Drugs used in the Therapy of Shock


It is an abnormal physiological state resulting from a widespread and serious reduction of tissue perfusion that if prolonged will lead to generalized impairment of cellular function.

  • A life-threatening clinical syndrome of cardiovascular collapse characterized by:
  1. An acute reduction of effective circulating blood volume (hypotension).
  2. Inadequate perfusion of cells and tissues (hypoperfusion).
  • If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
  • The clinical manifestations of shock are the result of stimulation of the sympathetic and neuroendocrine stress responses, inadequate oxygen delivery, end-organ dysfunction.
Therapy of Shock


  • Hypovolemic shock
  • Cardiogenic shock
  • Distributive shock
  1. Septic shock
  2. Neurogenic shock
  3. Anaphylactic shock

Management of Shock:

  • Ionotropic: An agent that changes myocardial contractility.
  • Vasopressor: An agent that increases blood pressure.
  • Chronotrope: An agent that changes heart rate.
  • Dromotrope: An agent that increases cardiac conduction velocity.


  • Most widely used vasopressor.
  • Potent α1 agonist causing vasoconstriction in tissue beds.
  • The resultant increase in SVR causes a rise in blood pressure.
  • Standard dose: 4 mg in 50 ml (0.08 mg/ml).


  • Nature’s vasopressor.
  • Most commonly used during resuscitation cardiac arrest and anaphylaxis.

α1: Increases SVR.

β1: Increases HR and myocardial contractility.

β2: Bronchial smooth muscle relaxation.

Standard dose: 10 mg in 50 ml (0.2mg/ml).


  • Vasopressor agent.
  • Use in cardiogenic and septic shock.
  • Receptor stimulation depends on the dose given.


  • A synthetic catecholamine.
  • An indicator.
  • β1 stimulation: Increase HR and increase cardiac contractility.
  • β2 mediated vasodilatation.
  • Reduction in MAP is common with dobutamine.
  • NE usually needed to offset vasodilatation.


  • Peptide hormone is released from the posterior pituitary.
  • Causes increase the permeability of DCT and CT, increases water retention. (V2 receptor).
  • V1 receptor present in the smooth muscle of an arteriolar wall and stimulation causes smooth muscle contraction and vasoconstriction.

1. Hypovolemic Shock

Improper tissue perfusion as a result of severe loss of blood or other fluid from the body or inadequate fluid intake, any of which decrease intravascular volume.


  • Hemorrhagic (acute blood loss)
  • Burns
  • Excessive vomiting and diarrhea
Pathophysiology of Hypovolemic shock

  Hemorrhage from small venules and veins (50%)
 Decreased filling of right heart
 Decreased filling of the pulmonary vasculature
 Decreased filling of left atrium and ventricle
 Left ventricular stroke volume decreases (Frank-Starling )
 Drop-in arterial blood pressure and tachycardia
 Poor perfusion to pulmonary arteries
 Cardiac depression and pump failure 


  • Hemorrhagic: Trauma, gastrointestinal bleeding.
  • Non-Hemorrhagic: external fluid loss, diarrhea, vomiting, polyurea, fluid redistribution, burns, anaphylaxis.

Signs and Symptoms:

  • Anxiety, restlessness, altered mental state.
  • Hypotension.
  • A rapid, weak, thready pulse.
  • Cool, clammy skin.
  • Rapid and shallow respirations.
  • Hypothermia.
  • Thirst and dry mouth.
  • Distracted look in the eyes.

Compensatory Mechanisms:

1. Adrenergic discharge.

2. Hyperventilation.

3. Vasoactive hormones Angiotensin, Vasopressin, Epinephrine.

4. Collapse.

5. Re-absorption of fluid from interstitial tissue.

6. Resorption of fluid from intracellular to extracellular space.

7. Renal conservation of body water and electrolyte.

Clinical Monitoring:

  • Blood pressure
  • Respiration
  • Urine output
  • Central venous pressure
  • ECG
  • Swan-Ganz catheter
  • cardiac output.
  • mixed venous oxygen level.
  • vascular pressure.
  • Pulmonary artery wedge pressure.


  • In the management of trauma patients, understanding the patterns of injury of the patient in shock will help direct the evaluation and management.
  • Blood loss sufficient to cause shock is generally of a large volume (e.g. external, intrathoracic, intra-abdominal, retroperitoneal, and long bone fractures).
  • Diagnostic and therapeutic tube thoracotomy may be indicated in unstable patients based on clinical findings and clinical suspicion.
  • Chest radiographs, pelvic radiography, diagnostic ultrasound, or diagnostic peritoneal lavage.



