Shock

Dr Yohannis C.(Assistant Professor of General Surgery)

Prepared for:C1 Medical students

September,2024
JUMC,Jimma,Ethiopia
Outline
• Overview
• Pathophysiology
• Clinical approach
• General Management Principle
• Types of shock
• End points of Resuscitation
• References
Overview
• Shock, regardless of the etiology, is the failure to meet the metabolic needs of the cell
and the consequences that ensue
• Modern definition: inadequate tissue perfusion marked by decreased delivery of required metabolic
substrates and inadequate removal of cellular waste products

• Six types of shock:

• Hypovolemic
• Septic (vasodilatory)
• Neurogenic
• Cardiogenic
• Obstructive
• Pulmonary embolism, tension pneumothorax, and cardiac tamponade
• Traumatic shock
Pathophysiology of Shock
• The initial physiologic responses in shock are driven by tissue
hypoperfusion and the developing cellular energy deficit

• This imbalance between cellular supply and demand leads to

neuroendocrine and inflammatory responses.

• Many of the organ-specific responses are aimed at maintaining perfusion

in the cerebral and coronary circulation
Cont.
Cont.
3 phases of shock
• Compensated phase: compensation though the neuroendocrine
response
• Decompensated phase: cellular death and ongoing tissue injury
• Microcirculatory dysfunction, parenchymal tissue damage, and inflammatory
cell activation
• The “vicious cycle of shock”
• Irreversible phase: hemodynamic derangements and cardiovascular
collapse as a result of persistent hypoperfusion
Cont.
• The “vicious cycle of shock”
• Regardless of the etiology, decreased tissue perfusion and shock results in a
feed-forward loop that can exacerbate cellular injury and tissue dysfunction
Cont.
• Types of responses
• Neuroendocrine response
• SNS
• Hormonal (cortisol, glucagon, RAAS, ADH)
• Immunologic and inflammatory response
Neuroendocrine responses to shock
• The goal of the neuroendocrine response to shock is to maintain
perfusion to the heart and the brain.

• The mechanisms include:

• 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
Cont.
• Afferent impulses transmitted from the periphery are processed within the
CNS and activate the reflexive effector responses or efferent impulses

• The effector responses are designed to expand plasma volume, maintain

peripheral perfusion and tissue O2 delivery, and restore homeostasis
Afferent Signals
• Afferent stimuli
• Baroreceptors
• Loss of circulating blood volume
• Chemoreceptors
• Hypoxemia
• Hypercarbia
• Acidosis
• Osmoreceptors
• Osmolality
• Pain receptors
• Pain
• Change in temperature
• Hypoglycemia
• Emotional arousal
• Infection/inflammation
• Mediated by a variety of protein and nonprotein mediators that are produced at the site of injury
• Cytokines, histamine, eicosanoids, and endothelins
Efferent Signals
• Neural responses
• Hormonal responses
• Immune and inflammatory responses
Immune and inflammatory responses to shock
Effects of Shock
• Cellular Hypoperfusion
• Microcirculations are affected
• Vasoconstrictions
• Capillary dysfunction
• Metabolic effects-glycolysis,gluconeogenesis,lipolysis,insulin
resistance.
Summary of Hemodynamic responses
Clinical approach to shock
• Symptoms
• History that suggests the cause
• Volume loss, infection, trauma, cardiac illness, anaphylaxis
• Orthostatic light headedness
• Weakness
Cont.
• Signs
• PR
• Usually elevated (bradycardia in neurogenic shock)
• Decrease in pulse volume
• Pulsus paradoxus
• Decrease in SBP with inspiration (Present in cardiac tamponade)
• BP
• Orthostatic hypotension
• Fall in DBP >15 to 20 mm Hg when the patient is sitting or standing
• Hypotension
• Shock may occur with a normal BP, and hypotension may occur without shock
• Shock index (HR/SBP): elevated in volume loss and LV dysfunction (normal is 0.5 to 0.7)
• RR
• Elevated
• Tempreature
• Hypothermia or fever
Cont.
• Splanchnic organs
• Respiratory system • Ileus
• Tachypnea
• Increased MV and dead space
• GI bleeding
• Respiratory failure • Acute cholecystitis
• ARDS • Mesenteric ischemia
• Cardiovascular system • Pancreatitis
• Neck veins…..distended or flattened • Renal
• Tachycardia and week pulse
• Decreased GFR and oliguria
• Decreaed capillary refill
• Muffled heart sounds
• Arrhythmias
• Murmurs
Cont.
• Skin
• Pallor
• Duskiness/cyanosis
• Sweating
• Altered temperature
• MSS
• Ischemia/gangrene
• CNS
• Restlessness, disorientation, confusion, coma
General Management Principle
• Core principles in the management of the critically ill or injured patient
include:
• Definitive control of the airway
• Control of active hemorrhage
• Volume resuscitation with blood products (red blood cells, plasma, and platelets)
with limited volume of crystalloid
• Excessive fluid resuscitation may exacerbate bleeding
Mgt..
• Establish airway and deliver oxygen
• Secure venous access with large bore cannula and start infusion of fluids
• Patient positioning
• Prevention of hypothermia
• Correcting acid-base and electrolyte disturbances
• DVT prophylaxis (for high risk patients)
• GI prophylaxis
• Analgesics (preferably IV narcotics)
• Treatment of specific causes of shock
Monitoring
• Minimum
• Electrocardiogram
• Pulse oximetry
• Blood pressure
• Urine output

