Shock Presentation Risk Factors Pathogenesis Management Treatment

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.

Shock2

Shock Presentation Risk Factors Pathogenesis Management Treatment


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

Shock 1

Shock Presentation Risk Factors Pathogenesis Management Treatment


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.
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