Shock by Karl Tapales

8/2/2019 Shock by Karl Tapales

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Karl Tapales, M.D.Reference:

Schwartz’s Principles of Surgery 9th Edition



Introduction• Shock

• inadequate delivery of oxygen and nutrients to maintainnormal tissue and cellular function

• cellular injury is initially reversible

• irreversible if hypoperfusion is severe and prolonged



Introduction• Clinical manifestations

– stimulation of the sympathetic and neuroendocrinestress 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 theorganism against external forces results in organ andcellular 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 orspinal anesthesia causes vasodilatation (acute loss of sympathetic vascular tone).

• Cardiogenic shock

– failure of the heart as a pump (arrhythmias or acuteheart 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 crystalloidsolution must occur while operative control of bleeding isachieved

(4) unrecognized or inadequately corrected hypoperfusionincreases morbidity and mortality

(5) both inadequate and uncontrolled volume resuscitation areharmful.



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 andinflammatory 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 andperipheral vascular tone via the autonomic nervoussystem

(2) hormonal response to preserve salt and intravascular volume

(3) changes in the local microcirculation to regulateregional 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 thispoint that continued volume resuscitation fails to reverse theprocess

• Vasodilatory response probably represents the commonlate 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 atthe expense of other organ systems

• Peripheral vasoconstriction occurs and fluid excretionis inhibited.



Neuroendocrine Response• Mechanisms:

autonomic control of peripheral vascular tone andcardiac contractility

hormonal response to stress and volume depletion

local microcirculatory mechanisms that are organspecific 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 isbased 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 efferentimpulses.

• The initial inciting event is usually loss of circulatingblood volume.



Afferent Signals Other stimuli that can produce the neuroendocrine

response includepain

hypoxemiahypercarbia

acidosis

infection

changes in temperatureemotional arousal

hypoglycemia



Afferent Signals Baroreceptors

• sensitive to changes in both chamber pressure and wallstretch (atria of the heart)

• activated with low volume hemorrhage or mildreductions in right atrial pressure

• centrally-mediated constriction of peripheral vessels



Afferent Signals• Chemoreceptors (aorta and carotid bodies)

• sensitive to changes in oxygen tension, H+ ionconcentration, 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 theheart 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 ormyocardial dysfunction will develop



Forms of Shock Hemorrhagic orHypovolemic 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 stretchreceptors in the large arteries, resulting in decreasedinhibition of vasoconstrictor centers in the brain stem

• increased chemoreceptor stimulation of vasomotor centers

• diminished output from atrial stretch receptors

these changes increase vasoconstriction and peripheralarterial resistance



Hemorrhagic or Hypovolemic Shock• Treatment of shock is initially empiric.

• The airway must be secured and volume infusion forrestoration of blood pressure initiated while the searchfor the cause of the hypotension is pursued.

• Shock in a trauma patient and postoperative patientshould 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 orhypotensive, this represents both significant bloodloss 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 120beats per minute (bpm)], and confusion may not beevident until more than 30% of the blood volume hasbeen 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 thepresence of significant peripheral hypoperfusion.



Hemorrhagic or Hypovolemic Shock• Factors affecting elderly patientsmedications that either promote bleeding (e.g., warfarin

or aspirin)

mask the compensatory responses to bleeding (e.g., betablockers)

atherosclerotic vascular disease

diminishing cardiac compliance with age

inability to elevate heart rate or cardiac contractility inresponse to hemorrhage

overall decline in physiologic reserve decrease theelderly patient's ability to tolerate hemorrhage



Cardiogenic Shock• Cardiogenic shock is defined clinically as circulatory

pump failure leading to diminished forward flow andsubsequent tissue hypoxia, in the setting of adequate

intravascular volume.



Cardiogenic Shock• Hemodynamic criteria include

sustained hypotension (SBP <90 mm Hg for at least 30minutes)

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 themost common cause of cardiogenic shock.

• Cardiogenic shock is the most common cause of deathin 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 causesmyocardial dysfunction, which results in moremyocardial ischemia.





