Shock is an acute clinical syndrome characterized by poor tissue perfusion with impaired cellular metabolism, which is manifested as different serious pathophysiological abnormalities.
CLASSIFICATION OF SHOCK
CAUSES OF SHOCK
Hypovolaemia shock:- due to reduction in total Blood volume.
Loss of blood:- hemorrhagic shock, RTA, major surgeries.
Loss of plasma:- burn shock, pancreatitis.
Loss of fluid:- diarrhea, vomiting , renal loss of water, DI etc.
Due to bacterial infxn and its toxins.
Acute MI, Acute carditis
Acute pulmonary thromboembolism
Toxaemia of any cause
Cardiac compression due to cardiac temponade or trauma.
Due to sudden anxious or painful stimuli causing splanchnic vasodilatation
Type I hypersensitivity rxn
Penicillin, anesthetics, stings, venoms, shellfish
PATHOPHYSIOLOGY OF SHOCK
- low CO
- vasoconstriction in vital organs(Brain, kidney, heart, liver.)
- Minute volume 1.5 – 2 times increased
- RR :- 2 – 3 times increased
- Decreased blood flow to kidney
- Decreased GFR and urinary output
- Release of ADH and activation of RAS and increased aldosterone.
- Increased water retention and decreased urine output.
- As CO falls
- hypotension and tachycardia
- Decreased coronary perfusion
- This in conjunction with hypoxia causes Metabolic Acidosis
- Release of specific cardiac depressant
- Further pump failure.
- Due to lack of oxygen in cells
- Anaerobic respiration- lactic acidosis
- Na+ K- pump failure -hyperkalaemia
- Calcium enters the cells- hypocalcaemia
- further intracellular lysosome breakdown and release powerful enzymes causing further damage
- Sick cell syndrome
- Platelets are activated forming small clots in many places
- DIC ( consumption coagulopathy)
- Further Bleeding
CONVERT COMPENSATED HYPOVOLAEMIA:-
Presence of reduced circulating blood volume without very obvious associated physical sign.
Often difficult to diagnose.
In conscious ptn CNS features are best guide
CF:- Nausea, drowsiness, hiccups, thirst.
Lab inv:- urine analysis:- increased urinary osmolality and decreased Na+ concn.
OVERT COMPENSATED HYPOVOLAEMIA
Here there is hypovolumia to an extent then reflex mechanism required to maintain perfusion to the vital organs.
O/E:- tachycardai, tachapnoea , wide arterial pulse pressure, systolic BP increased, pale, cool clammy extremities., drowsiness, confusion.
if diagnosis is uncertain:- Gentle head down ,bed tilting
Leg raising or administration of iv bolus fluid.
if diagnosis is true
Increase venous return , decrease HR, narrow pulse pressure , reduce RR, and overall well being improved.
ABG analysis:- hypoxaemia, metabolic acidosis.
Severe degree of hypovolaemia
reflex mechanism insufficient to compensate blood flow to vital organ. So decreased perfusion of vital organs.
C/F:- Mean arterial pressure falls
Tachycardia changes to Bradycardia
Conscious level severely compromised
Peripheral Pulses impalpable
HISTORY:- h/o blood loss, fluid loss, plasma loss.
C/F:- depends on the type of hypovolaemia.
DIAGNOSIS:- depends on clinical monitoring and investigation.
CLINICAL MONITORING :-
HR:- rate :- tachycardia then later bradycardia.
rhythm may be thready and irregular
BP:-systolic BP increased.
TEMP:- may be normal.
URINARY OUTPUT:- decreased.
PULSE OXYMETER:- to determine venous oxygen saturation.
ABG analysis:- hypoxemia , metabolic acidosis.
hyperkalaemia, hypocalcaemia, metabolic acidosis.
ECG:- to monitor or detect cardiac arrhythmia.
CHEST X-RAY:- mediastinal trauma or cardiac tamponade.