• Additional modalities
• Invasive blood pressure
• Central venous pressure
• Base deficit and serum lactate
• Cardiac output
Specific Types of shock
Hypovolemic/Hemorrhagic
• The most common cause of shock in the surgical or trauma patient
• Shock in a trauma patient or postoperative patient should be presumed to be due to
hemorrhage until proven otherwise

• Etiology
• Non-haemorrhagic
• Poor fluid intake
• Excessive fluid loss
• Vomiting, diarrhoea, urinary loss (e.g. diabetes)
• Third-spacing
• Hemorrhagic
• Most common cause of shock in the surgical or trauma patient
• Trauma: external, intrathoracic, intra-abdominal, retroperitoneal, and long bone fractures
• Non-trauma: GI bleeding, hemoptysis, urinary tract bleeding, and gynecologic bleeding
Cont.
• The clinical signs of shock may be evidenced by agitation, cool clammy
extremities, tachycardia, weak or absent peripheral pulses, and
hypotension
• Such apparent clinical shock results from at least 25% to 30% loss of the blood
volume
• However, substantial volumes of blood may be lost before the classic clinical
manifestations of shock are evident
• This is especially true in young healthy patients with vigorous compensatory mechanisms
• Elderly patients have an overall poor physiologic reserve
• They may also be taking medications that either promote bleeding (e.g., warfarin or aspirin) or
mask the compensatory responses to bleeding (e.g., β-blockers)
Cont.
Cont.
• Evaluation
• Clinical examination
• A systolic blood pressure (SBP) of less than 110 mmHg is a clinically relevant definition of
hypotension and hypoperfusion
• Hematocrit
• It must be noted that lack of a depression in the initial hematocrit does not rule out substantial
blood loss or ongoing bleeding
• Lactate and base deficit
• Serum lactate and base deficit are measurements that are helpful to both estimate and monitor
the extent of bleeding and shock
Cont.
• Treatment
• Secure the airway and provide adequate ventilation
• Control the source of blood loss (ASAP)
• The probability of death is increased by approximately 1% for each 3 minutes in the emergency
department in patients requiring emergency laparatomy
• Attempts to stabilize an actively bleeding patient anywhere but in the OR are inappropriate
• IV volume resuscitation
• Damage control resuscitation
• Begins in the emergency department, continues into the OR, and into the ICU
• Initial resuscitation is limited to keep SBP around 80 to 90 mmHg for penetrating and around 110 mmHg for
blunt injuries (to prevent secondary TBI) - “Hypotensive resuscitation”
• This prevents renewed bleeding from recently clotted vessels
• Warm patients and prevent coagulopathy
• Treat electrolyte and acid-base disturbances
• Control pain
Septic Shock (Vasodilatory Shock)
• Vasodilatory shock is characterized by peripheral vasodilation with
resultant hypotension and resistance to treatment with vasopressors

