SHOCK

DR.MUTHUVEL.D.M.

DEFINITION

Its a condition, in which circulation fails to meet the metabolic need of the tissue & at the same time fails to remove the metabolic waste products.

STAGES OF SHOCK

Non-progressive Stage Progressive Stage Irreversible Stage

NON-PROGRESSIVE STAGE

Reflex compensatory mechanisms are activated.

Profusion of vital organ is maintained

PROGRESSIVE STAGE

Tissue hypoperfusion.

Circulatory & metabolic imbalances leading to Acidosis.

IRREVERSIBLE STAGE

Cellular & tissue injury. Even with correction of haemodynamic defects, survival is not possible.

MECHANISM OF DIFFERENT STAGES OF SHOCK

NON-PROGRESSIVE STAGE

NEUROHUMORAL MECHANISMS MAINTAIN CARDIAC OUTPUT AND BLOOD PRESSURE: Baroreceptors reflexes Release of catecholamine Activation of renin-angiotensin axis ADH release Generalized sympathetic stimulation DIFFERENT CLINICAL OUTCOME OF THESE COMPENSATORY MECHANISMS: Tachycardia Peripheral vasoconstriction (cool & pale skin) Renal conservation of fluid

PROGRESSIVE STAGE

WIDESPREAD HYPOXIA:

Anaerobic glycolysis Production of lactic acidosis pH lead to blunting of vasomotor response leading to vasodilatation Peripheral pooling of blood cardiac output

DIFFERENT CLINICAL OUTCOME OF THESE FAILING MECHANISMS:

Feeble, failing pulse Mental confusion Urine output

IRREVERSIBLE STAGE

WIDESPREAD CELLULAR INJURY:

Damage to the organelle of cells Leakage of lysosomal enzymes Production of nitric oxide by cells Worsened myocardial contractility

DIFFERENT CLINICAL OUTCOME OF CELLULAR INJURY:

Septic shock (entry of intestinal flora into circulation) Complete renal shutdown (acute tubular necrosis) Downward clinical spiral

CLASSIFICATIONS OF SHOCK

Haematogenic or Hypovolumic Shock. Traumatic Shock. Neurogenic Shock. Cardiogenic Shock. Septic Shock. Miscellaneous.
- Anaphylactic & Insulin Shock.

HYPOVOLUMIC SHOCK

ETIOLOGY

Blood loss.

haemorrhage

Plasma / body water loss. Electrolytes imbalance.

Vomiting. Diarrhea. Dehydration.

PATHOPHYSIOLOGY

Sudden loss of blood volume / Loss of fluids from the vascular space. Mostly occurs from systemic venules & small veins Loss of blood will cause decreased filling of right heart. Which causes reduced filling of the pulmonary vasculature Which turns to reduced filling of left atrium and left ventricle. So left ventricular stroke volume reduce by starling hypothesis

COMPENSATORY MECHANISM

Adrenergic discharge. Hyperventilation. Release of vasoactie hormones. Collapse. Resorption of fluids from the interstitial tissue space. Resorption of fluids from the intracellular to extracellular space. Renal conversion of body water and electrolytes.

ADRENERGIC DISCHARGE

Occurs with in 60 seconds. Constriction of venules & small veins displace the blood to right atrium & ventricle, which increase the diastole & stroke volume leads to increase blood in pulmonary vasculature & so into left atrium & ventricle also left ventricle stroke volume. Also constricts vascular sphincters in the kidneys, Splanchnic viscera and Skin, this selective vasoconstriction improve the filling of right heart & increase cardiac output, also diverts blood to heart & brain. Increase the heart rate,

HYPERVENTILATION

Occurs with in 60 seconds. Response to metabolic acidaemia which develops shortly after haemorrhage. Spontaneous deep breathing sucks blood from extrathoracic sites to the heart & lungs.

RELEASE OF VASOACTIE HORMONES

Similar to Adrenergic discharge. Low perfusion of kidneys leads to release of renin from JUXTRAGLOMERULAR APPARATUS Renin liberate Angiotensin I from LIVER, which converted to Angiotensin II to by LUNGS Selective vasoconstriction by Angiotensin II to Kidneys, Splanchnic viscera and Skin

COLLAPSE

Assumption of recumbent posture due to collapse automatically displaces blood from lower part of the body to heart & lungs and increase the cardiac output.

RESORPTION OF FLUIDS FROM THE INTERSTITIAL TISSUE SPACE

Due to adrenergic discharge the arterioles, pre & post capillary sphincters, venules & small veins of the skin & Splanchnic organs & skeletal muscles constrict. Which decrease the capillary intravascular hydrostatic pressure, leads to influx of water, sodium, chloride from interstitial tissue to capillaries.

RESORPTION OF FLUIDS FROM THE INTRACELLULAR TO EXTRACELLULAR SPACE

Release of epinephrine from adrenal medulla, cortisol from adrenal cortex & glucagon from the pancreas & inhibition of release of insulin all leads to high extracellular Glucose concentration. Products of anaerobic metabolism also accumulate in the extracellular space. Both of these cause hyperosmolarity of the extracellular tissue, which draw the water out of the cells. Interstitial pressure increases, which forces water, sodium & chloride across the capillary endothelium into vascular space.

