Shock

Anas As’ad. MD. FACS

Consultant Hepato-Pancreato-Biliary + Transplant Surgery
BAU
Definition

► Shock is defined by global tissue hypoxia and occurs when the supply of
oxygen is insufficient to meet metabolic demands.

► Results in global tissue hypoperfusion and metabolic acidosis

Pathophysiology

► Inadequate systemic oxygen delivery activates autonomic responses to

maintain systemic oxygen delivery.
► Sympathetic nervous system
► NE, epinephrine, dopamine, and cortisol release
► Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac
output)

► Renin-angiotensin axis
► Water and sodium conservation and vasoconstriction
► Increase in blood volume and blood pressure
► Cellular response must switch from aerobic to anaerobic metabolism. The
product of anaerobic respiration is not carbon dioxide but lactic acid that
produces a systemic metabolic acidosis.
► Goal is to maintain cerebral and cardiac perfusion
► Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow
► The metabolic acidosis and increased sympathetic response result in an
increased respiratory rate and minute ventilation to increase the excretion of
carbon dioxide (and so produce a compensatory respiratory alkalosis).
Multiorgan Dysfunction Syndrome (MODS)

► Progression of physiologic effects as shock ensues

► Cardiac depression
► Respiratory distress
► Renal failure
► Liver failure
► DIC
► Result is end organ failure.
Classification and Recognition of Shock

► The patient's recent history, laboratory values, and physical examination are
usually sufficient for determining the etiology.
► Low Cardiac Output status
► Hypovolemic shock
► volume loss
► Internal volume loss

► Cardiac shock
► Primary pump dysfunction
► Impaired outflow
► Low peripheral resistance status
► Neurogenic shock
► Loss of sympathetic tone

► Vasogenic (Distributive) Shock ; In vasogenic shock, this circulatory failure results

from vasodilation. There is vascular hypo reactivity with reduced vascular smooth
muscle contraction in response to α1 adrenergic agonists.
► Septic
► Anaphylactic
Hypovolemic shock

► Results from loss of circulating blood volume caused by acute hemorrhage,

fluid depletion, or dehydration.
► Patients are peripherally vasoconstricted, tachycardic, and have low jugular
venous pressure.
► Decreased JP pressure.
► Hypovolaemia is probably the most common form of shock, and to some
degree is a component of all other forms of shock.
► Non-hemorrhagic
► Vomiting
► Diarrhea
► Bowel obstruction, pancreatitis
► urinary loss (e.g. diabetes)
► Burns
► Neglect, environmental (dehydration poor fluid intake)
► Hemorrhagic
► GI bleed
► Trauma
► Massive hemoptysis, GI bleeding
► AAA rupture
► Ruptured ectopic pregnancy, post-partum bleeding
Treatment

► ABCs
► Establish 2 large bore IVs
► Crystalloids
► Normal Saline or Lactate Ringers
► Up to 3 liters
► PRBCs
► cross matched or O blood group
► Control any bleeding
► Arrange definitive treatment
Evaluation of Hypovolemic Shock
► CBC
► ABG/lactate
► Electrolytes
► BUN, Creatinine
► Coagulation studies
► Type and cross-match
► As indicated
► CXR
► Pelvic x-ray
► Abd/pelvis CT
► Chest CT
► GI endoscopy
► Bronchoscopy
► Vascular radiology
► Therapy focuses on control of ongoing loss and restoration of intravascular
volume.

► Patients with blood losses of up to 20% can be resuscitated using crystalloid

solutions.

► volume replacement requires three times the estimated volume deficit.

Vasogenic (Distributive) shock

► Distributive shock describes the pattern of cardiovascular responses

characterizing a variety of conditions, including septic shock, anaphylaxis and
spinal cord injury.
► Inadequate organ perfusion is accompanied by vascular dilatation with
hypotension, low systemic vascular resistance, inadequate afterload and
resulting with abnormally high cardiac output.
► Patients are peripherally vasodilated and tachycardic.
► Jugular venous pressure is low.
Septic shock

► SEPSIS: is defined as SIRS + documented or presumed infection.

► SIRS requires two of the following:

► Body temperature >38C or <36C
► Heart rate >90 beats/minute
► Respiratory rate >20/minute or Paco2 <32
► WBC count >12 or <4 or >10% bands.
► Severe sepsis: Sepsis + multiple organ dysfunction.
► Septic shock: Severe sepsis + hypoperfusion or hypotension
► Diagnosis: Cultures should be obtained as part of the initial evaluation.
Management

► 1. Infection
► A. Broad-spectrum intravenous antibiotics should be initiated within the first
hour.
► B. Source control, drainage, debridement, or removal of the infectious source
is imperative.