• It is the result of dysfunction of the endothelium and vasculature

secondary to circulating inflammatory mediators or as a response to
prolonged and severe hypoperfusion
• Vasodilatory shock seems to represent the final common pathway for profound and
prolonged shock of any etiology
Cont.
• Causes of septic and vasodilatory shock
• Systemic response to infection (the most frequently encountered form of vasodilatory
shock)
• Non-infectious systemic inflammation
• Pancreatitis
• Burns
• Anaphylaxis
• Prolonged, severe hypotension
• Hemorrhagic shock
• Cardiogenic shock
• Metabolic
• Hypoxic lactic acidosis
• Carbon monoxide poisoning
• Acute adrenal insufficiency
Cont.
• Septic shock is a by-product of the body’s response to disruption of the
host-microbe equilibrium, resulting in invasive or severe localized
infection

• Despite advances in intensive care, the mortality rate for severe sepsis
remains at 30% to 50%
Cont.
• Definitions
• SIRS (≥2 of the following)
• Temp (core) >38°C or <36°C
• Heart rate >90 beats/min
• RR >20 breaths/min for patients spontaneously ventilating or a PaCO2 <32 mm
Hg
• WBC count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature (band)
cells in the peripheral blood smear
• Sepsis
• SIRS with a clearly established focus of infection
Cont.
• Severe Sepsis
• Sepsis associated with organ dysfunction and hypoperfusion
• Systolic blood pressure <90 mm Hg
• >40 mm Hg fall from normal systolic blood pressure
• Acute mental status changes
• Oliguria
• Lactic acidemia
• Septic shock
• Severe sepsis plus
• No response for iv fluid infusion (for at least 1 hr)
• Requiring inotropes or vasoactive agents to maintain SBP ≥90 mmHg or MABP ≥70
mmHg
Sequential organ failure assessment
qSOFA
Cont.
• qSOFA
• Provides simple bedside criteria to identify adult patients with suspected
infection who are likely to have poor outcomes
• Criteria (≥2)
• GCS score of ≤13
• SBP of ≤100 mm Hg
• Respiratory rate of ≥22/min
Cont.
• Sources of infection
• Respiratory (38%)
• Urinary tract (21%)
• Intra-abdominal (16.5%)
• Device (1.3%)
• CNS (0.8%)
• Others (11.3%)
Treatment of Septic shock
• Management of airway and breathing
• Severely obtunded patients and patients whose work of breathing is excessive require
intubation and ventilation to prevent respiratory collapse
• Fluid resuscitation
• It should be at least 30 mL/kg within the first 4 to 6 hours
• Empiric IV antibiotics
• Should be started within the first hour of recognition of severe sepsis
• Mortality increases by 7.6% for each hour delay to appropriate antibiotics
• Source control
• Drainage of infected fluid collections, removal of infected foreign bodies, debridement of
devitalized tissue, and removal/resection of infected organs
Cont.
• Vasopressors
• To maintain MABP ≥65 mmHg
• Catecholamines are the vasopressors used most often, with norepinephrine being the
first-line agent followed by epinephrine
• Dobutamine therapy is recommended for patients with cardiac dysfunction
• Dopamine should not be used for “renal protection”
• Steroids
• Severe sepsis often is associated with adrenal insufficiency or glucocorticoid receptor
resistance
• If SBP remains less than 90 mmHg despite appropriate fluid and vasopressor therapy,
hydrocortisone at 200 mg/d for 7 days in four divided doses or by continuous infusion
should be considered (dose ≤300 mg/d)
Cont.
• Management of end organ dysfunction
• ARDS (Use of lower ventilatory tidal volumes, higher levels of PEEP, alveolar recruitment
maneuvers, and prone positioning)
• Tight glucose management
• Maintenance of blood glucose between 80 and 110 mg/dL (upper blood glucose target of 180 mg/dL)
• Transfusion
• RBCs: when hemoglobin decreases to 7 g/dL
• FFP: when there is bleeding or planned invasive procedures
• Platelets
• Counts are <5000/mm3 regardless of bleeding
• Counts are 5000–30,000/mm3 and there is significant bleeding risk
• Any number with bleeding
• DVT and GI prophylaxis
• Pain control
• Counseling
Cardiogenic Shock
• Defined clinically as circulatory pump failure leading to diminished forward
flow and subsequent tissue hypoxia, in the setting of adequate intravascular
volume

