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Failure to meet the metabolic demands of cells and tissues, & the consequences that ensue
Inadequate tissue perfusion marked by decreased delivery of required metabolic substrates &
inadequate removal of cellular waste products

Initial cell injury = reversible

Prolonged = irreversible

Table 4. Categories of Shock

HYPOVOLEMIC Most common; loss of circulating blood volume

CARDIOGENIC Failure of the heart as a pump

SEPTIC (VASOGENIC) Decreased resistance within capacitance vessels

NEUROGENIC Form of vasogenic shock, spinal cord injury / anesthesia causes vasodilation due to
acute loss of sympathetic tone

TRAUMATIC Soft tissue and bony injury lead to activation of inflammatory cells & release of
circulating factors that modulate the immune response
Effects of tissue injury are combined wtith effects of hemorrhage

OBSTRUCTIVE Form of cardiogenic shock; from mechanical impediment to circulation leading to

depressed cardiac output

III. Pathophysiology: Tissue hypoperfusion

Cellular energy deficit

Organ-specific responses to maintain cerebral & coronary perfusion:
Stretch receptors, baroreceptors, chemoreceptors, cerebral ischemia responses, endogenous
vasoconstrictors, fluid shift into intravascular space, renal absorption & conversion of salt &
water
 NONPROGRESSIVE (EARLY) STAGE
NONPROGRESS
COMPENSATED PHASE
Body can compensate for initial loss of blood volume/perfusion
Neuroendocrine response maintain hemodynamics
Increased HR & peripheral resistance

PROGRESSIVE STAGE / DECOMPENSATED PHASE

Tissue hypoperfusion
Onset of circulatory & metabolic imbalance
Lactic Acidosis metabolic acidosis
Compromise of function at Organ System level

IRREVESIBLE STAGE
Peristenthypoperfusion
Hemodynamic derangements & cardiovascular collapse
Volume resuscitation fails to reverse process

DEATH - eventually

Compensated Shock
Exists when inadequate tissue perfusion persists despite normalization of blood pressure & heart rate
Even with normal BP, 80-85%85% of trauma patients have inadequate tissue perfusion
Increased lactate or decreased O2 sat
IV. FORMS OF SHOCK

HYPOVOLEMIC / HEMORRHAGIC
Loss of circulating volume
Most common cause of shock in surgical / trauma patient

Acute blood loss

Reflexive decreased baroreceptor stimulation from stretch receptors in large arteries
Decreased inhibition of vasoconstrictor receptors in brainstem
Increased chemoreceptor stimulation of vasomotor centers
Decreased output from atrial stretch receptors

Increase in Vasoconstriction & Peripheral Arterial Resistance

Sympathetic stimulation
NE & E release
RAS cascade
Vasopressin release

Classification of Hemorrhage:
Class
Parameter 1 11 111 1V
Blood Loss (mL) <750 750 - 1500 1500 - 2000 >2000
Blood Loss (%) <15 15 – 30 30 - 40 >40
Heart rate (bpm) <100 >100 >120 >140
Blood pressure Normal Orthostatic hypotension Severe
hypotension
CNS symptoms Normal Anxious Confused Obtunded

Young healthy patents

may maintain near normal blood pressure until precipitous cardiovascular collapse occurs
Elderly patients
may be taking medications that promote bleeding (warfarin, ASA) or mask compensatory
response to bleeding (e.g. beta blockers)

Diagnosis
Shock in trauma & post-op patient should be presumed to be due to hemorrhage until proven
otherwise.

Clinical Signs
agitation, cool clammy extremities, tachycardia, weak/absent peripheral pulses, hypotension
25-30% blood loss + physiologic decompensation

Systolic BP
99% of patients had a BP < 120 mmHg
93% of patients had a BP < 100 mmHg

Tachycardia
Not a reliable sign of hemorrhage following trauma
Present in only 65% of hypotensive patients
Serum Lactate & Base Deficit
Helpful to estimate & monitor extent of bleeding & shock
SERUM LACTATE
Initial & serial
ial levels are reliable predictors of morbidity & mortality with hemorrhage following
trauma

BASE DEFICIT (ABG)

Indirect estimation of tissue acidosis from hypoperfusion
Base deficit upon admission correlates with transfusion requirements, development of multiorgan
failure and death