USG ABDOMEN:- to detect intra abdominal Hge from spleen and liver
OBJECTIVE:- to treat the cause
to increase CO
to improve tissue perfusion( coronary, cerebral, renal and mesenteric vascular beds)
Hospitalize the patient:-
Airway / Breathing should be secured
O2 inhalation, intubation, artificial ventilation if required.
Intravenous line:- to be opened with wide bore canula as soon as possible.
infuse crystalloid (R/L) or colloid ( albumin, gelatin, haemaccel ,hetastarch
If it is a case of HAEMORRHAGE:-
Take specific measure to control hemorrhage :-
Position and rest
immediately send the blood for cross matching and transfusion of Blood as soon as possible.
CORRECT ACID BASE AND ELECTROLYTE BALANCE
Cause:- due to Gm -ve and Gm +ve organism, fungi, viruses and protozoa
Gm -ve septicaemia is also known as endotoxic shock.
Commonly seen in strangulated intestine, peritonitis m GI fistula, urinary infxn, pancreatitis, major surgical wounds etc.
Pathophysiology of septic shock
- Toxins , endotoxins from Gm -ve organism( E.coli, klebsiella, pseudomonas and proteus)
- Inflammation, cellular activation( macrophages,neutrophils, monocytes)
- Release of cytokines free radicals
- Chemotaxis of cells. Endothelial injury, altered coagulation cascade-SIRS.
- Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea
- Severe circulatory failure wit MODS ( failure of lungs, kidneys, liver , heart) with DIC
- Hypodynamic, irreversible cold stage of septic shock.
STAGES OF SEPTIC SHOCK
HYPERDYNAMIC ( WARM ) SHOCK:-
Pyrogenic response is still intact.
C/F:- fever , tachycardia and tachypnoea
warm dry skin
HYPODYNAMIC ( COLD) SHOCK:-
Pyrogenic response is lost.
Irreversible stage along with MODS.
Generalized capillary permeability , leakage causes hypovolaemia, decreased CO , tachycardia, vasoconstriction
C/F:- cold clammy skin, drowsy, tachapnoeic
Culture & sensitivity :- Blood, Pus , Urine.
USG/ CT:-To find out source of infection.
Treatment of septic shock
- Correction of fluid and electrolyte by crystalloids , blood transfusion.
- Start antibiotics of high generation like cephalosporin, aminoglycosides, metronidazole.
- Treat the cause or focus:- drainage of abscess, laparotomy for peritonitis, resection of gangrenous bowel wound excision.
- Critical care, O2, ventilator support, dobutamine /dopamine /NA to maintain BP and urine output.
- Activated protein C :- prevent release and block the effect of inflammatory mediator on cellular function.
- Monitor:- pulse, BP, RR, urinary output, level of consciousness.
Here intravascular volume is Normal or increased.
Cardiac dysfunction limits the cardiac output and leads to:-
Raised lf atrial pressure
Increased pulmonary artery pressure
Raised Rt ventricular overload and failure.
myocarditis, Acute MI, cardiomyopathy, dysarrhythmia
congenital and acquired heart disease ,metabolic derangement,
Drug intoxication and poisons.
Volume expansion( iv fluids)
Drugs:- dopamine or
dobutamine + epinephrine.
After load reducing agent:- nitroprusside , milrinone.
Deteriorating Cardiogenic shock:- Lf ventricular assisted device
Rt ventricular assisted device.
PATHOPHYSIOLOGY- antigens combine with IgE of mast cells and basophils , releasing histamine and large amount of SRS-A
CAUSES– Injections- penicillin , anaesthetics , stings, venoms
C/F– sudden onset
bronchospasm , laryngeal oedema
Generalised rashes, oedema
respiratory distress , hypotension , feeble pulse
T/T– Oxygen with foot end elevation
Adrenaline, Antihistaminics, steroids,
Ventilator in severe cases
Cardiac massage , defibrillation