Karl Tapales, M.D.

Reference: Schwartzs Principles of Surgery 9th Edition

Introduction
Shock inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function cellular injury is initially reversible irreversible if hypoperfusion is severe and prolonged

Introduction
Clinical manifestations stimulation of the sympathetic and neuroendocrine stress responses inadequate oxygen delivery end-organ dysfunction. Management is empiric securing the airway restoration of vascular volume and tissue perfusion

Introduction
The organism's ability to survive was related to

maintenance of homeostasis. The failure of physiologic systems to buffer the organism against external forces results in organ and cellular dysfunction

Introduction
Categories of shock: Hypovolemic Vasogenic Cardiogenic Neurogenic Obstructive shock Traumatic shock

Introduction
Hypovolemic shock most common type loss of circulating blood volume (hemorrhagic shock bowel obstruction) Vasogenic shock decreased resistance within capacitance vessels, usually seen in sepsis

Introduction
Neurogenic shock form of vasogenic shock in which spinal cord injury or spinal anesthesia causes vasodilatation (acute loss of sympathetic vascular tone). Cardiogenic shock failure of the heart as a pump (arrhythmias or acute heart failure).

Introduction
Obstructive shock pulmonary embolism or tension pneumothorax results in depressed cardiac output mechanical impediment to circulation Traumatic shock soft tissue injury and long bone fractures that occur in association with blood loss yield an upregulation of proinflammatory mediators

Introduction
Core principles in the early management of the critically-ill

or injured patient include:

(1) definitive control of the airway (2) delay in control of ongoing bleeding increases mortality (3) volume resuscitation with red blood cells and crystalloid solution must occur while operative control of bleeding is achieved (4) unrecognized or inadequately corrected hypoperfusion increases morbidity and mortality (5) both inadequate and uncontrolled volume resuscitation are harmful.

Pathophysiology
Shock is defined as tissue hypoperfusion that is

insufficient to maintain normal aerobic metabolism. Imbalance

substrate delivery (supply) cellular substrate requirements (demand).

The initial insult, whether hemorrhage, injury, or

infection, initiates both a neuroendocrine and inflammatory mediator response.

Pathophysiology
Persistent hypoperfusion will result in hemodynamic derangements end-organ dysfunction cell death death of the patient Hemorrhagic shock is seen most often clinically,

bleeding and resuscitation produce a "whole body" ischemia-reperfusion injury.

Pathophysiology
The physiologic responses to hypovolemia are directed

at preservation of perfusion to the heart and brain

vasoconstriction occurs fluid excretion is curtailed fluid is shifted into the intravascular space

Pathophysiology
The major mechanisms achieving physiologic

response:
(1) prompt increase in cardiac contractility and peripheral vascular tone via the autonomic nervous system (2) hormonal response to preserve salt and intravascular volume (3) changes in the local microcirculation to regulate regional blood flow

Pathophysiology
Compensated phase of shock compensatory mechanisms for small volume blood loss (neuroendocrine response) Decompensation phase of shock cellular dysfunction can be reversed with appropriate volume resuscitation

Pathophysiology
Irreversible phase of shock volume loss continues or volume resuscitation is insufficient vicious physiologic cycle will develop persistent hypoperfusion with low cardiac output sufficient tissue injury and cell death have occurred to this point that continued volume resuscitation fails to reverse the process Vasodilatory response probably represents the common

late phase of all forms of shock, regardless of etiology.

Neuroendocrine Response
The goal of the neuroendocrine response to

hemorrhage:
maintain perfusion to the heart and the brain, even at

the expense of other organ systems

Peripheral vasoconstriction occurs and fluid excretion

is inhibited.

Neuroendocrine Response
Mechanisms: autonomic control of peripheral vascular tone and cardiac contractility hormonal response to stress and volume depletion local microcirculatory mechanisms that are organ specific and regulate regional blood flow

Neuroendocrine Response
The initial stimulus is loss of circulating blood volume

in hemorrhagic shock. The magnitude of the neuroendocrine response is based on both the volume of blood lost and the rate at which it is lost.

Afferent Signals
Afferent impulses transmitted from the periphery are

processed within the central nervous system (CNS) and activate the reflexive effector responses or efferent impulses. The initial inciting event is usually loss of circulating blood volume.