MILD -35 to -5 mmol/L

MODERATE -6 to -9 mmol/L

SEVERE < -10 mmol/L

Management
ABC of life support
Search for cause of hypotension

TRAUMA
Bleeding sources located along known / suspected path of wounding object
Operative intervention
Multisystem injuries from blunt trauma
Multiple sources of potential hemorrhage
Blood loss generally of large volume
Sites that harbor
arbor extravascular blood loss: external, intrathoracic, intraabdominal, long bone
fractures
NON-TRAUMA
GI Bleed ; GI Tract - Always be considered as a site for blood loss
Sites of Hemorrhage
Pleural Cavity - Each can hold 2-3 L blood
Diagnostic & therapeutic CTT
Retroperitoneal Hemorrhage
Pelvic fractures - Pelvic radiography
Intraperitoneal Hemorrhage - Most common source of blood loss inducing shock
PE is unreliable
Abdominal distention, abdominal tenderness, visible abdominal wounds- Adjunct

Treatment
: ABC
Control of ongoing hemorrhage
If fail to respond to initial resucitation - assume to have active hemorrhage from large vessels
Trauma patients with major abdominal injuries requiring ex-lap have increased probability of
death with increasing length of time in ER: Increase in 1% for every 3 minutes in ER

Damage Control Resuscitation

Strategy aimed at halting &/or preventing rather than treating the lethal triad:
Coagulopathy
Acidosis
Hypothermia

ER → OR→ ICU

ER
Initial resuscitation to keep SBP at 90 mmHg
Prevents renewed rebleed from recently clotted vessels
Blood products & limited crystalloids

OR
Control of hemorrhage

ICU
Keep patient normothermic
Prevent coagulopathy with blood products & medications
TRAUMATIC SHOCK
Multiple organ failure & ARDS more common
Hypoperfusion deficit is magnified by proinflammatory activation
Damage Associated Molecular Patterns (DAMPS)
Cellular products released that activate the same cell surface receptors (Pattern Recognition
Receptors /PRRs)
Similar effects with septic shock

Examples:
Small volume hemorrhage accompanied by soft tissue injury (femur fracture, crush injury)
Any combination of hypovolemic, cardiogenic, neurogenic & obstructive shock that precipitate
rapidly progressive proinflammatory reaction

Treatment
Correction of the individual elements to diminish cascade of proinflammatory activation:
Prompt control of hemorrhage
Adequate volume resuscitation to correct O2 de
Debridement of nonviable tissue
Stabilization of bony injuries
Treatment of soft tissue injuries

SEPTIC / VASODILATORY SHOCK

Sepsis (most common)
Noninfectious systemic inflammation:
Pancreatitis
Burns
Anaphylaxis
Acute adrenal insufficiency
Prolonged & severe hypotension
Hemorrhagic, Cardiogenic shock
Cardiopulmonary bypass
Metabolic
Hypoxic lactic acidosis
Carbon monoxide poisoning

Vasodilatory shock
The final common pathway for profound & prolonged shock of any etiology
Mortality rate = 30-50%
Findings:
Increased cardiac output
Peripheral vasodilatation (upregulation of Nitric Oxide Synthase in vessel wall)
Fever
Leukocytosis
Hyperglycemia
Tachycardia

Diagnosis
Identify offending organism
Search for infection:
Thorough PE
Inspect all wounds, catheters, foreign bodies
Cultures
Imaging studies

Treatment
ABC
Empiric antibiotics based on most likely organism (gram negative rods &cocci, anaerobes)
Tailor with narrower spectrum antibiotics once cultures available
IV fluids
Vasopressors (catecholamines)
ARGININE VASOPRESSIN - If with arterial resistance to catecholamines

Source Control
IV antibiotics are insufficient to treat infections in settings of infected fluid collections,
infected foreign bodies & devitalized tissue
Involves percutaneous drainage & operative management to target focus of infection

Goal-directed therapy during first 6 hous of hospital stay:

Higher mean venous O2 saturation
Lower lactate levels
Lower base deficit
Higher pH
Decreased mortality

CARDIOGENIC SHOCK

Circulatory pump failure leading to diminished forward flow & subsequent tissue hypoxia in the
setting of adequate intravascular volume
50-80% mortality rate

Causes
Acute extensive MI (most common)
Infarction in patient with left ventricular dysfunction
-Average of 7 hours after onset of infarction
Hemodynamic Criteria
Sustained hypotension
SBP < 90 mmHg for at least 30 minutes
Elevated pulmonary artery wedge pressure
> 15 mmHg