Cardiogenic ShockCauses of Cardiogenic Shock

Acute myocardial infarction

• Pump failure

• Mechanical complications – Acute mitral regurgitation

from papillary musclerupture

– Ventricular septal defect

–

Free-wall rupture – Pericardial tamponade

• Right ventricular infarction



Cardiogenic ShockOther causes of cardiogenicshock

• End-stage cardiomyopathy • Myocarditis• Severe myocardial contusion• Prolonged cardiopulmonary

bypass• Septic shock with severe

myocardial depression• Left ventricular outflow

obstruction – Aortic stenosis –

Hypertrophic obstructivecardiomyopathy

• Obstruction to left ventricularfilling – 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 leadto:

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, precordialheave, or distal heart tones.



Cardiogenic Shock• Diagnostic Tests:electrocardiogram

echocardiography

chest radiographarterial blood gases

electrolytes

complete blood count

cardiac enzymes invasive cardiac monitoring can be useful to exclude

right ventricular infarction, hypovolemia, and possiblemechanical complications



Cardiogenic Shock• Treatment

ensuring that an adequate airway

ventilation is sufficient

support of the circulation

• Intubation and mechanical ventilation are oftenrequired, 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, orcardioversion if necessary.

• Early consultation with cardiology is essential incurrent 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 orfentanyl.



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 Epinephrine

increase cardiac contractility and heart rate

may have intense peripheral vasoconstrictor effects thatimpair 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 othertreatment



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 volumerestoration

minimizing sympathetic discharge through adequaterelief of pain

correcting electrolyte imbalances



Cardiogenic Shock• Anticoagulation and aspirin

given for acute myocardial infarction

thrombolytic therapy reduces mortality in patients withacute myocardial infarction

role in cardiogenic shock is less clear



Cardiogenic Shock• Additional pharmacologic tools :

-blockers to control heart rate and myocardial oxygenconsumption

nitrates to promote coronary blood f low through vasodilatation

ACE inhibitors to reduce ACE-mediated vasoconstrictiveeffects 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 than75 years.

• When feasible, PTCA (generally with stent placement)is the treatment of choice.

• Coronary artery bypass grafting seems to be moreappropriate for patients with multiple vessel disease orleft main coronary artery disease.



Vasodilatory Shock (Septic Shock)• In the peripheral circulation, profound

vasoconstriction is the typical physiologic response toarterial pressure that is insufficient for tissue

perfusion, usually causing cardiogenic or hemorrhagicshock.

• In vasodilatory shock, hypotension results from failureof 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 levelsare elevated and the renin-angiotensin system isactivated in vasodilatory shock



Vasodilatory Shock (Septic Shock)• The most frequently encountered form of vasodilatory

shock is septic shock .

• Final common pathway for profound and prolongedshock of any etiology.



Vasodilatory Shock (Septic Shock)• Causes of Vasodilatory Shock

Sepsis

prolonged and severe hypotension

hemorrhagic shock

cardiogenic shock

cardiopulmonary bypass

inadequate tissue oxygenationhypoxic 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 severelocalized infection, typically from bacterial or fungal

pathogens in attempt to eradicate the pathogens

• enhance macrophage and neutrophil killing effectormechanisms

• increase procoagulant activity and fibroblast activity tolocalize the invaders

• increase microvascular blood flow to enhance delivery of killing forces to the area of invasion




• When this response is overly exuberant or becomessystemic rather than localized, manifestations of sepsis

may be evident. enhanced cardiac output

peripheral vasodilation

fever

leukocytosis hyperglycemia

tachycardia




• 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 vasodilatorsuppresses 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




• requires the presence of the above

• associated with more significant evidence of tissue

hypoperfusion and systemic hypotension

• maldistribution of blood flow and shunting in themicrocirculation 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 thesource of an organism is identified.