(a) Increase Cardiac Output

(b) Increase Tissue Perfusion

The plan of action should be based on:

(a) Primary problem

(b) Adequate fluid replacement

(c) Improving myocardial contractility

(d) Correcting acid-base disturbances

  • Resuscitation
  • Immediate control of bleeding: Rest, Pressure Packing.
Operative Methods:
  • Extracellular fluid replacement:
  1. Infusion of fluid is the fundamental treatment.
  2. Crystalloids, for initial resuscitation for most forms of hypovolemic shock.
  3. After the initial resuscitation, with up to several liters of crystalloid fluid, use of colloids.

1. Sedatives

2. Chronotropic agents

3. Inotropic

2. Distributive Shock

  • As in hypovolemic shock, there is an insufficient intravascular volume of blood.
  • This form of “relative” hypovolemia is the result of dilation of blood vessels which diminishes systemic vascular resistance.
  • Examples of this form of shock:

1. Septic shock

2. Anaphylactic shock

3. Neurogenic shock

1. Septic Shock:

A type of distributive shock resulting from sepsis.

  • Sepsis: An abnormal body-wide inflammatory response to an infection that can result in death.


Pathogenesis of Septic Shock
Fig.1: Pathogenesis of Septic Shock

Clinical Signs:

  • Hyperthermia
  • Tachycardia
  • Wide pulse pressure
  • Low blood pressure (SBP < 90)
  • Mental status changes


  • Fluid replacement.
  • Supplemental oxygen.
  • Antibiotics: Survival correlates with how quickly the correct drug is given cover gram-positive and gram-negative bacteria:
  • Ceftriaxone 1 gram IV BD or
  • Imipenem 1 gram IV TDS.

Add additional coverage for:

  • Pseudomonas: Gentamicin or Cefepime.

2. Anaphylactic Shock:

It develops following exposure to:

  • Allergen and cross-links IgE on mast cells causing mediator release (release of Histamine, Eicosanoids-LTs, PGs).

Clinical Presentation:

  • Urticaria and angioedema.
  • Bronchospasm.
  • Hypertension and CV collapse.


Epinephrine is 1st line drug:

  • Standard Dose: Inj. 0.5 ml (1:1000) IM.
  • Repeat every 5-10 min if not improve.
  • Inj. 0.5 ml (1: 10000),(1:100000) IV.


  • Diphenhydramine (H1) administered IV.
  • Ranitidine (H2) administered IV.
  • β2 agonist: Salbutamol.
  • Corticosteroid: Hydrocortisone 200 mg IV followed by oral prednisolone for 3 days.

3. Neurogenic Shock:

Develops secondary to a sudden loss of ANS functions following spinal cord injury resulting in vasomotor tone and impaired cellular metabolism.


  • Hypotension
  • Bradycardia
  • Poikilothermia


  • Airway support.
  • Fluid replacement.
  • Dopamine (>10 mcg/kg/min).
  • Ephedrine (12.5 – 25 mg IV every 3-4 hr).
  • Atropine for bradycardia. (0.5 mg IV every 3 to 5 mins − 3 mg).
  • Treatment of the underlying cause.

3. Cardiogenic Shock

A state of inadequate cardiac output despite the adequate intravascular volume, resulting in hypoxia.

  • Cool, mottled skin
  • Tachypnea
  • Hypotension
  • Altered mental status
  • Narrowed pulse pressure


  • Acute myocardial infarction
  • Myocarditis
  • Myocardial contusion
  • Aortic or mitral stenosis
  • Acute aortic insufficiency


  • Often after ischemia, loss of LV function
  • CO reduction = lactic acidosis, hypoxia
  • Stroke volume is reduced
  • Tachycardia develops as compensation
  • Ischemia and infarction worsens


  • Aspirin, beta-blocker, morphine, heparin
  • If no pulmonary edema, IV fluid
  • If pulmonary edema
  • Dopamine – will ↑ HR and thus cardiac work
  • Dobutamine – May drop blood pressure
  • Combination therapy may be more effective
  • Thrombolytics(streptokinase, rt-PA)


Treatment of shock
Fig.2: Treatment of shock
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