Approach to shock

Outline
• Definition
• Pathophysiology
• Diagnosis
• Managment
• Shock is a pathophysiologic state in which the oxygen supply to body
tissues inadequately meets metabolic demands, resulting in
dysfunction of end-organs
• The aim of oxygenation is to maintain adequate cellular oxygenation
Which requires red cell oxygenation and red cell delivery to the tissues
 DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] +
(PaO2 x 0.003) Abbreviations: DO2, oxygen delivery; PaO2; partial
oxygen pressure; SaO2, arterial oxygen saturation
Consequences of shock
• Inadequate tissue perfusion results in:
Poor cellular Oxygenation
Shift from aerobic to anaerobic circulation
 Ultimate
Effects of
Inadequate
Anaerobic Cellular
Metabolism Oxygen
Delivery

Lactic
Inadequate
Energy Anaerobic Acid
Production Metabolism Production

Metabolic Metabolic
Failure CELL Acidosis
DEATH
COMPENSATORY MECHANISMS IN
SHOCK
Central Nervous System
• Autonomic (Sympathetic, Fight or Flight)
• Rapid onset
• Increased heart rate (chronotropic), increased force of contraction
(inotropic), increased conduction (dromotropic) Beta 1
• Stimulates Adrenal Medulla to secrete Norepinepherine and
Epinephrine
• Nor Epinephrine-Alpha 1 peripheral vasoconstriction, Epinephrine-
Beta 2 dilate vessels to coronary and skeletal muscle, bronchodilation
Respiratory System

• Decreased Po2 sensed by peripheral chemoreceptors, increased

acidosis sensed by central chemoreceptors
• Stimulates increased respiratory rate, maximizes FiO2, compensates
for acid base imbalance
Hormonal Compensation

• Decreased blood flow to Kidneys-> Hypoprofusion sensed by

Juxtaglomerular Cells, causes kidneys secrete renin->Renin acts on
Angiotensinogen (protein from liver)->Angiotensine 1->at lungs
converted to Angiotensine 2 by ACE-> Angiotensine 2 powerful
vasoconstrictor and stimulates Adrenal Cortex to secrete Aldosterone
• Aldosterone stimulates kidneys to retain sodium with that water
overall increasing fluid volume
Anti-diuretic Hormone - ADH

• Secreted by posterior pituitary if stimulated by hypothalamus (Senses

increased osmotic pressure)
• volume =  Tonicity (sodium)
• Causes tubules of kidney to be more permeable to water therefore
more volume retained
ACTH - Adrenocorticotropic Hormone