• Hemodynamic criteria include:

• Sustained hypotension (i.e., SBP <90 mmHg for at least 30 minutes)
• Elevated pulmonary artery wedge pressure (>15 mmHg)
• Reduced cardiac index (<2.2 L/min per square meter)

• Other causes of hypotension must be excluded

• Mortality rates for are 50% to 80%

Cont.
• Acute, extensive MI is the most common cause of cardiogenic shock
• Other causes
• VHD
• Arrhythmia
• End-stage cardiomyopathy
• Myocarditis
• Severe myocardial contusion
Cont.
• Treatment
• Maintenance of adequate oxygenation
• To ensure adequate myocardial O2 delivery
• Judicious fluid administration
• To avoid fluid overload and development of cardiogenic pulmonary edema
• Inotropic support
• May be indicated to improve cardiac contractility and cardiac output
• Dopamine may be preferable to dobutamine
• Correction of electrolyte abnormalities
• Commonly hypokalemia and hypomagnesemia
• Adequate treatment of pain
• To minimize sympathetic discharge
Obstructive Shock
• Due to etiologies that result in mechanical obstruction of venous return
• Tension pneumothorax
• Pericardial tamponade
• Pulmonary embolus
• IVC obstruction
• Deep venous thrombosis
• Gravid uterus on IVC
• Neoplasm
• Increased intrathoracic pressure
• Excess positive end-expiratory pressure
• Neoplasm

• Reduced filling of the right side of the heart results in decreased cardiac output
associated with increased central venous pressure
Cont.
• Tension pneumothorax
• Most common cause of obstructive shock in trauma patients
• Classic clinical findings
• Respiratory distress (in an awake patient)
• Hypotension
• Diminished breath sounds over one hemithorax
• Hyperresonance to percussion (may be difficult to appreciate in a noisy resuscitation area)
• Jugular venous distention (may be absent in a hypovolemic patient)
• Shift of mediastinal structures to the unaffected side with tracheal deviation (is a late finding
and often is not apparent on clinical examination)

• Practically, 3 findings are sufficient to make the diagnosis

• Respiratory distress or hypotension, decreased lung sounds, and hypertympany to percussion
Cont.
• Chest x-ray findings
• Deviation of mediastinal structures
• Depression of the hemidiaphragm
• Hypo-opacification with absent lung markings

• Treatment
• Definitive treatment of a tension pneumothorax is immediate tube
thoracostomy
• Most recommend placement in the fourth intercostal space (nipple level) at the
anterior axillary line
Cont.
• Cardiac tamponade
• It results from the accumulation of blood within the pericardial sac, usually from
penetrating trauma or chronic medical conditions such as heart failure or uremia
• The hemodynamic abnormalities are due to elevation of intracardiac pressures with
resultant decrease in cardiac output
• Acutely, the pericardium does not distend; thus small volumes of blood may produce
cardiac tamponade
• If the effusion accumulates slowly, the quantity of fluid producing cardiac tamponade may reach
2000 mL
• Signs
• Beck’s triad: hypotension, muffled heart tones, and neck vein distention
• Pulsus paradoxus: decreased systemic arterial pressure with inspiration
• Elevated CVP
• Elevated right atrial and right ventricular pressure
Cont.
• Diagnosis
• Echocardiography
• It has become the preferred test for the diagnosis
• Pericardiocentesis
• To diagnose pericardial blood and potentially relieve tamponade
• Diagnostic pericardial window
• It represents the most direct method to determine the presence of blood within the
pericardium
• The procedure is best performed in the operating room under general anesthesia