RENAL CONVERSION OF BODY WATER AND ELECTROLYTES

Adrenocorticotropic hormone is released by any stress even shock. This hormone & angiotensin II stimulate the synthesis and release of aldosterone from adrenal cortex. Aldosterone is concerned with resorption of sodium from glomerular ultrafiltrate into the vascular space. Resorption of sodium & water by kidneys helps to maintain the vascular volume.

CLINICAL FEATURES

Features of hypovolumic shock depend on the degree of loss of blood volume & on duration of shock

Types Mild shock. Moderate shock. Severe shock.

MILD SHOCK

Blood loss less then 20% Features;

Collapse of subcutaneous veins of extremities esp. the feet, which become pale and cool Sweat on forehead, hand and feet due to adrenergic discharge Urine output normal. Pulse rate normal. Blood pressure normal. Patient feels thirsty and cold.

MODERATE SHOCK

Blood loss 20% - 40%. Features;

Collapse of subcutaneous veins of extremities esp. the feet, which become pale and cool Sweat on forehead, hand and feet due to adrenergic discharge Oliguria

due to adrenergic discharge along with aldosterone & vasopressin

Pulse rate increased usually less then 100/min. Blood pressure normal initially then falls in later stage.

SEVERE SHOCK

Blood loss more then 40%. Features;

Pallor. Low urine output. Rapid pulse. Low blood pressure.

CLINICAL MONITORING OF SHOCK

MONITORING OF SHOCK

BLOOD PRESSURE;

Normal in mild shock.

Lower in moderate and severe cases.

MONITORING OF SHOCK

RESPIRATION;

Increase rate & depth of respiration, its normal response at early shock. If the patient is not hyperventilating patient may suffer with CNS / Respiratory system damage. Persistent hyperventilation is an ominous sign & indicates improper treatment shock.

MONITORING OF SHOCK

PHSYCHOLOGIC STATES

General monitoring Heart rate Breathing

MONITORING OF SHOCK

COLOR AND TEMPERATURE OF SKIN

ELECTROCARDIOGRAM

SHOWS SIGNS OF MYOCARDIAL INFARCTION WITH DEPRESSION OF ST T SEGMENTS.

SPECIAL MONITORING

CENTRAL VENOUS PRESSURE;

Normal ; 5-10cmH2O, If CVP<5cmH2O

INADEQUACY OF BLOOD VOLUME CARDIAC DYSFUNCTION

CVP>12cmH2O

LUNG ARTERIAL PRESSURE CARDIAC OUTPUT BLOOD GAS

PO2 75-100mmHg Pco2 40mmHg PH 7.357.45

COAGULATION TEST

TREATMENT OF THE HYPOVOLUMIC SHOCK

STEPS OF TREATMENTS;

Resuscitation. Immediate control of bleeding. Extracellular fluid replacement. Drug treatments.

RESUSCITATION

Establishment of a clear airway & maintains ventilation and O2. Lowering the head improves the venous return, preventing stasis of blood in muscles of legs & preventing oedema. Which also improve the cerebral blood flow. If airway obstruction present need artificial ventilation is need to supply.

IMMEDIATE CONTROL OF BLEEDING

Highly important in case of haemorrhagic shock, it may achieved by raising the foot end by compressing bandage to tamponade external haemorrhage. Surgical procedure may need after resuscitation

EXTRACELLULAR FLUID REPLACEMENT.

Fluid administration should be starts after bleeding is controlled. May need plasma replacement therapy

DRUG TREATMENTS

Sedatives;

Morphine by intravenously. Atropine to increase HR. Dopamine to improve the strength of cardiac muscle contraction.

Chronotropic agents;

Ionotropic agents;

Vasodilators;

Nitroprusside & nitroglycerin for septic shock.

Phenylephrine & metaraminol to improve the BP. Propranolol increases the efficiency of ventricular contraction. Reduce the vascular volume & decrease the filling pressure.

Vasoconstrictor;

Beta-blockers;

Diuretics;

TRAUMATIC SHOCK

ETIOLOGY

Major fractures. Crush injuries. Burns. Extensive soft tissue injuries. Intra abdominal injuries.

PATHOPHYSIOLOGY

Traumatised tissues activate the coagulation system & release of microthrombi into the circulation These may occlude / constrict parts of pulmonary micro vasculature to increase the pulmonary vascular resistance. Which increase the right ventricular diastolic & right atrial pressure. Humoral products of microthrombi induce a generalised increase in capillaries permeability, which leads to loss of plasma in interstitial tissue throughout the body This depletes the vascular volume to great extent.

CLINICAL FEATURES

Features are similar to hypovolumic shock. Special features

Presence of peripheral and pulmonary oedema Infusion of large volume of fluid may need

TREATMENT OF TRAUMATIC SHOCK

Resuscitation

Mechanical ventilation necessary.

Local treatment of trauma & control of bleeding. Fluid replacement.