• Hypothalamus stimulates anterior pituitary to secrete ACTH

• ACTH stimulates metabolism of carbohydrates, proteins and fats
• Decreases permeability of capillary walls helping prevent loss of
intravascular fluid
Clinically shock is recognized by:
• Hypotension : SBP<90 mm Hg, Tachycardia>100/min is common
• Altered mental status or fainting
• Poor peripheral perfusion : Cool peripheries, clammy/sweaty skin,
pallor, delayed capillary return
• Oliguria
• Tachypnea
• HR > 100 RR > 22 or PC02 < 32
• Base deficit < -5 or lactate > 4
• Urine output < 0.5 ml/kg/hr
• Hypotension > 20 minute duration
• NOTES Base deficit = amount of base required to neutralize the pH
(normal is > -2
• Shock index : HR/SBP > 0.9 suggest shock
Classification of shock based on Etiology
1.Hypovolemic shock
 Decreased intravascular volume resulting in decreased preload, stroke
volume, and cardiac output
 Causes
• Hemorrhagic : major trauma, gastrointestinal bleeding, ruptured
ectopic pregnancy, etc.
• Non-hemorrhagic : vomiting, diarrhea, burns, etc.
2. Cardiogenic: Impaired cardiac output secondary to cardiac pump
function, rhythm aberrancy or structural defect
• Arrhythmogenic (brady- or tachydysrhythmia)
• Cardiomyopathic (myocardial infarction, heart failure, etc.)
• Cardiotoxicity from medication
• Structural (valvular insufficiency, ventricular septal wall defect, e
3. Distributive
Pathologic vasodilatation leading to relative intravascular volume
depletion
• Anaphylactic (IgE mediated allergic reaction)
• Septic (pneumonia, pyelonephritis, etc.)
• Neurogenic (spinal cord injury)
• Toxicologic (vasodilatory medication)
4. Obstructive
 Impaired cardiac output due to pulmonary vascular or mechanical
obstruction
• Pulmonary vascular obstruction (pulmonary embolism, venous air
embolism, etc.)
• Mechanical obstruction (tension pneumothorax, pericardial
tamponade, left ventricular outflow tract obstruction, etc.
Mixed / Other: Any of the above may be present concurrently
• Cellular poisons (carbon monoxide, cyanide, etc.)
• Endocrinologic (adrenal insufficiency, myxedema coma, etc.)
• Environmental (hypothermia, etc.)
• Toxicologic etiology with cardiac and vasoplegic manifestations
(calcium channel blocker, etc.)
Initial treatment
• Primary survey
• Focused history and physical examination
• intravenous access (i.e. two large-bore IVs, intraosseous access, or
central venous catheter)
• Continuous monitoring, noninvasive blood pressure monitoring, and
pulse oximetry.
• An ECG and chest radiograph should generally be obtained.
• Bedside ultrasonography (i.e. FAST examination)
• intravenous fluid resuscitation should be started
• Hypovolemic shock due to hemorrhage is suggested by the report of
trauma or bleeding from other source (melena or hematemesis from
a gastrointenstinal source, vaginal bleeding from a gynecologic
source, etc.).
• Non-hemorrhagic hypovolemic shock may be suggested by decreased
oral intake, diarrhea, vomiting or high ostomy output.
• Cardiogenic or obstructive shock may be suggested by chest pain,
shortness of breath, recent leg swelling, or syncope.
• Anaphylactic shock may present as the sudden onset of pruritus,
hives, or swelling following exposure to an inciting trigger.
• Septic shock may be associated with signs of infection such as fever,
cough, dysuria, abdominal or flank pain, or rigors.
• Hypotension alone should not be used as the sole determinant of shock, as early shock
may present with normal or even elevated blood pressure, and normal heart rate.
• Without prompt treatment of the patient in early shock, hypotension and tachycardia
frequently follow.
• Altered mental status is common.
• Thready pulses, tachycardia and tachypnea are frequently present.
• Patients in shock often exhibit cool, pale or ashen skin with decreased capillary refill and
dry mucous membranes; however, in distributive shock states the extremities may be
inappropriately warm.
• In cardiogenic shock, arrhythmias, dependent edema, or new murmurs may be present,
while jugular venous distention is seen in both cardiogenic and obstructive shock states.
• Focused bedside ultrasonography is beneficial to assess for
intraperitoneal hemorrhage, pneumothorax, or pericardial
tamponade, and to assess global cardiac function and intravascular
volume status.
• Vascular catastrophes such as abdominal aortic aneurysm with
rupture may also be identified on bedside ultrasonography.
• The pump refers to cardiac function as measured by cardiac output in
terms of cardiac contractility and heart rate (HR). The tank refers to
the amount of preload present, often measured by central venous
pressure (CVP), and the pipes are assessed by systemic vascular
resistance (SVR).
Diagnostic tests
• CBC with differential
• Electrolytes, BUN, creatinine, glucose
• Lactate
• Coagulation studies
• Hepatic function panel
• Calcium
• Urinalysis
• ECG
• Chest radiograph
• Pregnancy test (blood or urine)
• Blood gas
Treatment
• airway, breathing, and circulation (i.e. “the ABCs”) should be emergently addressed.
• If peripheral IV access is unable to be established, intraosseous access or a
percutaneous introducer catheter may be inserted.
• Generally, volume expansion with crystalloid fluids (normal saline or Ringer’s
lactate) should be administered as rapid bolus infusion
• The Trendelenburg position does not improve cardiopulmonary performance
compared with the supine position. It may worsen pulmonary gas exchange and
predispose to aspiration.
• Passive leg raising above the level of the heart with the patient supine may be
effective. If passive leg raising results in an increase in blood pressure or CO, fluid
resuscitation is indicated.
• Patients with a modest degree of hypovolemia usually require an
initial 20 to 30 mL/kg of isotonic crystalloid,
• Restore arterial oxygen saturation to ≥91%.
• In shock states, consider a transfusion of packed red blood cells to
maintain hemoglobin ≥7 grams/dL.34
• Blood products may be indicated in hemorrhagic shock, particularly in
the trauma patient, in whom crystalloid infusion should be minimized
to reduce clotting factor dilution and hyperchloremic acidemia.
• If volume resuscitation does not improve the patient’s hemodynamic
state, initiation of vasopressor medications such as norepinephrine or
epinephrine may be indicated.
• The underlying etiology of shock should be aggressively treated:
Indications of appropriate resuscitation and
resolution of a shock states include:
• Normalization of hemodynamic parameters (i.e. BP, HR, and urine
output)
• Lactate clearance with reduction in lactate concentration below 2
mmol/L
• Volume status restored
• Resolution of acidosis and return to normal metabolic parameters