Historical background ● The mitochondria is the most

● In 1934,Blalock proposed four susceptible to inadequate oxygen

categories of shock, hypovolemic, delivery to the tissues, therefore,
vasogenic, cardiogenic, neurogenic. In generation of ATP slow or stops
recent clinical practice, 6 types of ● Under hypoxic conditions, the
shock have been described: mitochondrial pathways or oxidative
Obstructive and traumatic catabolism are impaired.
● As cellular ATP is depleted, activity of
Introduction the membrane NA+, K+ ATPase
● Shock maybe defined as inadequate slows.
delivery of oxygen and nutrients to ● Sodium accumulates intracellularly
maintain normal tissue and cellular while K+ leaks into the extracellular
function space.
● The intestinal mucosal cell apoptosis
Shock may compromise bowel integrity and
Concepts in the maintenance of tissue lead to translocation of bacteria.
perfusion:
1. Cardiac output Immune and Inflammatory Response
2. Circulating volume ● The immune response to shock
3. Systemic vascular resistance encompasses the elaboration of
4. ANS response mediators with both proinflammatory
5. Hormones (ADH and RAAS) and anti-inflammatory properties.

Pathophysiology Inflammatory Response

● The initial insult initiates both ● Innate immune response can help
neuroendocrine and inflammatory restore homeostasis, or if it is
mediator response. Persistent excessive, promote cellular and organ
hypoperfusion will result in dysfunction.
hemodynamic derangements, end-
organ Forms of Shock
● Hemorrhagic or hypovolemic
Neuro Endocrine Response ● Cardiogenic shock
● The mechanism include autonomic ● Distributive/ Vasodilatory (Septic/
control of peripheral vascular tone and Toxic, Anaphylactic, Neurogenic)
cardiac contractility, hormonal ● Traumatic shock
response to stress and volume ● Obstructive shock
depletion and local microcirculatory
mechanism. Stages of Shock
1. Initial/ Compensated/ Non-progressive
Hormonal Response ➔ Vital organs remain adequately
● The stress response includes perfused because of activation of
activation of the ANS and compensatory mechanisms
Hypothalamic-pituitary adrenal axis ➔ SAMR (systematic autonomic
medullary response)
Hormones: 2. Progressive/ Decompensated
● Cortisol ➔ Vital organs become underperfused
● Renin-angiotensin and compensatory mechanisms
● Aldosterone become ineffective, resulting in
● ADH systemic manifestations.

Microcirculation Organ Damage in Progressive Shock

● After hemorrhage, larger arterioles 1. Kidneys
vasoconstrict while smaller, distal 2. Brain
arterioles dilate, presumably due to 3. Heart
local mechanism 4. Lungs
● The dec in capillary perfusion and 5. GIT
blood flow result in diminished 6. Liver
capillary hydrostatic pressure.
3. Irreversible
Cellular Effects
 ➔ Extent of shock is so severe that ➢ End stage cardiomyopathy
therapeutic interventions become ➢ Acute aortic insufficiency, acute mitral
useless regurgitation
➔ Death eventually occurs ➢ Obstruction to left ventricular filling

Physiologic Responses to Shock Diagnosis

1. Vasoconstriction ● In evaluation of possible cardiogenic
2. Tachycardia shock, other causes of hypotension
3. Tachypnea must be excluded.
4. Skin color and temperature changes ● Making the diagnosis of cardiogenic
5. Hypotension shock involves the identification of
6. Coagulation abnormalities cardiac dysfunction or acute heart
7. Hyperglycemia failure in susceptible patient.
8. Fluid shifts
9. Activation of RAAS Treatment
10. End organ damage ● Maintain adequate oxygenation
● Judicious fluid administration
Hemorrhagic Shock ● Pain is treated with IV morphine
● Acute blood loss results in reflexive sulfate
decreased baroreceptor stimulation, ● Antiarrhythmic drugs
increased chemoreceptor stimulation ● Cardioversion
of vasomotor centers, increase
vasoconstriction and peripheral Vasodilatory Shock
arterial resistance. ● Hypotension results from failure of the
vascular smooth muscle to constrict
Diagnosis appropriately, resistant to treatment
● The clinical signs of shock maybe with vasopressors.
evident with agitated patient, cool
clammy extremities, tachycardia, Other causes of vasodilatory shock:
hypotension ● Hypoxic lactic acidosis
● Marked tachycardia, hypotension, ● Carbon monoxide poisoning
confusion may be evident. ● Terminal cardiogenic shock

Treatment Represent the FINAL COMMON PATHWAY

● Secure the airway for profound and prolonged shock of any
● Control the source of blood loss etiology.
● Intravenous volume resuscitation
● The actively bleeding patient cannot Septic/ Toxic Shock
be resuscitated until control of ongoing ● Results from severe and profound
hemorrhagic is achieved. conditions of generalized vascular
collapse secondary to a systemic
Cardiogenic shock infection commonly caused by gram
● Defined as circulatory pump failure (-) organisms
leading to decrease blood flow and ● Endotoxins cause massive
hypoxia. vasodilation

