Shock

Shock is a clinical syndrome due to inadequate tissue perfusion. A clinical syndrome marked by inadequate perfusion and oxygenation of cells, tissues, and organs, usually as a result of marginal or markedly lowered blood pressure. Shock is the physiologic state characterized by significant reduction of systemic tissue perfusion, resulting in decreased tissue oxygen delivery.

• This leads to Cellular dysfunction leading to produc­tion and release of inflammatory mediators which act on the microvasculature.
• Cellular injury  —–>  Multiple Organ Failure  ——> Death
• The cellular injury is reversible or irreversible.

Aims of Treatment in Shock

• Restore perfusion by expansion of blood volume
• Check the cause like:
  • – Haemorrhage
  •   Impairment of cardiac functions
  • Infections.

History in Shock

• Hypovolemic shock: Burns, trauma, bleeding wound(s), hematemesis, vomiting, abdominal pain, melena, diarrhea, vaginal bleeding
• Cardiogenic shock: Dizziness, chest pain, dyspnea, palpitations
• Septic shock: Fever, chills, rigors, malaise, myalgias, cough, shortness of breath, productive sputum, dysuria, suprapubic pain, flank pain
• Neurogenic: Spinal trauma

Risk Factorsfor Shock

• Hypovolemic shock: Hemorrhage, dehydration, burns, anaphylactic (decreased effective circulating volume)
• Cardiogenic shock: Heart disease such as MI and congestive heart failure (CHF)
• Septic shock: Elderly, immunosuppression, critical illness, malnutrition, cancer
• Neurogenic: Spinal cord injury

Pathogenesis of Shock

• Cardiac output falls below 60%.
• There is hypotension i.e. mean <60 mmHg.

• Systemic vascular response increases so that there is :

  • Increased perfusion of brain and heart.
  • · Decreased perfusion of skin, muscles, GIT. Cerebral and coronary perfusion is maintained spite fall of blood pressure.
  •   Arterioles have vascular smooth muscle.
  • Vascular smooth muscles have Alfa and Beta adrenergic receptors.
  • Alfa-1 receptors cause Vasoconstriction.
  • Beta-2 receptors cause Vasodilatation.
  • Norepinephrine released from efferent sympathetic fibers act on ~ receptors.
  • Epinephrine and norepinephrine are released by adrenal medulla.
• Other vasoconstrictors are :
  • angiotensin II,
  • vaso­pressin,
  • endothelins,
  • thromboxane A2.

Vasodilator substances in shock:

• Prostacyclin
• PG 1₂
• Nitric oxide
• Adenosine.

Derangement of cellular metabolism leads to cell death resulting in organ failure.‘ There is :

• · Hypovolemia
• · Hypotension
• · Hypoxia.
  • Autonomic response —> decreased vagal response, increased heart rate, increased cardiac output, in­creased glycogenolysis and gluconeogenesis.
• Severe pain, severe stress leads to increased ACTH and increased blood volume.
  • Release of renin —> Angiotensin I  —> angiotensin Il  —> Vasoconstriction  —> aldosterone release by adrenal cortex  —> Vasopressin by posterior pituitary.
• Aldosterone and Vasopressin enhance water reabsorp­tion and cause vasoconstriction.

 Cardiovascular response

• Decreased cardiac output
• Decreased stroke volume
• Increased heart rate
• Increased systemic vascular resistance
• Vasoconstriction and peripheral vasoconstriction are compensatory responses.

Pulmonary response

• Tachypnea  —> Hypoxia  —> Respiratory alkalosis  —> Atelectasis  —> Acute Lung Injury  —> Acute respira­tory distress syndrome

Renal response

• Shock —> acute tubular necrosis —> decreased GFR —> increased Angiotensin —> increased aldosterone and vasopressin —> decreased urine formation Low dose dopamine may be useful.

Metabolic effects

• Disruption of Lipid,
• Carbohydrate and protein metabo­lism.

Monitoring the Patient with shock

• · ICU admission
• · Monitor arterial pressure (intraarterial)
• · Pulse
• · Respiratory rate
• · Urine flow (Foley’s catheter)
• · Mental status
• · Pulmonary arterial catheter (for Right atrial, Pulmonary arterial, and Pulmonary wedge pressure)
• · Cardiac output
• · 02 consumption, 02 delivery
• · Systemic vascular resistance to be maintained.

TYPES OF SHOCK

HYPOVOLEMIC SHOCK

Causes

• · Haemorrhage
• · Loss from GIT, urinary, insensible loss (extravas­cular fluid sequestration)
• · Tachycardia

Presentation

• Postural hypotension, Severe hypotension
• Oliguria
• Agitation
•  Confusion
• Mental obtundation
• Differentiation from cardiogenic shock by ab­sence of S3, rales, jugular venous distension.~

Management

• Give volume:
  • · Isotonic saline (2-3 litres in 112 hour)
  • · Blood transfusion (0 +ve packed RBCs).
  • · Dopamine
  • · Vasopressin
  • · Dobutamine (No norepinephrine)
  • · Oxygen
  • · Endotracheal intubation.

TRAUMATIC SHOCK

• · Haemorrhage
• · Hypovolemia
• · Pain
• · Tissue ischemia
• Pericardial tamponade
• Tension Pneumothorax
• Myocardial injury.

Management

• · Airway
• · Breathing
• · Circulation
• · Control haemorrhage
• · Antioxidants.

INTRINSIC CARDIOGENIC SHOCK

• It is complication of Myocardial Infarction.

Presentation

• · Decreased cardiac output
• · Pulmonary congestion
• · Increased systemic vascular resistance / Left ventricular failure / Right ventricular failure / Pulmonary arterial hypertension ~ alveolar edema
• · There is no hypovolemia.

Treatment —

• Management of AMI to be done Dopamine
• Norepinephrine
• Vasopressin
• Dobutamine
• Furosemide
• Intra Aortic Balloon Pump
• Revascularization
• Ventricular Assist Device
• Heart transplantation.

COMPRESSIVE CARDIOGENIC SHOCK

Causes

• · Tamponade
• · Increased intrathoracic pressure
• · Tension pneumothorax
• · Intermittent positive pressure ventilation (exces­sive)
• ·Acute right heart failure in pulmonary embolism. There is pulsus paradoxus.

NEUROGENIC SHOCK

• · High cervical cord injury
• · Spinal anaesthesia (Cephalad migration)
• · Head injury.

Management

• · Give fluids
• · Norepinephrine.

HYPOADRENAL SHOCK

• Adrenal insufficiency in stress, surgery, illness, trauma, sepsis, (due to previous high dose of exog­enous corticosteroids) in patients of :
• · Tuberculosis
• · Metastatic disease
• · Bilateral haemorrhage
• · Amyloidosis

 Treatment

• Dexamethasone – 4 mg· IV
• Hydrocortisone – 100 mg IV 6 – 8 hourly.

OTHER THERAPIES IN SHOCK

• · Elevation of foot
• · Pneumatic antishock garment
• · Rewarming.

SEPTIC SHOCK

Systemic responses to infection:

• · Fever
• · Hypothermia
• · Tachypnea
• · Tachycardia.