Types of Shock

Dr Umme Salma
Department of Surgery
 Objectives

To Recognise and Understand:

▪ Definition
▪ Physiology and pathophysiology
▪ Types
▪ Causes
▪ Resuscitation
▪ Golden hours
 Definition
A life-threatening disorder of the circulatory system that results in inadequate
organ perfusion and tissue hypoxia, leading to metabolic disturbances and, ultimately,
irreversible organ damage

A Physiologic state
Inadequate oxygen delivery to meet metabolic
demand

Reduction of systemic Global tissue hypo-perfusion and metabolic acidosis

tissue perfusion

Decreased tissue
oxygen delivery
General Homeostasis
In shocked State
Cell death

End organ damage

Multi-system organ
failure

Death
Pathophysiology
• Oxygen delivery is the function of the
circulatory system

• This system is basically:

• - Pump (heart)
• - Pipes (vessels)
• - Solution (blood)

• Needs to function at adequate pressure,

volume and carrying capacity
 Pathophysiology
• Changes at Cellular Level
• Change from aerobic to anaerobic
metabolism

• Production of……..Lactic Acid

• Metabolic Acidosis
 Later glucose exhausted
Cessation of anaerobic respiration

Failure of Na+ / K+ pump

in cell membranes & organelles

Lysosymes release auto digestive enzymes ….. Cell lysis

Inc K+ in circulation …. Hyperkalemia

At Microvascular level…
Tissue
Hypoxia/ Tissue ischemia
Acidosis

Activate complement system & prime

neutrophils to release Oxygen FR and Activation of immune and
cytokines coagulation system

Damaged endothelium…leaky
capillaries
 Changes at Systemic Level

Inc CO2 production  Inc Dec preload  increase

Resp rate & Minute sympathetic release  VC and
ventilation  Resp Alkalosis CVS tachycardia

Resp
Dec. perfusion  Dec Urine
OP and activation of Renin
Link:
Renal Angiotensis Axis Inc
sodium and water
Pathophysiology of shock reabsorption
Ischemia- Reperfusion syndrome
During ischemia….
• Tissue hypoxia and local activation of inflammation Cellular and organ damage progresses

• Once normal circulation is restored after initial insult

Further injury
• Acid and potassium load that has built up  direct myocardial depression, vascular
dilatation and further hypotension.

• Cellular and humoral elements* activated by the hypoxia are flushed back into the
circulation  further endothelial injury to organs  Acute lung injury, acute renal injury,
multiple organ failure and death

• Reperfusion injury can be reduced by decreasing the extent and duration

of tissue hypoperfusion
Clinically
• The goal of the body response….
• Maintain perfusion to the heart and the brain,
• even at the expense of other organ systems

• Stimulation of CVS, neuroendocrine, and organ-specific responses.

• Loss of blood volume is usually the main trigger.

• Other stimuli : Pain, hypoxemia, hypercarbia, acidosis, infection,

change in temperature or hypoglycemia
Diagnosis of Shock
➢The diagnosis of shock is based on clinical recognition of the
presence of inadequate tissue perfusion and oxygenation.

➢The first step in the initial management of shock is to

recognize its presence
Types Of Shock
Low Cardiac Output states Low peripheral resistance states
(narrow Pulse Pressure) (↑↑pipes)
• Hypovolemic shock (↓↓ solution) (Widened Pulse Pressure)
• bleeding • Neurogenic shock
• Dehydration • Loss of sympathetic tone

• Cardiogenic shock (↓↓ pump) • Vasogenic Shock

• Impaired inflow • Septic
• Primary pump dysfunction • Anaphylactic
• Impaired outflow
 Types of Shock
Volume loss or shift
• Hypovolemic:
• Due to reduced intravascular volume (reduced preload)

• Distributive:
• Characterized by severe peripheral vasodilatation (vasodilatory shock).

Output Failure:
• Restrictive ( Obstructive ):
• Extracardiac causes of cardiac pump failure

• Cardiogenic:
• Due to intracardiac causes of cardiac pump failure

• Endocrine
Types of Shock
Hypovolemic shock
 Cardiogenic Shock
Pump failure: heart is not pumping properly

Main hemodynamic abnormality: Dec cardiac output

• Causes
• Pulmonary vascular: mostly due to right ventricular failure.
• Pul embolism, severe pul hypertension, valvular stenosis

• Mechanical:
 Tension pneumothorax.
 Pericardial tamponade (Beck’s triad?).
 Constrictive pericarditis and Restrictive cardiomyopathy.
 Abdominal compartment syndrome (ACS)
Obstructive shock
Distributive shock
• Includes septic shock, anaphylaxis and spinal cord
injury.

• Primary abnormality
• Vascular dilatation with hypotension low systemic
vascular resistance
• Inadequate afterload
• A resulting abnormally high cardiac output.
Anaphylaxis:
• vasodilatation due to histamine release

High spinal cord injury:

• failure of sympathetic outflow and adequate vascular tone
(neurogenic shock).

Septic shock
• Vasodilatation due to release of bacterial products (endotoxin)
Cardiogenic shock
Decreased cardiac output due to pump failure

Causes
• Cardiomyopathic:
MI, Myocarditis
• Arrhythmic:
Tachy and bradyrhythmias
• Mechanical
Atrial and ventricular septal defects
Endocrine shock:
Present as a combination of
• Hypovolaemic
• Cardiogenic
• Distributive shock
Causes:
Hypothyroidism:
• Like Neurogenic shock … disordered vascular & cardiac responsiveness low inotropy and
bradycardia.
• There may also be an associated cardiomyopathy.