Afferent Signals
Other stimuli that can produce the neuroendocrine

response include
pain hypoxemia

hypercarbia
acidosis infection changes in temperature emotional arousal hypoglycemia

Afferent Signals
Baroreceptors sensitive to changes in both chamber pressure and wall stretch (atria of the heart) activated with low volume hemorrhage or mild reductions in right atrial pressure centrally-mediated constriction of peripheral vessels

Afferent Signals
Chemoreceptors (aorta and carotid bodies) sensitive to changes in oxygen tension, H+ ion concentration, and CO2 levels Stimulation results in: vasodilatation of the coronary arteries slowing of the heart rate vasoconstriction of the splanchnic skeletal circulation inflammatory response, act as afferent impulses and induce a host response (histamine, cytokines, eicosanoids, and endothelins)

Efferent Signals
Cardiovascular Response hemorrhage results in diminished venous return to the heart and decreased cardiac output compensated to increase cadiac output

increased cardiac heart rate and contractility (1-adrenergic receptors) venous and arterial vasoconstriction

Efferent Signals
Increased myocardial oxygen consumption occurs as a

result of the increased workload Myocardial oxygen supply must be maintained or myocardial dysfunction will develop

Forms of Shock
Hemorrhagic or

Hypovolemic Shock Cardiogenic Shock Vasodilatory Shock (Septic Shock)

Vasodilatory Shock (Septic Shock) Neurogenic Shock Obstructive Shock Traumatic Shock

Hemorrhagic or Hypovolemic Shock

The most common cause of shock in the surgical or trauma

patient Acute blood loss results in:

reflexive decreased baroreceptor stimulation from stretch

receptors in the large arteries, resulting in decreased inhibition of vasoconstrictor centers in the brain stem increased chemoreceptor stimulation of vasomotor centers diminished output from atrial stretch receptors
these changes increase vasoconstriction and peripheral

arterial resistance

Hemorrhagic or Hypovolemic Shock

Treatment of shock is initially empiric.
The airway must be secured and volume infusion for

restoration of blood pressure initiated while the search for the cause of the hypotension is pursued. Shock in a trauma patient and postoperative patient should be presumed to be due to hemorrhage until proven otherwise.

Hemorrhagic or Hypovolemic Shock

Clinical signs : cool clammy extremities tachycardia weak or absent peripheral pulses hypotension (25 to 30% loss of the blood volume)

Hemorrhagic or Hypovolemic Shock

Substantial volumes of blood may be lost before the

classic clinical manifestations of shock are evident. When a patient is significantly tachycardiac or hypotensive, this represents both significant blood loss and physiologic decompensation. The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss.

Hemorrhagic or Hypovolemic Shock

Loss of up to 15% of the circulating volume (700 to 750

mL for a 70-kg patient)

may produce little in terms of obvious symptoms

loss of up to 30% of the circulating volume (1.5 L) mild tachycardia tachypnea anxiety hypotension (marked tachycardia [pulse >110 to 120 beats per minute (bpm)], and confusion may not be evident until more than 30% of the blood volume has been lost)

Hemorrhagic or Hypovolemic Shock

loss of 40% of circulating volume (2 L) immediately life threatening generally requires operative control of bleeding
Young healthy patients with vigorous compensatory

mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs despite the presence of significant peripheral hypoperfusion.

Hemorrhagic or Hypovolemic Shock

Factors affecting elderly patients medications that either promote bleeding (e.g., warfarin or aspirin) mask the compensatory responses to bleeding (e.g., beta blockers) atherosclerotic vascular disease diminishing cardiac compliance with age inability to elevate heart rate or cardiac contractility in response to hemorrhage overall decline in physiologic reserve decrease the elderly patient's ability to tolerate hemorrhage

Cardiogenic Shock
Cardiogenic shock is defined clinically as circulatory

pump failure leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume.

Cardiogenic Shock
Hemodynamic criteria include sustained hypotension (SBP <90 mm Hg for at least 30 minutes) reduced cardiac index (<2.2 L/min per square meter) elevated pulmonary artery wedge pressure (>15 mm Hg)

Cardiogenic Shock
Mortality rates for cardiogenic shock are 50 to 80%.
Acute, extensive myocardial infarction (MI) is the

most common cause of cardiogenic shock. Cardiogenic shock is the most common cause of death in patients hospitalized with acute MI.

Cardiogenic Shock
Inadequate cardiac function can be a direct result of

cardiac injury
profound myocardial contusion blunt cardiac valvular injury direct myocardial damage.