• Rx-Therapeutic pericardiocentesis
• Pericardiotomy
Traumatic Shock
• In traumatic shock, soft tissue and bony injury leads to the activation
of inflammatory cells and the release of circulating factors (DAMPs)
which are recognized by pattern recognition receptors (PRRs)
• Small-volume hemorrhage accompanied by soft tissue injury or any
combination of the other types of shock that precipitates rapidly
progressive pro-inflammatory activation
• Even simple hemorrhage induces pro-inflammatory activation that
results in many of the cellular changes typically ascribed only to septic
shock
• Attributable to the release of cellular products termed DAMPs
Cont.
• Treatment
• Prompt control of hemorrhage
• Adequate volume resuscitation
• Management of injured tissue
• Stabilization of bony injuries
• Appropriate treatment of soft tissue injuries
• Débridement of non-viable tissue
Neurogenic Shock
• It 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,
and decreased cardiac output

• It 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
• Other causes
• Spinal cord neoplasm
• Spinal/epidural anesthetic

• Hypotension contributes to the worsening of acute spinal cord injury as the result of further
reduction in blood flow to the spinal cord
Cont.
• 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
• With or without radiographic evidence of a vertebral column fracture

• Other causes of shock must be sought and excluded

Cont.
• Difficulties in diagnosis
• Spinal cord injuries often have head injuries that may make identification of motor
and sensory deficits difficult in the initial evaluation
• In the multiply injured patient, other causes of hypotension, including hemorrhage,
tension pneumothorax, and cardiogenic shock may mask neurogenic shock
Cont’d
• Treatment
• Airway and breathing
• Fluid resuscitation
• Most patients with neurogenic shock will respond to restoration of intravascular volume alone
• Vasoconstrictors
• They will improve peripheral vascular tone, decrease vascular capacitance, and increase
venous return
• They should only be considered once hypovolemia is excluded as the cause of the
hypotension
• Stabilize the vertebral fracture
• Restoration of normal blood pressure and adequate tissue perfusion should precede any
operative attempts to stabilize the vertebral fracture
Endpoints in Resuscitation
• The goal in the treatment of shock is restoration of adequate organ
perfusion and tissue oxygenation
• Resuscitation is complete when O2 debt is repaid, tissue acidosis is corrected, and
aerobic metabolism is restored

• Recognition of subclinical hypoperfusion requires information beyond

vital signs and urinary output
• Even with normalization of blood pressure, heart rate, and urine output, 80% to
85% of trauma patients have inadequate tissue perfusion, as evidenced by
increased lactate or decreased mixed venous O2 saturation
Cont.
• Goals of initial resuscitation
• Mean arterial pressure ≥65mmHg
• Urine output ≥0.5 mL/kg/hr
• Central venous pressure 8–12 mmHg
• Central venous or mixed venous oxygen saturation ≥70% or ≥65%, respectively
Cont.
• Endpoints in resuscitation
• Systemic/global
• Vital signs
• Cardiac output
• Oxygen delivery and consumption
• Lactate
• Base deficit
• Tissue specific
• Gastric tonometry
• Tissue pH, oxygen, carbon dioxide levels
• Near infrared spectroscopy
• Cellular
• Membrane potential
• ATP
Cont.
• Surrogate parameters have been sought to estimate the O 2 debt
• Lactate
• It is generated by conversion of pyruvate to lactate by lactate dehydrogenase
in the setting of insufficient O2
• Time interval to normalize the serum lactate is important prognostic
indicators for survival
• Base Deficit
• It usually is measured by arterial blood gas analysis in clinical practice as it
is readily and quickly available
• It may be better predictors of mortality than the plasma lactate alone
References
• Schwartz’s principle of surgery 11th ed.
• Sabiston Textbook of surgery 21th ed.
• Bailey and Love’s short practice of surgery 27 th ed.
• Uptodate 2018