Hyperthyroidism:
• Thyrotoxicosis may cause a high-output cardiac failure.

Adrenal insufficiency:
• Shock due to hypovolaemia and a poor response to circulating and exogenous catecholamines.
• May be due to pre-existing Addison’s disease or be a relative insufficiency due to a pathological
disease state, such as systemic sepsis
Hemodynamics

Preload
Initial assessment
Preshock
• Peripheral vasoconstriction
• Cold, clammy extremities and increased capillary refill time
• Decreased capillary hydrostatic pressure→ increased absorption of interstitial
fluids into intravascular space to help maintain blood pressure
• Peripheral vasoconstriction may be absent in distributive shock
• Tachycardia
• Exception to the rule: Neurogenic shock ---bradycardia)
• Oliguria
Initial assessment
• Shock (Progressive Phase :
• Worsening hypotension
• Hypoperfusion of peripheral tissues → generalized tissue hypoxia
→ anaerobic metabolism in the underperfused organs → lactic
acidosis , which in turn causes:
• Worsening tachypnea
• Precapillary dilation and postcapillary constriction of the blood vessels
→ pooling and stasis of blood in the capillary bed → decreased CO and
formation of microthrombi in the capillaries → DIC and further hypoxic injury to
tissues
• Acidosis, cerebral hypoperfusion → altered mental status
Initial assessment
End-Organ Dysfunction:
• Cerebral hypoxia → autonomic dysfunction
• Myocardial ischemia → decreased cardiac output
• Widespread cell necrosis causes:
• Release of lysosomal enzymes → further tissue injury → worsening of shock
• Activation of the immune system→ release of cytokines → DIC, further tissue
damage
• Bowel ischemia → bacteremic sepsis
• Can create a vicious cycle, leading to irreversible multiple organ
failure
Initial assessment
Manifestation
• Tachycardia
• Tachypnea
• Hypotension
• Oliguria or anuria
• Abnormal mental status
• Cool, clammy, cyanotic skin
• Weak peripheral pulses and prolonged capillary refill
• Narrowing of the pulse pressure
Preshock
• Peripheral vasoconstriction
• Manifests with cold, clammy extremities and increased capillary refill time
• Decreased capillary hydrostatic pressure → increased absorption of interstitial
fluids into intravascular space to help maintain blood pressure
• Peripheral vasoconstriction may be absent in distributive shock.
• Tachycardia (Patients with neurogenic shock may present with
bradycardia.)
• Oliguria
Stages of Shock
 Goal: Restore perfusion

Treatment of Method: Depends on type

Shock of Shock

Reverse the cause.

Microscopy
All patients
• Target ABC in your management.
• Oxygen
• IVF and blood (directed according to the type of shock).
• Response to resuscitation should be monitored.

Further therapy should be guided by type of shock

Types Of Shock
Cardiogenic shock:
• Initial resuscitation:
• Start with ionotropes (Dobutamine)  if shock persists vasopressors

• If dry…fluid resuscitation trial initially

• Interventions include:
• Pharmacologic agents (antiplatelet agents, heparin),
• Coronary revascularization procedures (balloon angioplasty),
• Intra-aortic balloon pump.
Obstructive Shock:
Tension Pneumothorax:
• Needle decompression followed by immediate tube thoracostomy.

Pericardial Tamponade:
• Pericardiocentesis
• Avoid it --if due to aortic dissection or myocardial rupture
Anaphylactic:
• Epinephrine
• Intramuscular 0.3 mg of 1:1000 epinephrine
• Repeat every 5 to 15 minutes as needed.
• Other pharmacologic agents:
• Antihistamines, nebulized albuterol, and methylprednisolone.
 Central venous line (CVL)
Begin immediate hemodynamic monitoring.
Continuous cardiac monitoring and pulse oximetry
Consider invasive monitoring for severe shock (e.g., central
venous pressure, arterial line).
Classify the type of shock (see “Overview of types of shock”).
Check vital signs, signs of end-organ hypoperfusion, and
other distinguishing clinical features.
Identify likely etiology of shock.
Perform rapid diagnostic studies, e.g., POCUS,
portable CXR, ECG, serum lactate, ABG/VBG.
Provide immediate hemodynamic support: can be started
for undifferentiated shock
Begin fluid resuscitation immediately if there are no
clinical signs of fluid overload or diagnostic evidence of
cardiogenic shock.
Consider a fluid challenge or passive leg raise test if
fluid responsiveness is in doubt.
Determine the need for vasopressors, inotropes, or
blood transfusions.
Determine the need for other critical therapy (e.g.,
corticosteroids for adrenal crisis, epinephrine for
anaphylaxis, needle thoracostomy for
tension pneumothorax).
Call for help early: critical care consult or rapid-response team
Reference

Bailey and Love’s Short Practice of Surgery 26th Edition

Case 1
• 68 yo M with hx of HTN and DM presents to the ER with abrupt onset
of diffuse abdominal pain with radiation to his low back. The pt is
hypotensive, tachycardic, afebrile, with cool but dry skin.

• What this patient is suffering from?

• What’s the first line management in this patient?

Case 2:
• A 34F presents to the ER after dining at a restaurant where shortly
after eating the first few bites of her meal, became anxious,
diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and
a sensation of her “throat closing off”. She is currently hypotensive,
tachycardic and ill appearing.

• What this patient is suffering from?

• What’s the first line option after starting resuscitation in this patient?
Thank You