The pathophysiology of cardiogenic shock involves a

vicious cycle of myocardial ischemia which causes myocardial dysfunction, which results in more myocardial ischemia.

Cardiogenic Shock
When sufficient mass of the left ventricular wall is

necrotic or ischemic and fails to pump, the stroke volume decreases. Autopsy series of patients dying from cardiogenic shock have found damage to 40% of the left ventricle.

Cardiogenic Shock
Causes of Cardiogenic Shock Acute myocardial infarction Pump failure Mechanical complications
Acute mitral regurgitation

from papillary muscle rupture Ventricular septal defect Free-wall rupture Pericardial tamponade

Right ventricular infarction

Cardiogenic Shock

Other causes of cardiogenic shock End-stage cardiomyopathy Myocarditis Severe myocardial contusion Prolonged cardiopulmonary bypass Septic shock with severe myocardial depression 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

Cardiogenic Shock
Diminished cardiac output or contractility in the face

of adequate intravascular volume (preload) may lead to:

underperfused vascular beds

reflexive sympathetic discharge

decrease coronary artery blood flow accumulation in the pulmonary microcirculatory bed,

decreasing myocardial oxygen delivery even further

Cardiogenic Shock
Other causes of hypotension must be excluded,

including
hemorrhage sepsis pulmonary embolism aortic dissection

Cardiogenic Shock
Signs of circulatory shock include hypotension cool and mottled skin depressed mental status tachycardia diminished pulses. Cardiac exam may include dysrhythmia, precordial

heave, or distal heart tones.

Cardiogenic Shock
Diagnostic Tests: electrocardiogram echocardiography chest radiograph arterial blood gases electrolytes complete blood count cardiac enzymes invasive cardiac monitoring can be useful to exclude right ventricular infarction, hypovolemia, and possible mechanical complications

Cardiogenic Shock
Treatment ensuring that an adequate airway ventilation is sufficient support of the circulation Intubation and mechanical ventilation are often

required, if only to decrease work of breathing and facilitate sedation of the patient. Rapidly excluding hypovolemia and establishing the presence of cardiac dysfunction is essential.

Cardiogenic Shock
Significant dysrhythmias and heart block must be

treated with antiarrhythmic drugs, pacing, or cardioversion if necessary. Early consultation with cardiology is essential in current management of cardiogenic shock, particularly in the setting of acute myocardial infarction.

Cardiogenic Shock
Electrolyte abnormalities, commonly hypokalemia and

hypomagnesemia, should be corrected. Pain is treated with intravenous morphine sulfate or fentanyl.

Cardiogenic Shock
Inotropic support may be indicated to improve cardiac

contractility and cardiac output.

Dobutamine (cardiac 1 receptors)

increase cardiac output vasodilate peripheral vascular beds lower total peripheral resistance lower systemic blood pressure through effects on 2 receptors

Cardiogenic Shock
Dopamine stimulates

receptors (vasoconstriction) 1 receptors (cardiac stimulation) 2 receptors (vasodilation)

Dopamine may be preferable to dobutamine in

treatment of cardiac dysfunction in hypotensive patients. Tachycardia and increased peripheral resistance from dopamine infusion may worsen myocardial ischemia.

Cardiogenic Shock
Epinephrine increase cardiac contractility and heart rate may have intense peripheral vasoconstrictor effects that impair further cardiac performance Catecholamine infusions must be carefully controlled to maximize coronary perfusion, while minimizing myocardial oxygen demand

Cardiogenic Shock
The phosphodiesterase inhibitors amrinone and

milrinone may be required on occasion in patients with resistant cardiogenic shock

long half-lives

induce thrombocytopenia and hypotension

use is reserved for patients unresponsive to other

treatment

Cardiogenic Shock
Preservation of existing myocardium and preservation

of cardiac function are priorities of therapy for patients who have suffered an acute myocardial infarction.

