/MONITORING
UO (50 ml/hr, or 1-3 ml/KBW/hr)
pH, specific gravity, osmolality
Cardiac index (3.2 +/- 0.2 L/min/m2)
Decrease in all forms, except in hyperdynamic septic
shock
ECG monitoring
Blood gases
• pH: 7.4 +/- 0.2
• PaO2: 95-100 torr
• PaCO2: 40 torr
• Provide information as to the efficiency of alveolar gas
exchange, O2 transport, O2 utilization
EVALUATION/MONITORING
Electrolyte measurement
Arterial blood lactate (1M/L)
^ with shifts from aerobic to anaerobic
^ initial level  poorer prognosis
 ORGANS IN SHOCK
“shock lung”, ARDS, fall in PaO2 < 50 torr
• ARF- major problem in shock
• Fluid exchange between capillary and lung interstitium
governed by balance forces:
 Capillary hydrostatic pressure, interstitial oncotic
pressure- those that tend to drive fluid out
 Plasma oncotic pressure, interstitial hydrostatic
pressure- those that tend to pull fluid out
• Thin/flagile wall separates capillary fluid from lung
interstitiummay be disrupted by various factors
interference w/ the alveolar-capillary gas exchange
lung water accumulates
 ORGANS IN SHOCK
“shock Lung”, causes:
Aggravation of chronic airway obstruction
Acute forces acting on previously (N) lung
• ARDS, “stiff lung”, shock lung
• Develops within 24-48 hours post injury
• Very rapidly fatal
• S/sx: tachypnea, severe dyspnea
• Basic defect: leaky capillary
• Capillary dilation  pulmonary edema, alveolar
hemorrhage atelectasis
• Etio: bacterial agents, microemboli (from BT, etc.),
pulmonary immune responses
 ORGANS IN SHOCK
Brain
Early shock  flow redistributed to
brain
Persistent shock  brain becomes
hypoperfused
Sensitive to hypoxia  decrease O2
anaerobic metabolism
S/Sx: sensorial changes
 ORGANS IN SHOCK
Heart
Struggles to maintain blood flow and
pressure
Failure plays a major role in irreversible
shock
Adequate myocardial O2 essential
Decrease coronary O2  anaerobic
energy production inadequate O2
decrease cardiac function
 ORGANS IN SHOCK
Kidney
• Renal vasoconstriction  decrease flow to
outer cortex  ATN  ARF= acute renal
failure
Liver derangements
• CHON, CHO synthesis
• Excretion, degradation of toxins
• AA catabolism
• FA catabolism for gluconeogenesis
 ORGANS IN SHOCK
Cell
• First changes occur at cell membrane
• Decrease O2 transport  decrease cation pump
mechanism
 Decrease energy production (ATP)
 Loss of cell membrane potential
 ^Na influx  ^ H2O influx  swelling cell, mitochondria
 mitochondrial leak, lysosomes rupture  release of
hydrolytic enzymes  cell destruction
• Anaerobic metabolism
 2 moles of ATP vs 38 moles (aerobic)
• Anaerobic glycolysis  pyruvate  converted to
lactic acid  lactic acidemia
 HYPOVOLEMIC SHOCK
Hemorrhagic shock (trauma)