Vasodilatory Shock (Septic Shock)• Diagnosis:

• thorough physical exam

• inspection of all wounds

• evaluation of intravascular catheters or other foreignbodies

• 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 patientsand patients whose work of breathing is excessive toprevent respiratory collapse

fluid resuscitation and restoration of circulatory volume

with balanced salt solutions is essential




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




Long-term empiric broad-spectrum antibiotic useshould be minimized to reduce the development of

resistant organisms, and to avoid the potentialcomplications of fungal overgrowth and antibiotic-associated colitis from overgrowth of Clostridiumdifficile



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 incritically-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 toperipheral 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 orhigh 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 spinalcord, 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 ref lex 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, andhemodynamics, essentially optimizing perfusion of an

already ischemic spinal cord, seems to result inimproved 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 cordinjury

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 torestoration of intravascular volume alone, withsatisfactory improvement in perfusion and resolutionof hypotension.



Neurogenic Shock• Administration of vasoconstrictors will

improve peripheral vascular tone

decrease vascular capacitance

increase venous return

• It should only be considered once hypovolemia isexcluded as the cause of the hypotension, and thediagnosis of neurogenic shock established.



Obstructive Shock Reduced filling of the right side of the heart results indecreased cardiac output associated with increasedcentral venous pressure.

increased intrapleural pressure secondary to airaccumulation (tension pneumothorax)

increased intrapericardial pressure precluding atrialfilling 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 spacecan 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 physicalexam.

• Hyperresonance may be difficult to appreciate in anoisy resuscitation area.

• Jugular venous distention may be absent in ahypovolemic patient.

• Tracheal deviation is a late finding and often notapparent 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 structuresdepression of the hemidiaphragm

hypo-opacification with absent lung markings



Obstructive Shock• Definitive treatment of a tension pneumothorax isimmediate tube thoracostomy



Obstructive Shock• Chest tube should be inserted rapidly, but carefully,and should be large enough to evacuate any blood thatmay be present in the pleural space.

• Fourth intercostal space (nipple level) at the anterioraxillary line.



Obstructive Shock• Cardiac tamponade may also be associated withDyspnea

Orthopnea

Coughperipheral 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 besufficient to exclude cardiac injury and cardiactamponade.



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 themin critically-injured patients, and their inability toexclude cardiac injury in the absence of tamponade)



Obstructive Shock• Chest radiographs may provide information on thepossible trajectory of a projectile, but rarely arediagnostic 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 andpotentially relieve tamponade may be utilized.

• Pericardiocentesis under ultrasound guidance

safer and more reliable

• Indwelling catheter

may be placed for several days in patients with chronicpericardial effusions.



Obstructive Shock• Needle pericardiocentesis may not evacuate clottedblood 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 inthe blunt trauma patient, but rarely after purehemorrhagic shock (such as a gastrointestinal bleed)



Traumatic Shock• The hypoperfusion deficit in traumatic shock is

magnified by the proinflammatory activation thatoccurs following the induction of shock



Traumatic Shock Examples of traumatic shock

small volume hemorrhage accompanied by soft tissueinjury (femur fracture, crush injury)

any combination of hypovolemic, neurogenic,cardiogenic, and obstructive shock that precipitaterapidly progressive proinflammatory activation



Traumatic Shock• Treatment of traumatic shock is focused on correction

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

prompt control of hemorrhageadequate volume resuscitation to correct oxygen debt

débridement 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 metabolismrestored.

• Hemorrhagic shock, septic shock, and traumatic shockare the most common types of shock encountered onsurgical services.



Endpoints in Resuscitation• To optimize outcome in bleeding patients, early

control of the hemorrhage and adequate volumeresuscitation, 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 mediatorsystems and to abort the microcirculatory changes,

which may evolve insidiously into the cascade thatends 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 actively-

bleeding trauma patient would be expected to increasemortality.



Use of Blood in Transfusion• In contrast, blood transfusion carries inherent risks

including transfusion reaction, infection, andimmunosuppression.



Thank You!

Reference:Schwartz’s Principles of Surgery 9th Edition

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Shock by Karl Tapales