Cardiogenic Shock
Summary in improving cardiac function to prevent

further cardiac complications:

ensuring adequate oxygenation and oxygen delivery maintaining adequate preload with judicious volume

restoration minimizing sympathetic discharge through adequate relief of pain correcting electrolyte imbalances

Cardiogenic Shock
Anticoagulation and aspirin given for acute myocardial infarction thrombolytic therapy reduces mortality in patients with acute myocardial infarction role in cardiogenic shock is less clear

Cardiogenic Shock
Additional pharmacologic tools : -blockers to control heart rate and myocardial oxygen consumption nitrates to promote coronary blood flow through vasodilatation ACE inhibitors to reduce ACE-mediated vasoconstrictive effects that increase myocardial workload and myocardial oxygen consumption

Cardiogenic Shock
Current guidelines of the American Heart Association

recommend percutaneous transluminal coronary angiography for patients with cardiogenic shock, ST elevation, left bundle-branch block, and age less than 75 years. When feasible, PTCA (generally with stent placement) is the treatment of choice. Coronary artery bypass grafting seems to be more appropriate for patients with multiple vessel disease or left main coronary artery disease.

Vasodilatory Shock (Septic Shock)

In the peripheral circulation, profound

vasoconstriction is the typical physiologic response to arterial pressure that is insufficient for tissue perfusion, usually causing cardiogenic or hemorrhagic shock. In vasodilatory shock, hypotension results from failure of the vascular smooth muscle to constrict appropriately.

Vasodilatory Shock (Septic Shock)

Vasodilatory shock peripheral vasodilatation with resultant hypotension resistance to treatment with vasopressors despite the hypotension, plasma catecholamine levels are elevated and the renin-angiotensin system is activated in vasodilatory shock

Vasodilatory Shock (Septic Shock)

The most frequently encountered form of vasodilatory

shock is septic shock. Final common pathway for profound and prolonged shock of any etiology.

Vasodilatory Shock (Septic Shock)

Causes of Vasodilatory Shock

Sepsis
prolonged and severe hypotension hemorrhagic shock cardiogenic shock cardiopulmonary bypass inadequate tissue oxygenation

hypoxic lactic acidosis

carbon monoxide poisoning

Vasodilatory Shock (Septic Shock)

Other causes of vasodilatory shock hypoxic lactic acidosis carbon monoxide poisoning decompensated and irreversible hemorrhagic shock terminal cardiogenic shock postcardiotomy shock

Vasodilatory Shock (Septic Shock)

Septic shock by-product of the body's response to invasive or severe localized infection, typically from bacterial or fungal pathogens in attempt to eradicate the pathogens

enhance macrophage and neutrophil killing effector mechanisms increase procoagulant activity and fibroblast activity to localize the invaders increase microvascular blood flow to enhance delivery of killing forces to the area of invasion

Vasodilatory Shock (Septic Shock)

Septic shock When this response is overly exuberant or becomes systemic rather than localized, manifestations of sepsis may be evident.

enhanced cardiac output peripheral vasodilation fever leukocytosis hyperglycemia tachycardia

Vasodilatory Shock (Septic Shock)

Septic shock vasodilatory effects are due in part to the upregulation of the inducible isoform of nitric oxide synthase (iNOS or NOS 2) in the vessel wall. iNOS produces large quantities of nitric oxide for sustained periods of time. This potent vasodilator suppresses vascular tone and renders the vasculature resistant to the effects of vasoconstricting agents.

Vasodilatory Shock (Septic Shock)

Sepsis evidence of an infection systemic signs of inflammation (e.g., fever, leukocytosis, and tachycardia) Severe sepsis. hypoperfusion with signs of organ dysfunction

Vasodilatory Shock (Septic Shock)

Septic shock requires the presence of the above associated with more significant evidence of tissue hypoperfusion and systemic hypotension maldistribution of blood flow and shunting in the microcirculation further compromise delivery of nutrients to the tissue beds

Vasodilatory Shock (Septic Shock)

Prompt the initiation of treatment is needed before

bacteriologic confirmation of an organism or the source of an organism is identified.

Vasodilatory Shock (Septic Shock)

Diagnosis: thorough physical exam inspection of all wounds evaluation of intravascular catheters or other foreign bodies obtaining appropriate cultures adjunctive imaging studies as needed

Vasodilatory Shock (Septic Shock)

Treatment assessment of the adequacy of their airway and ventilation intubation is required for severely obtunded patients and patients whose work of breathing is excessive to prevent respiratory collapse fluid resuscitation and restoration of circulatory volume with balanced salt solutions is essential

Vasodilatory Shock (Septic Shock)

Treatment Empiric antibiotics based on the most likely pathogens (gram-negative rods, gram-positive cocci, and anaerobes) Antibiotics should be tailored to cover the responsible organisms once culture data are available, and if appropriate, the spectrum of coverage narrowed

Vasodilatory Shock (Septic Shock)

Treatment Long-term empiric broad-spectrum antibiotic use should be minimized to reduce the development of resistant organisms, and to avoid the potential complications of fungal overgrowth and antibioticassociated colitis from overgrowth of Clostridium difficile

Vasodilatory Shock (Septic Shock)

After first-line therapy of the septic patient with

antibiotics, intravenous fluids, and intubation if necessary, vasopressors may be necessary to treat patients with septic shock. Catecholamines are the vasopressors used most often.