Table 6. Causes of Cardiogenic Shock

Table 5 – 7 Causes of Cardiogenic Shock
Acte myocardial infarction
Pump failure
Mechanical Complications
Acute Mitral regurgitation
Acute ventricular septal defect
Free wall rupture
Pericardial tamponade
Arrhythmia
End-stage cardiomyopathy
Myocarditis
Severe Myocardial contusion
Left Ventricular outflow obstruction
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Obstruction to left ventricular filling
Mitral stenosis
Left atrial myxoma
Acute mitral regurgitation
Acute aortic insufficiency
Metabolic

Diagnosis
Identify cardiac dysfunction/ acute heart failure in vulnerable patient
Exclude other causes of hypotension
Hemorrhage, sepsis, pulmonary embolism, aortic dissection
Signs of circulatory shock:
Hypotension, cool mottled skin, depressed mental status, tachycardia, diminished pulses
Cardiac exam:
Dysrhythmia, precordial heave, distal heart tones
Diagnostics:
ECG, cardiography, CBC, ABG, Electrolytes, cardiac enzymes

Blunt cardiac injury

In blunt traumatic injury
Rule out hemorrhage before implicating cardiogenic shock
Relatively few patients will develop cardiac pump dysfunction
Those who do exhibit cardiogenic shock early in their evaluation
Pulmonary artery catheter:
diminished cardiac output
Elevated pulmonary artery pressure
Treatment
Intubation &mech vent - decrease work of breathing & facilitate sedation
Circulatory support:
Maintenance of adequate oxygenation to ensure adequate myocardial O2 delivery
Judicious fluid administration to avoid fluid overload & cardiogenic pulmonary edema
Pain control - morphine / fentanyl
Antiarrhythmic drugs, pacing, cardioversion
Correct electrolyte abnormalities
Beta agonists (dopamine, dobutamine, epinephrine, catecholamine)

Treatment of Choice:
Percutaneous Transluminal Coronary Angiography + Stent Placement
For patients with cardiogenic shock, ST elevation, LBB, age < 75 years old
Early definition of coronary anatomy & revascularization
Coronary Artery Bypass Grafting
Patients with multiple vessel disease or Left Main Coronary artery disease

OBSTRUCTIVE SHOCK
Causes:
Tension pneumothorax (most common)
Pericardial tamponade
Pulmonary embolus
IVC obstruction
DVT, gravid uterus on IVC, neoplasm
Increased intrathoracic pressure
Excessive PEEP
Neoplasm

Table 7. Diagnosis & Treatment

Condition Diagnosis Treatment

TENSION Respiratory distress, JVD, Hypotension, Pleural

PNEUMO- decreased breath sounds, hypertympany, decompression
THORAX CTT

CARDIAC Muffled heart sounds, JVD, inc CVP, Pericardial

TAMPONADE Beck’s Triad decompression
2-D Echo/ transesophageal Pericardiocentesis
Echocardiography
Diagnostic pericardial window

NEUROGENIC SHOCK
Diminished tissue perfusion due to loss of vasomotor tone to peripheral arterial beds:
Increased vascular capacitance
Decreased venous return
Decreased cardiac output
Caused by spinal cord injuries:
Fractures / impingement of cervical / high thoracic region that disrupt sympathetic regulation of
peripheral vascular tone
Spinal cord neoplasm
Spinal / epidural anesthesiaAcute spinal injury results in activation of multiple secondary injury
mechanisms:
Vascular compromise to spinal cord
Loss of autoregulation, vasospasm, thrombosis
Dec in blood flow to spinal cord worsens spinal cord injury
Loss of cellular membrane integrity & impaired energy metabolism
Neurotransmitter accumulation & release of free radicals
Diagnosis
Decreased BP + Bradycardia
No reflexive tachycardia
Warm extremities
Loss of peripheral vasoconstriction
Motor & sensory deficits
Radiographic injuries of vertebral column fracture

Management
Attention to BP, oxygenation, hemodynamics
Optimize perfusion of spinal cord
Most patients respond to restoration of intravascular volume alone
Stabilize vertebral fracture
Life threatening cardiac dysrhythmias & hypotension may occur up to 14 days after injury

________________
Reference
Brunicardi FC et al. Schwartz’s Principles of Surgery, 10th Edition.McGraw-Hill.2014.