SHOCK Flashcards
DEFINE SHOCK
A STATE OF TISSUE HYPOPERFUSION AND CELLULAR HYPOXIA RESULTING IN REDUCE CO AND REDUCE ECV.
TYPES OF SHOCK
- HYPOVOLAEMIC SHOCK
- CARDIOGENIC SHOCK
- ANAPHYLACTIC SHOCK
- SEPTIC SHOCK
- NEUROGENIC SHOCK
HYPOVOLAEMIC SHOCK
INADEQUATE BLOOD OR PLASMA VOLUME
CAUSE OF HYPOVOLAEMIC SHOCK
HAEMORRHAGIC
- POST PARTUM BLEEDING
- BLEEDING OESOPHAGEAL VARICES
- TRAUMA
- ANEURYSM RUPTURE
- MASSIVE HAEMOPTYSIS
NON HAEMORRHAGIC
- SEVERE VOMITING/ DIARRHEA
- BURN
- INCREASED URINE OUTPUT SUCH AS IN DKA, HHS
- ACUTE PANCREATITIS
- DENGUE SHOCK SYNDROME
MECHANISM OF HYPOVOLAEMIC SHOCK
REDUCED ECV D/T BLOOD / PLASMA LOSS -> REDUCE VR -> REDUCE CO -> SYSTEMIC TISSUE HYPOPERFUSION -> WIDESPREAD OF CELLULAR HYPOXIA -> IMPAIRED IN THE CELLULAR METABOLISM AND CELL DEATH -> IRREVERSIBLE CELL INJURY -> MULTIPLE ORGAN DYSFUNCTION
CAUSE OF CARDIOGENIC SHOCK
- MYOCARDIAL INFARCTION
- VENT. RUPTURE
- MYOCARDIAL CONTUSION
- ARRHYTHMIA
- CARDIOMYOPATHY
- VALVULAR DEFECTS
- TENSION PNEUMOTHORAX
- CARDIAC TAMPONADE
- LARGE PE
MECHANISM OF CARDIOGENIC SHOCK
CARDIAC PUMP FAILURE D/T
1. INTRINSIC DAMAGE
2. EXTRINSIC COMPRESSION
3. OUTFLOW OBSTRUCTION
-> REDUCE CO -> SYSTEMIC TISSUE HYPOPERFUSION -> WIDESPREAD OF CELLULAR HYPOXIA -> IMPAIRED IN THE CELLULAR METABOLISM AND CELL DEATH -> IRREVERSIBLE CELL INJURY -> MULTIPLE ORGAN DYSFUNCTION
DEFINE SEPTIC SHOCK
MICROBIAL INFECTION A/W SYSTEMIC HOST INFLAMMATORY RESPONSE
MECHANISM OF SEPTIC SHOCK
REFER TO NOTES
DEFINE ANAPHYLACTIC SHOCK
IG-E MEDIATED HYPERSENSITIVITY REACTION TOWARDS ALLERGEN
MECHANISM OF ANAPHYLACTIC SHOCK
REFER NOTES
DEFINE NEUROGENIC SHOCK
SPINAL CORD INJURY RESULTING IN AUTONOMIC DYSFUNCTION
EXAMPLE CAUSES OF NEUROGENIC SHOCK
MVA
SPORTS INJURY
FALLS
ACTS OF VIOLENCE
OCCUPATIONAL ACCIDENT
NATURAL DISASTER
MECHANISM OF NEUROGENIC SHOCK
REFER NOTES
STATE THE STAGE OF SHOCK
- NON PROGRESSIVE (COMPENSATED) STAGE
- PROGRESSIVE (DECOMPENSATED) STAGE
- IRREVERSIBLE STAGE
BRIEFLY DESC COMPENSATED STAGE
- NEURAL REGULATION
- REDUCE CO AND PERFUSSION PRESSURE
- DETECTED BY THE BARORECEPTOR
- ACTIVATION OF THE SYMPATHETIC STIMULATION
- INCREASE IN THE MYOCARDIAL CONTRACTILITY
- INCREASE IN THE HR
- VASOCONSTRICTION SUPPLYING THE NON VITAL ORGAN -> SHUNTING OF BLOOD TO THE VITAL ORGAN
- INCREASE RESP. RATE - HORMONAL REGULATION
- RAAS PATHWAY ACTIVATION
- ADH AND ALDOSTERONE SECRETION
- NA+ REABSORPTION
- WATER RETENTION
- VASOCONSTRICTION - BIOCHEMICAL REGULATION
- STIMULATING THE RESP CENTRE
- D/T CELLULAR HYPOXIA -> LACTIC ACIDOSIS
- INCREASE IN THE H+ PRODUCTION
- REDUCE THE PH
- COMPENSATE: HYPERVENTILATION
BRIEFLY DESC PROGRESSIVE STAGE
PERSISTENT SHOCK -> COMPENSATORY MECHANISM OVERWHELMED -> OXYGEN DEFICIT INCREASE -> ANAEROBIC GLYCOLYSIS -> LACTIC ACID PRODUCTION INCREASE -> INCREASE H+ -> METABOLIC ACIDOSIS AND FALL OF PH -> BLUNT THE VASOMOTOR RESPONSE -> PERIPHERAL VASODILATION AND POOLING OF BLOOD -> TISSUE HYPOPERF. -> CELLULAR HYPOXIA
VITAL ORGAN START TO FAIL:
- REDUCE CO
- RESP DISTRESS
- OLIGURIA
- ALTERED MENTAL STATUS
BRIEFLY DESC IRREVERSIBLE SHOCK
WIDESPREAD CELLULAR HYPOXIA -> ABNORMALITIES IN METABOLIC FUNCTION AND CELL DEATH -> IRREVERSIBLE INJURY D/T:
- LEAKAGE OF LYSOSOMAL ENZYME
- WORSENING OF THE MYOCARDIAL CONTRACTILE F(X) D/T INCREASE NO SYNTHESIS
- ISCHAEMIC BOWEL -> INTESTINAL FLORA TO ENTER THE CIRCULATION -> SUPERIMPOSED SEPTIC SHOCK
- ISCHAEMIC KIDNEY -> RENAL FAILURE
BY TIME, IT CAN LEAD TO DEATH
5 COMPLICATIONS OF SHOCK
BRAIN: COMA
HEART: MYOCARDIAL INFARCTION
KIDNEY: ATI
RESP: RESP FAILURE/ ARDS
GI: BOWEL INFARCTION
LAB FINDINGS OF DIC
- THROMBOCYTOPENIA (LOW PLATELET)
- PROLONGED PT/APTT (CLOTTING FACTOR REDUCE)
- LOW FIBRINOGEN
- ELEVATED FIBRIN DEGRADATION PRODUCT SUCH AS D- DIMER
BAD PROGNOSIS
SEPTIC
CARDIOVASCULAR
SHORTER DURATION OF SHOCK HAVE __ OUTCOME
BETTER