Vasodilatory Shock (Septic Shock)

Occasionally, patients with septic shock will develop

arterial resistance to catecholamines. Arginine vasopressin, a potent vasoconstrictor, is often efficacious in this setting. Hyperglycemia and insulin resistance are typical in critically-ill and septic patients, including patients without underlying diabetes mellitus.

Neurogenic Shock
Neurogenic shock refers to diminished tissue

perfusion as a result of loss of vasomotor tone to peripheral arterial beds. Loss of vasoconstrictor impulses results in
increased vascular capacitance
decreased venous return decreased cardiac output

Neurogenic Shock
Neurogenic shock is usually secondary to spinal cord

injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone.

Neurogenic Shock
Rarely, a spinal cord injury without bony fracture, such

as an epidural hematoma impinging on the spinal cord, can produce neurogenic shock.

Neurogenic Shock
Sympathetic input to the heart is disrupted: increased heart rate and cardiac contractility input to the adrenal medulla, which increases catecholamine release Preventing the typical reflex tachycardia that occurs

with hypovolemia.

Neurogenic Shock
Acute spinal cord injury results in activation of

multiple secondary injury mechanisms:

(1) vascular compromise to the spinal cord with loss of autoregulation, vasospasm, and thrombosis (2) loss of cellular membrane integrity and impaired energy metabolism (3) neurotransmitter accumulation and release of free radicals

Neurogenic Shock
Management of acute spinal cord injury with attention

to blood pressure control, oxygenation, and hemodynamics, essentially optimizing perfusion of an already ischemic spinal cord, seems to result in improved neurologic outcome.

Neurogenic Shock
Acute spinal cord injury bradycardia hypotension cardiac dysrhythmias reduced cardiac output decreased peripheral vascular resistance

Neurogenic Shock
The classic description of neurogenic shock decreased blood pressure associated with bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge) warm extremities (loss of peripheral vasoconstriction) motor and sensory deficits indicative of a spinal cord injury radiographic evidence of a vertebral column fracture

Neurogenic Shock
Treatment secure airway and ventilation fluid resuscitation restoration of intravascular volume Most patients with neurogenic shock will respond to

restoration of intravascular volume alone, with satisfactory improvement in perfusion and resolution of hypotension.

Neurogenic Shock
Administration of vasoconstrictors will improve peripheral vascular tone decrease vascular capacitance increase venous return It should only be considered once hypovolemia is

excluded as the cause of the hypotension, and the diagnosis of neurogenic shock established.

Obstructive Shock
Reduced filling of the right side of the heart results in

decreased cardiac output associated with increased central venous pressure.

increased intrapleural pressure secondary to air

accumulation (tension pneumothorax) increased intrapericardial pressure precluding atrial filling secondary to blood accumulation (cardiac tamponade)

Obstructive Shock
The diagnosis of tension pneumothorax should be

made on clinical examination. The classic findings:

respiratory distress (in an awake patient) hypotension diminished breath sounds over one hemithorax hyperresonance to percussion

jugular venous distention

shift of mediastinal structures to the unaffected side

with tracheal deviation.

Obstructive Shock
In most instances, empiric treatment with pleural

decompression is indicated rather than delaying to wait for radiographic confirmation. When a chest tube cannot be immediately inserted, such as in the prehospital setting, the pleural space can be decompressed with a large caliber needle. Immediate return of air should be encountered with rapid resolution of hypotension.

Obstructive Shock
Unfortunately, not all of the clinical manifestations of

tension pneumothorax may be evident on physical exam. Hyperresonance may be difficult to appreciate in a noisy resuscitation area. Jugular venous distention may be absent in a hypovolemic patient. Tracheal deviation is a late finding and often not apparent on clinical examination.