Hemodynamic Criteria: Diagnosis

● Sustained hypotension ● Evidence of infection
● Reduced cardiac index ● Fever
● Elevated pulmonary artery wedge ● Tachycardia
pressure ● Leukocytosis
● Tachypnea
Causes of Cardiogenic Shock ● Signs of hypoperfusion such as
● Acute Myocardial Infarction confusion, malaise, oliguria or
➢ Pump failure hypotension
➢ Mechanical complications
➢ Right ventricular infarctions Treatment
● Adequacy of airway and ventilation
● Other causes ● Empiric antibiotics
➢ Myocarditis ● IV fluids
 ● Arginine vasopressin
● Tight glucose management Traumatic Shock
● Corticosteroids ● In traumatic shock, soft tissue injury
and long bone fractures that occur in
Neurogenic Shock associated with blood loss yield an
● Defined as diminished tissue perfusion upregulation of proinflammatory
as a result of loss of vasomotor tone mediators that is more complex than
to peripheral arterial beds usually sec simple hemorrhagic shock.
to spinal cord injury.
● Affects medulla and SNS Treatment
● Interference with SNS ● Secure airway
● Control bleeding
Diagnosis ● IV fluids
➔ Classic description consist of: ● Debridement of non viable tissue
● Decrease blood pressure associated ● Stabilisation bony injuries
with bradycardia ● Treatment of soft tissue injuries
● Warm extremities
● Motor and sensory deficit Differential Diagnosis of Shock BAsed on
● Radiographic evidence of vertebral Hemodynamic Parameters
column fracture
-insert pic
Treatment
● Secure airway
● IV fluids Signs and Symptoms
● Administration Of vasoconstrictors, ● Early signs
dopamine ➢ Increase SNS activity
➢ Increase HR
➢ Increase shallow respiration
Anaphylactic Shock ➢ Increase BP
● There is profound peripheral vascular ➢ Diaphoresis
collapse induced by severe allergic ➢ Cool clammy skin
response. ➢ Thirst
● Mediated by histamine, kinims, PgE, ➢ Dry mucous membranes
Leukotrienes ➢ Decrease urine output
● Large quantities of fluid may leak out ➢ N/V
of capillaries causing severe ➢ Weakness
hypovolemia ➢ Restlessness
➢ Increase alertness
Treatment
● Epinephrine ● Late stage
➢ Apathetic
➢ Unresponsive
Obstructive Shock ➢ Confusion
● Caused by pulmonary embolism or ➢ Decrease LOC
tension pneumothorax, resulting in ➢ Eyes sunken with vacant expression
depressed cardiac output, which ➢ Dilated pupils
results from mechanical impediment to ➢ Mottled skin appearance
circulation rather than a primary ➢ Hypotension
cardiac failure. ➢ Decrease temperature
➢ Oliguria, Anuria
Diagnosis ➢ Decreased bowel sounds
● The diagnosis of tension ➢ Metabolic/ Respiratory acidosis
pneumothorax is made on clinical ➢ DIC
examination, includes respiratory
distress, hypotension, diminished BS, Assessment Parameters
shift of mediastinal structures 1. Hemodynamic monitoring
● Definitive tube of tension 2. Respiratory monitoring
pneumothorax immediate to the 3. Fluid electrolyte monitoring
thoracostomy. 4. CNS monitoring
5. Hematologic monitoring
First Aid and Preventive Management in
Shock
1. Proper position
2. Proper body heat

Collaborative Management
1. Assess primary cause of shock in
case of 3rd space shifting to prevent
further volume loss
2. Assess hemodynamic status and all
major body systems
3. Maintain airway and provide cardiac
and pulmonary support
4. Assisting with renal support
5. Assisting with GI support
6. Promoting safety
7. Institute management for specific
causes
8. Provide supportive care as indicated

Pharmacologic Therapy
1. Vasoconstrictors
2. Vasodilators
3. NaHCO3
4. Antibiotics
5. Heparin/ LMWH
6. Steroids
7. Glucagon, D50% W
8. H2 blockers/ proton pump inhibitors
9. Naloxone
10. Analgesics
11. Antidysrhythmics

Endpoints in Resuscitation
● The goal in the treatment of shock is
restoration of adequate organ
perfusion and tissue oxygenation.
● Resuscitating is complete when
oxygen debt is repaid, tissue acidosis
is corrected and aerobic metabolism is
restored.

Systemic/Global
● Lactate, base deficit, cardiac output

Tissue specific
● Gastric tonometry, tissue pH,O2 level

Cellular level
● Membrane potential
● ATP