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It’s 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
Profusion of vital organ is maintained .NON-PROGRESSIVE STAGE Reflex compensatory mechanisms are activated.
PROGRESSIVE STAGE Tissue hypoperfusion. . Circulatory & metabolic imbalances leading to Acidosis.
. Even with correction of haemodynamic defects.IRREVERSIBLE STAGE Cellular & tissue injury. 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 .
Cardiogenic Shock. Neurogenic Shock. Septic Shock. Traumatic Shock. Miscellaneous. .CLASSIFICATIONS OF SHOCK Haematogenic or Hypovolumic Shock.Anaphylactic & Insulin Shock. .
HYPOVOLUMIC SHOCK .
Electrolytes imbalance. Vomiting. haemorrhage Plasma / body water loss. Diarrhea.ETIOLOGY Blood loss. . Dehydration.
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 .PATHOPHYSIOLOGY Sudden loss of blood volume / Loss of fluids from the vascular space.
Resorption of fluids from the interstitial tissue space.COMPENSATORY MECHANISM Adrenergic discharge. . Renal conversion of body water and electrolytes. Release of vasoactie hormones. Collapse. Resorption of fluids from the intracellular to extracellular space. Hyperventilation.
also diverts blood to heart & brain. Increase the heart rate. this selective vasoconstriction improve the filling of right heart & increase cardiac output. . Also constricts vascular sphincters in the kidneys. which increase the diastole & stroke volume leads to increase blood in pulmonary vasculature & so into left atrium & ventricle also left ventricle stroke volume. Splanchnic viscera and Skin. Constriction of venules & small veins displace the blood to right atrium & ventricle.ADRENERGIC DISCHARGE Occurs with in 60 seconds.
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.
Splanchnic viscera and Skin .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.
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. sodium. chloride from interstitial tissue to capillaries. pre & post capillary sphincters. Which decrease the capillary intravascular hydrostatic pressure. venules & small veins of the skin & Splanchnic organs & skeletal muscles constrict. leads to influx of water.
which draw the water out of the cells. cortisol from adrenal cortex & glucagon from the pancreas & inhibition of release of insulin all leads to high extracellular Glucose concentration. sodium & chloride across the capillary endothelium into vascular space. . which forces water. Products of anaerobic metabolism also accumulate in the extracellular space.RESORPTION OF FLUIDS FROM THE INTRACELLULAR TO EXTRACELLULAR SPACE Release of epinephrine from adrenal medulla. Both of these cause hyperosmolarity of the extracellular tissue. Interstitial pressure increases.
RENAL CONVERSION OF BODY WATER AND ELECTROLYTES Adrenocorticotropic hormone is released by any stress even shock. 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. . This hormone & angiotensin II stimulate the synthesis and release of aldosterone from adrenal cortex.
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.
Patient feels thirsty and cold. Collapse of subcutaneous veins of extremities esp. Pulse rate normal.MILD SHOCK Blood loss less then 20% Features. the feet. Blood pressure normal. . hand and feet due to adrenergic discharge Urine output normal. which become pale and cool Sweat on forehead.
Blood pressure normal initially then falls in later stage. which become pale and cool Sweat on forehead. Collapse of subcutaneous veins of extremities esp. Features. hand and feet due to adrenergic discharge Oliguria due to adrenergic discharge along with aldosterone & vasopressin Pulse rate increased usually less then 100/min. .40%. the feet.MODERATE SHOCK Blood loss 20% .
Rapid pulse.SEVERE SHOCK Blood loss more then 40%. Low urine output. Pallor. Features. . Low blood pressure.
CLINICAL MONITORING OF SHOCK .
• Lower in moderate and severe cases. • Normal in mild shock. .MONITORING OF SHOCK • BLOOD PRESSURE.
Persistent hyperventilation is an ominous sign & indicates improper treatment shock. . its normal response at early shock. If the patient is not hyperventilating patient may suffer with CNS / Respiratory system damage. Increase rate & depth of respiration.MONITORING OF SHOCK RESPIRATION.
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. If CVP<5cmH2O INADEQUACY OF BLOOD VOLUME CARDIAC DYSFUNCTION CVP>12cmH2O LUNG ARTERIAL PRESSURE CARDIAC OUTPUT BLOOD GAS PO2 75-100mmHg Pco2 40mmHg PH 7.35—7. 5-10cmH2O.45 COAGULATION TEST . Normal .
. Drug treatments. Resuscitation.TREATMENT OF THE HYPOVOLUMIC SHOCK STEPS OF TREATMENTS. Immediate control of bleeding. Extracellular fluid replacement.
. preventing stasis of blood in muscles of legs & preventing oedema. Lowering the head improves the venous return. Which also improve the cerebral blood flow. If airway obstruction present need artificial ventilation is need to supply.RESUSCITATION Establishment of a clear airway & maintains ventilation and O2.
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 .
Nitroprusside & nitroglycerin for septic shock. Dopamine to improve the strength of cardiac muscle contraction. Morphine by intravenously. Atropine to increase HR. Ionotropic agents. Vasoconstrictor. Chronotropic agents. . Beta-blockers. Vasodilators. Phenylephrine & metaraminol to improve the BP. Reduce the vascular volume & decrease the filling pressure. Diuretics.DRUG TREATMENTS Sedatives. Propranolol increases the efficiency of ventricular contraction.