Non-hemorrhagic shock ( vomiting,

LBM, & burns)
 HYPOVOLEMIC SHOCK
S/sx:
Include:
• Signs of adrenergic discharge to skin
• Oliguria
• Hypotension
• EKG myocardial ischemia
• neurologic
 HYPOVOLEMIC SHOCK
Diagnosis and monitoring
• Moderate and severe shock  easy to recognize
• Mild shock  subtle signs
• Monitor UO, serial Hct, postural changes in BP, CR
• UO: insert FC, maintain 1-3
dependable except in alcoholics
• Hct  decreasing hct w/ ^ IVF= hypovolemic shock
 Decrease hematocrit of 3-4 pts w/ fluid resuscitation means
a loss of 500 ml of blood
• Falling systolic BP > 10 mm Hg > 30 sec = hypovolemia
• CR not reliable
• In patients w/ shock do hgt to r/o hypoglycemia
 HYPOVOLEMIC SHOCK
Treatment:
• Initial resuscitation- adequate ventilation
and O2
 Control of bleeders
 Venous access
• Crystalloid infusion- non-sugar, non-CHON
soln w/ electrolytes approximating plasma
LRS
• Blood administration
 Type specific blood or blood type “O”, Rh +
 TRAUMATIC SHOCK
External blood or plasma loss +/- internal
losses
From wound or burn surfaces, loss into
damaged tissues
Same s/sx
Treatment:
• Control airway- if RR > 30-35/min, pO2 < 70 ET + MV
• Correct hypovolemia  IVF’s  BT
• Control of bleeders
• Prompt debridement
• Immobilize fracture
 CARDIOGENIC SHOCK
Circulatory pump failure  diminished forward
flow, tissue hypoxia
Intrinsic heart abnormality: ischemiamyocardial
dysfunction ^ ischemia
Congenital abnormalities, arrhythmias, ischemia,
VSD, cardiomyopathies, air embolism
Acute MI- most common cause
R ventricular dysfunction distended neck veins
L ventricular dysfunction rales, third heart sound
Chronic dysfunction cardiomegaly, distended
neck veins
 CARDIOGENIC SHOCK
Hemodynamic criteria
• Sustained hypotension (< 90 mm Hg>30’)
• Reduced cardiac index (<2.2 LPM/m2)
• ^ PCWP (> 15 mm Hg)
Mortality rate: 50-80%
Complicates 5-10% of MI
• Most common cause of death in patients w/
MI
 CARDIOGENIC SHOCK
Diagnosis
• ID cardiac dysfunction
• Rapid identification is the clue to survival
• R/O other causes: hemorrhage, sepsis,
pulmo embolism, aortic dissection
• Tests: EKG, 2D echo, CXR, ABG’s,
electrolytes, CBC, cardiac enzymes ( trop)
 CARDIOGENIC SHOCK
Treatment
1. Opioids: relieve pain,provide
sedation,lessen stress on the heart
2. Diuretics: decrease R&L atrial
pressures which alleviates peripheral
and pulmonary edema
3. Chronotropic agents: (atropine and
Isoproterenol) increase heart
contractility and and dilates systemic
arterioles
 CARDIOGENIC SHOCK
Treatment
4. Inotropic agents: (dopamine or
dobutamine) in low doses,, increases
contractility. Dopamine dilates renal
vessels increasing blood flow and urine
output
 CARDIOGENIC SHOCK
Treatment
5. Vasodilators(morphine,nitroprusside,
nitroglycerine) for high arterial
pressures to dec per res= better heart
pump
6. Beta Blockers
7. Vasoconstrictors
CARDIAC COMPRESSIVE
SHOCK
Compression of great veins, cardiac
chamber or both
Seen in:
Pericardial tamponade, tension
pneumothorax, ascites,
hemoperitoneum, diaphragmatic
rupture,
CARDIAC COMPRESSIVE
SHOCK
Signs/ Symptoms
^ CVP in patients w/ suggestive hx
Kussmauls sign:
Pathognomonic of pericardial tamponade
Increase right heart pressure plus
distended neck vein
Paradoxic pulse: fall of >10mm Hg in
systolic pressure on inspiration
CARDIAC COMPRESSIVE
SHOCK
Dx:
• PE: Beck’s triad
• Definitive: Swan-Ganz catheter decr Co,
^PCWP
• Oliguria
Tx:
• Airway
• Circulation
• Treat cause!
 VASODILATORY
(SEPTIC)SHOCK

Results from the body’s attempt to

eradicate pathogens.
When the response of body is overly
exuberant, signs of sepsis becomes
evident
In response to toxins, gm (-)
bacteriaseptic shock
 VASODILATORY
(SEPTIC)SHOCK
Characteristics: Hypotension is due to:
• Failure of vascular smooth muscle
constriction
• Peripheral vasodilatation
• Loss of plasma into tissues and blood
sequestration into cutaneous vasculature
• Resistance to vasopressor treatment
• Septic shock- most common
Mortality rate= 30- 50%
Sepsis accounts for 9.3% of deaths
 VASODILATORY
(SEPTIC)SHOCK
Causes
1. Sepsis
2. Prolonged and severe Hypotension
• Hemorrhagic shock
• Cardiogenic
• Cardiopulmonary bypass
3. Inadequate tissue perfusion
• Lactic acidosis
• Carbon monoxide poisoning
 VASODILATORY
(SEPTIC)SHOCK
Early septic shock/ Red Shock
Hypermetabolic state
Fever, ^ heat production opening of
cutaneous A-V shunts  blood diverted
to skinheat loss
 VASODILATORY
(SEPTIC)SHOCK
Late septic shock
Hypoperfusion of vital organs cutaneous
pressor mechanisms activated  blood
diverted from skin to vital organs  decr
skin temp  cold sensation  chills
Cutaneous vasoconstriction compromises
body’s ability to dissipate heat rapid rise
in body temp
^CO  decr systemic resistance  decr
BP
 VASODILATORY
(SEPTIC)SHOCK
Treatment:
• Prevention- early recognition, ID source,
antibiotics, I & D
• Correct hypovolemia
• Almost all require ET + MV
 NEUROGENIC SHOCK
Loss of vascular tone w/ venous pooling, decr.
return flow to the heart
Pooling of blood in denervated venous beds,
excess perfusion of unessential vascular beds
Spinal cord injury, regional anesthetic, fright,
hysterics
Similar to warm septic shock
Treatment:
• Balanced salt solution
• Vascoconstrictors…elevate legs
 ENDPOINTS IN
RESUSCITATION
Resuscitation complete:
• O2 debt repaid
• Tissue acidosis corrected
• Aerobic metabolism restored
Parameters:
Systemic parameters: lactate, base deficit, CO,
O2 delivery and consumption
Tissue parameters: gastric tonometry, tissue
pH, O2, CO2 levels
Cellular : membrane potential, ATP
 ENDPOINTS IN
RESUSCITATION
O2 transport
• Related to lactate and base deficit
Lactate
• ^ serum lactate- indirect measure of O2 debt,
approximation of magnitude of shock
• Generated by conversion of pyruvate to lactate (LDH)
• Metabolism: Liver (50%), kidneys ( 30%)
Base deficit- measured by ABG
• Base deficit > 15 mmol/L mortality 70%
• Mild (3-5), mod (6-14), severe (>15)
• ^ base deficit ^ acidosis ^ mortality
“The patients are your textbooks,
the sickbed is your study room”