► 2. Circulatory support
► A. Volume resuscitation. volume resuscitation for a CVP of 8 to 12, MAP >65,
UOP >0.5 mL/kg/hour, and mixed SvO2 >70%.
► B. Vasoactive medications: norepinephrine for its vasoconstrictive properties
as well as its ability to increase cardiac output.
Neurogenic shock

► Results from interruption of the spinal cord at or above the thoracolumbar

sympathetic nerve roots, which produces loss of sympathetic tone, causing
vasodilation.
► Warm, flushed, flaccid extremities; paraplegia; confusion; oliguria; and
hypotension are the classic clinical findings.
► Patients are peripherally vasodilated and bradycardia.
► Jugular venous pressure is low.
Treatment

► The initial intervention is volume infusion.

► A peripheral vasoconstrictor, phenylephrine or norepinephrine, is
administered to increase vascular tone if hypotension is refractory to volume
infusion.
► Dopamine is used in patients with neurogenic shock and bradycardia.
Cardiogenic shock

► Cardiogenic shock is due to primary failure of the heart to pump blood to the
tissues.
► Causes of cardiogenic shock include myocardial infarction, cardiac
dysrhythmias, valvular heart disease, blunt myocardial injury and
cardiomyopathy.
► Diagnosis may require ECG and echocardiography.
► These patients typically are peripherally vasoconstricted and tachycardic with
an elevated jugular venous pressure (venous hypertension).
Treatment

► Management is directed toward maintaining adequate myocardial perfusion

and cardiac output with volume expansion and vasoactive medications with
inotropes.
► Dopamine and dobutamine are the drugs of choice to improve cardiac
contractility, with dopamine the preferred agent in patients with
hypotension.
► Initial treatment is often guided by CVP measurements or PA catheter data,
while the precipitating cause is identified and treated.
► If perfusion remains inadequate, the only remaining option is mechanical
circulatory support.
Obstructive shock

► In obstructive shock there is a reduction in preload due to mechanical

obstruction of cardiac filling.
► Caused by PE, tension pneumothorax, or cardiac tamponade.
► Reduced filling of the left and/or right sides of the heart leading to reduced
preload and a fall in cardiac output.
► Jugular venous pressure is elevated while the peripheral tissues demonstrate
vasoconstriction.
Treatment

► Tension pneumothorax is treated by needle decompression thoracostomy,

Followed by chest tube.
► Pericardial tamponade is treated by needle decompression, often with
catheter placement for drainage.
► The treatment of a PE varies based on the degree of hemodynamic
compromise. Options include systemic anticoagulation, thrombolysis, and
surgical clot removal.
Severity of shock
Symptoms and Signs

► Looking ill
► Altered mental status
► Skin cool and mottled or hot and flushed
► Weak or absent peripheral pulses
► SBP <110
► Tachycardia/bradycardia
How to approach?

► ABCs
► Cardiorespiratory monitor
► Pulse oximetry
► Supplemental oxygen
► IV access
► ABG, labs
► Foley catheter
► Vital signs including rectal temperature
How to approach?

► History
► Recent illness
► Fever
► Chest pain, SOB
► Abdominal pain
► Comorbidities
► Medications
► Toxins/Ingestions
► Recent hospitalization or surgery
► Baseline mental status
How to approach?

► Physical examination
► Vital Signs
► CNS – mental status
► Skin – color, temp, rashes, sores
► CV – JVD, heart sounds
► Respiratory – lung sounds, RR, oxygen sat, ABG
► GI – abd pain, rigidity, guarding, rebound
► Renal – urine output
Diagnosis

► Physical exam (VS, mental status, skin color, temperature, pulses, etc)
► Infectious source
► Labs:
► CBC
► Chemistries
► Lactate
► Coagulation studies
► Cultures
► ABG
Further Evaluation

► CT of head/sinuses
► Lumbar puncture
► Wound cultures
► Acute abdominal series
► Abdominal/pelvic CT or US
► Cortisol level
► Fibrinogen, FDPs, D-dimer
Optimizing Circulation

► Isotonic crystalloids
► Titrated to:
► CVP 8-12 mm Hg
► Urine output 0.5 ml/kg/hr (30 ml/hr)
► Improving heart rate
► May require 4-6 L of fluids
► No outcome benefit from colloids
► Goal directed approach
► Urine output > 0.5 mL/kg/hr
► CVP 8-12 mmHg
► MAP 65 to 90 mmHg
► Central venous oxygen concentration > 70%
Questions?

Thank you