TRAUMATIC SHOCK .
. Burns. Crush injuries.ETIOLOGY Major fractures. 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. which leads to loss of plasma in interstitial tissue throughout the body This depletes the vascular volume to great extent. Humoral products of microthrombi induce a generalised increase in capillaries permeability. .
CLINICAL FEATURES Features are similar to hypovolumic shock. Special features Presence of peripheral and pulmonary oedema Infusion of large volume of fluid may need .
. Local treatment of trauma & control of bleeding. Fluid replacement.TREATMENT OF TRAUMATIC SHOCK Resuscitation Mechanical ventilation necessary.
NEUROGENIC SHOCK .
Quadriplegia. Trauma to spinal cord. . Spinal anesthesia.ETIOLOGY Paraplegia.
so right heart filling & stroke volume reduce. so left ventricular output decreases. Discharge of adrenergic nervous system innervated parts & release of angiotensin & vasopressin. Which reduces pulmonary blood volume & left heart filling. are compensatory mechanisms which of course fail to restore cardiac output to normal.PATHOPHYSIOLOGY Dilatation of systemic vasculature which lowers the systemic arterial pressure Blood pools in the systemic venules and small veins. .
CLINICAL FEATURES Peculiar features Skin remains warm. Heart rate is rapid. . pink. Low blood pressure. & well perfused. Urine output may be normal.
TREATMENT OF NEUROGENIC SHOCK
ELEVATION OF LEG
Position of Body 30 degree
TREATMENT OF NEUROGENIC SHOCK
Increase the filling of right heart so cardiac output also increase.
TREATMENT OF NEUROGENIC SHOCK
to improve the BP.
CARDIOGENIC SHOCK .
Cardiac arrhythmias. Congestive cardiac failure. .ETIOLOGY Injuries to the heart. Myocardial infarction.
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.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.
Tension pnumothorax. . Pericardial tamponade. Heart compressed enough from outside to decrease the cardiac output. Diaphragmatic rupture with herniation of bowel to chest.CARDIAC COMPRESSIVE SHOCK ETIOLOGY. PATHOPHYSIOLOGY.
Urine output is low. Left ventricle dysfunction leads to bronchial rales & IIIrd heart sound heard. Gradually pulse become rapid. .CLINICAL FEATURES Skin is pale & cool. Blood pressure become low. Right ventricle dysfunction leads to neck vein distention and liver enlargement. Gradually heart become enlarged.
In right side failure caused by massive embolism so IV heparin should be given. In left side failure produce pain. so treat with sedatives.TREATMENT Airway must be clear with adequate O2. Fulminant pulmonary oedema are treat with diuretic .
hypotension despite adequate fluid resuscitation and cardiac output. through a positive blood culture. Refractory hypotension . or a reduction of 40 mmHg in the systolic blood pressure from baseline. . without the requirement for inotropic support. To diagnose septic shock the following two criteria must be met: Evidence of infection. or a MAP < 60 mmHg.SEPTIC SHOCK In adults it is defined as a systolic blood pressure < 90 mmHg. In children it is BP < 2 SD of the normal blood pressure.
.SEPTIC SHOCK In addition to the two criteria above. a PaCO2 less than 32 mmHg. two or more of the following must be present: Tachypnea (high respiratory rate) > 20 breaths per minute or. White blood cell count < 4000 cells/mm³ or > 12000 cells/mm³ (< 4 x 109 or > 12 x 109 cells/L). on blood gas.
Approximately 70% of septic shock cases are due to gram-negative bacilli that produce endotoxins. septic shock. and death. other cytokines involved in the development of septic shock include interleukin-1β.ETIOLOGY The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. Besides TNFα. In rough order of increasing severity. The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators. refractory septic shock. interleukin-6 and interleukin-8. these are bacteremia or fungemia. . multiple organ dysfunction syndrome. septicemia. severe sepsis or sepsis syndrome. these act to stimulate immune response. sepsis. such as tumor necrosis factors (TNF).
 If this is given. Antimediator agents may be of some limited use in severe clinical situations: Corticosteroids. Early antibiotic administration. Rapid source identification and control. a randomized controlled trial concluded that there was no difference between norepinephrine (plus dobutamine as needed for cardiac output) versus epinephrine. . Support of major organ dysfunction. heparin should probably be continued. Among the choices for pressors. 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.TREATMENT Treatment primarily consists of the following. However dopamine has more beta adrenergic activity and therefore is more likely to cause arrhythmia or myocardial infarction. especially if combined with a mineralocorticoid. can reduce mortality among patients who have relative adrenal insufficiency. Volume resuscitation.
MISCELLANEOUS TYPES Anaphylactic shock Insulin Shock .
laryngeal oedema. & respiratory distress along with massive vasodilatation.ANAPHYLACTIC SHOCK ETIOLOGY. anasthetics CLINICAL FEATURES. This histamine & slow release substance causes bronchospasm. laryngeal oedema. Which aggravates vasodilatation & causes hypotension and ultimately shock. & respiratory distress which totally leads to HYPOXIA. . dextrose. Commonly seen after penicillin administration or serum. Bronchospasm. Which increase the release of histamine & slow release substance of anaphylaxis by combination of antigen with IgE on the mast cells & basophils.
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