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:
- An acute reduction of effective circulating blood volume (hypotension).
- 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.
TYPES OF SHOCK
- Hypovolemic shock
- Cardiogenic shock
- Distributive shock
- Septic shock
- Neurogenic shock
- 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)
- 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.
- A rapid, weak, thready pulse.
- Cool, clammy skin.
- Rapid and shallow respirations.
- Thirst and dry mouth.
- Distracted look in the eyes.
1. Adrenergic discharge.
3. Vasoactive hormones Angiotensin, Vasopressin, Epinephrine.
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.
- Blood pressure
- Urine output
- Central venous pressure
- 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
- Immediate control of bleeding: Rest, Pressure Packing.
- Extracellular fluid replacement:
- Infusion of fluid is the fundamental treatment.
- Crystalloids, for initial resuscitation for most forms of hypovolemic shock.
- After the initial resuscitation, with up to several liters of crystalloid fluid, use of colloids.
2. Chronotropic agents
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.
- 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).
- Urticaria and angioedema.
- 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.
- 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
- Altered mental status
- Narrowed pulse pressure
- Acute myocardial infarction
- 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
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