Obstructive Shock
Three findings are sufficient to make the diagnosis of

tension pneumothorax:
respiratory distress or hypotension decreased lung sounds hypertympany to percussion

Chest x-ray findings deviation of mediastinal structures depression of the hemidiaphragm hypo-opacification with absent lung markings

Obstructive Shock
Definitive treatment of a tension pneumothorax is

immediate tube thoracostomy

Obstructive Shock
Chest tube should be inserted rapidly, but carefully,

and should be large enough to evacuate any blood that may be present in the pleural space. Fourth intercostal space (nipple level) at the anterior axillary line.

Obstructive Shock
Cardiac tamponade may also be associated with Dyspnea Orthopnea Cough peripheral edema chest pain Tachycardia muffled heart tones jugular venous distention elevated central venous pressure.

Obstructive Shock
Beck's triad hypotension muffled heart tones neck vein distention Absence of these clinical findings may not be

sufficient to exclude cardiac injury and cardiac tamponade.

Obstructive Shock
Invasive hemodynamic monitoring elevated central venous pressure pulsus paradoxus (i.e., decreased systemic arterial pressure with inspiration) elevated right atrial and right ventricular pressure by pulmonary artery catheter are present. (These hemodynamic profiles suffer from lack of specificity, the duration of time required to obtain them in critically-injured patients, and their inability to exclude cardiac injury in the absence of tamponade)

Obstructive Shock
Chest radiographs may provide information on the

possible trajectory of a projectile, but rarely are diagnostic since the acutely filled pericardium distends poorly. Echocardiography has become the preferred test for the diagnosis of cardiac tamponade.

Obstructive Shock
Pericardiocentesis to diagnose pericardial blood and

potentially relieve tamponade may be utilized. Pericardiocentesis under ultrasound guidance

safer and more reliable

Indwelling catheter may be placed for several days in patients with chronic pericardial effusions.

Obstructive Shock
Needle pericardiocentesis may not evacuate clotted

blood and has the potential to produce cardiac injury, making it a poor alternative in busy trauma centers.

Traumatic Shock
Different physiologic insult than simple hemorrhagic

shock Multiple organ failure, including acute respiratory distress syndrome (ARDS), develops relatively often in the blunt trauma patient, but rarely after pure hemorrhagic shock (such as a gastrointestinal bleed)

Traumatic Shock
The hypoperfusion deficit in traumatic shock is

magnified by the proinflammatory activation that occurs following the induction of shock

Traumatic Shock
Examples of traumatic shock small volume hemorrhage accompanied by soft tissue injury (femur fracture, crush injury) any combination of hypovolemic, neurogenic, cardiogenic, and obstructive shock that precipitate rapidly progressive proinflammatory activation

Traumatic Shock
Treatment of traumatic shock is focused on correction

of the individual elements in order to diminish the cascade of proinflammatory activation

prompt control of hemorrhage

adequate volume resuscitation to correct oxygen debt

dbridement of nonviable tissue stabilization of bony injuries

appropriate treatment of soft tissue injuries

Endpoints in Resuscitation
Shock is defined as inadequate perfusion to maintain

normal organ function. With prolonged anaerobic metabolism, tissue acidosis and oxygen debt accumulate. Thus the goal in the treatment of shock is restoration of adequate organ perfusion and tissue oxygenation.

Endpoints in Resuscitation
Resuscitation is complete when oxygen debt is repaid,

tissue acidosis is corrected, and aerobic metabolism restored. Hemorrhagic shock, septic shock, and traumatic shock are the most common types of shock encountered on surgical services.

Endpoints in Resuscitation
To optimize outcome in bleeding patients, early

control of the hemorrhage and adequate volume resuscitation, including both red blood cells and crystalloid solutions, are necessary.

Endpoints in Resuscitation
Expedient operative resuscitation is mandatory to

limit the magnitude of activation of multiple mediator systems and to abort the microcirculatory changes, which may evolve insidiously into the cascade that ends in irreversible hemorrhagic shock.

Use of Blood in Transfusion

Volume resuscitation in the trauma patient requires

restoration of intravascular volume and repletion of sufficient oxygen-carrying capacity with red blood cell transfusion. Delay of transfusion of red blood cells in the activelybleeding trauma patient would be expected to increase mortality.

Use of Blood in Transfusion

In contrast, blood transfusion carries inherent risks

including transfusion reaction, infection, and immunosuppression.

Thank You!
Reference: Schwartzs Principles of Surgery 9th Edition