NEUROGENIC SHOCK

ETIOLOGY

Paraplegia. Quadriplegia. Trauma to spinal cord. Spinal anesthesia.

PATHOPHYSIOLOGY

Dilatation of systemic vasculature which lowers the systemic arterial pressure Blood pools in the systemic venules and small veins, so right heart filling & stroke volume reduce, Which reduces pulmonary blood volume & left heart filling, so left ventricular output decreases. Discharge of adrenergic nervous system innervated parts & release of angiotensin & vasopressin, are compensatory mechanisms which of course fail to restore cardiac output to normal.

CLINICAL FEATURES

Peculiar features

Skin remains warm, pink, & well perfused.

Urine output may be normal. Heart rate is rapid. Low blood pressure.

TREATMENT OF NEUROGENIC SHOCK

ELEVATION OF LEG

Position of Body 30 degree

TREATMENT OF NEUROGENIC SHOCK

FLUID ADMINISTRATION

Increase the filling of right heart so cardiac output also increase.

TREATMENT OF NEUROGENIC SHOCK

VASOCONSTRICTOR;

Phenylephrine, Metaraminol.

to improve the BP.

CARDIOGENIC SHOCK

ETIOLOGY

Injuries to the heart. Myocardial infarction. Cardiac arrhythmias. Congestive cardiac failure.

PATHOPHYSIOLOGY

Primary dysfunction of one ventricle

Right ventricle dysfunction leads to reduce blood flow to lungs, so filling of left heart reduces leads to left ventricular output reduced. In left ventricle dysfunction unable to maintains the stroke volume so left ventricular output systemic arterial pressure reduced leads to pulmonary engorgement due to normal right ventricular output.

CARDIAC COMPRESSIVE SHOCK

ETIOLOGY;

Tension pnumothorax. Pericardial tamponade. Diaphragmatic rupture with herniation of bowel to chest.

PATHOPHYSIOLOGY;

Heart compressed enough from outside to decrease the cardiac output.

CLINICAL FEATURES

Skin is pale & cool. Urine output is low. Gradually pulse become rapid. Blood pressure become low. Right ventricle dysfunction leads to neck vein distention and liver enlargement. Left ventricle dysfunction leads to bronchial rales & IIIrd heart sound heard. Gradually heart become enlarged.

TREATMENT

Airway must be clear with adequate O2. In right side failure caused by massive embolism so IV heparin should be given. In left side failure produce pain, so treat with sedatives. Fulminant pulmonary oedema are treat with diuretic

SEPTIC SHOCK

In adults it is defined as a systolic blood pressure < 90 mmHg, or a MAP < 60 mmHg, without the requirement for inotropic support, or a reduction of 40 mmHg in the systolic blood pressure from baseline. In children it is BP < 2 SD of the normal blood pressure.

To diagnose septic shock the following two criteria must be met:

Evidence of infection, through a positive blood culture. Refractory hypotension - hypotension despite adequate fluid resuscitation and cardiac output.

SEPTIC SHOCK

In addition to the two criteria above, two or more of the following must be present:

Tachypnea (high respiratory rate) > 20 breaths per minute or, on blood gas, a PaCO2 less than 32 mmHg. White blood cell count < 4000 cells/mm or > 12000 cells/mm (< 4 x 109 or > 12 x 109 cells/L).

ETIOLOGY

The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. Approximately 70% of septic shock cases are due to gram-negative bacilli that produce endotoxins. In rough order of increasing severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death. The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response. Besides TNF, other cytokines involved in the development of septic shock include interleukin-1, interleukin-6 and interleukin-8.

TREATMENT

Treatment primarily consists of the following.

Volume resuscitation. Early antibiotic administration. Rapid source identification and control. Support of major organ dysfunction.

Among the choices for pressors, a randomized controlled trial concluded that there was no difference between norepinephrine (plus dobutamine as needed for cardiac output) versus epinephrine. However dopamine has more beta adrenergic activity and therefore is more likely to cause arrhythmia or myocardial infarction. Antimediator agents may be of some limited use in severe clinical situations:

Corticosteroids, especially if combined with a mineralocorticoid, can reduce mortality among patients who have relative adrenal insufficiency. Recombinant activated protein C (drotrecogin alpha) has been shown in large randomized clinical trials to be associated with reduced mortality (Number needed to treat (NNT) of 16) in patients with multi-organ failure.[5] If this is given, heparin should probably be continued.

MISCELLANEOUS TYPES

Anaphylactic shock

Insulin Shock

ANAPHYLACTIC SHOCK

ETIOLOGY; Commonly seen after penicillin administration or serum, dextrose, anasthetics CLINICAL FEATURES; Bronchospasm, laryngeal oedema, & respiratory distress which totally leads to HYPOXIA. Which aggravates vasodilatation & causes hypotension and ultimately shock. Which increase the release of histamine & slow release substance of anaphylaxis by combination of antigen with IgE on the mast cells & basophils. This histamine & slow release substance causes bronchospasm, laryngeal oedema, & respiratory distress along with massive vasodilatation.

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