DEFINITION:-

Shock is an acute clinical syndrome characterized by poor tissue perfusion with impaired cellular metabolism, which is manifested as different serious pathophysiological abnormalities.

Shocked patient

CLASSIFICATION OF SHOCK

Hypovolaemia

Cardiogenic

Intrinsic

Compressive

Septic

Hyperdynamic

Hypodynamic

Anaphylactic

Traumatic

Neurogenic

Hypoadrenal

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.

Septic shock:-

Due to bacterial infxn and its toxins.

Cardiogenic shock:-

Acute MI, Acute carditis

Acute pulmonary thromboembolism

Toxaemia of any cause

Cardiac compression due to cardiac temponade or trauma.

Neurogenic shock:-

Due to sudden anxious or painful stimuli causing splanchnic vasodilatation

Anaphylactic shock

Type I hypersensitivity rxn

Penicillin, anesthetics, stings, venoms, shellfish

Others:-

Addison’s disease

myxoedema

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
• 
  

HYPOVOLAEMIC SHOCK

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.

DECOMPENSATED HYPOVOLAEMIA:-

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

Coma

Peripheral Pulses impalpable

Decreased CO

V/P- mismatch.

MANAGEMENT

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 :-

VITALS:-

HR:- rate :- tachycardia then later bradycardia.

rhythm may be thready and irregular

RR:- tachapnoea

BP:-systolic BP increased.

TEMP:- may be normal.

URINARY OUTPUT:- decreased.

INVESTIGATIONS:-

PULSE OXYMETER:- to determine venous oxygen saturation.

ABG analysis:- hypoxemia , metabolic acidosis.

SERUM  ELECTROLYTE:-

hyperkalaemia, hypocalcaemia, metabolic acidosis.

CVP:-

PCWP:-

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

TREATMENT

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 :-

Pressure packing,

Position and rest

Tourniquet

Surgical methods.

immediately send the blood for cross matching and transfusion of Blood as soon as possible.

IONOTROPHIC DRUGS:-

DOPAMINE ( 3 – 10gm/kg/min) .iv-improves renal and splanchnic blood

DOBUTAMINE ( 2 – 8 gm/kg/min) :- Improves CO

CORRECT ACID BASE AND ELECTROLYTE BALANCE

SEPTIC SHOCK

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:-

Reversible stage

Pyrogenic response is still intact.

C/F:- fever , tachycardia and tachypnoea

warm dry skin

HYPODYNAMIC ( COLD) SHOCK:-

Decompensated 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

Investigation:-

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.

CARDIOGENIC SHOCK

Here intravascular volume is Normal or increased.

Cardiac dysfunction limits the cardiac output and leads to:-

Raised lf atrial pressure

Increased pulmonary artery pressure

Pulmonary edema

Raised Rt ventricular overload and failure.

Causes:-

myocarditis, Acute MI, cardiomyopathy, dysarrhythmia

congenital and acquired heart disease ,metabolic derangement,

Drug intoxication and poisons.

Treatment

Bed rest

Propped position

O2 inhalation

Vitals monitoring

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.

Anaphylactic shock

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

IV fluids

Adrenaline 100g IV, Antihistaminics, steroids,

Ventilator  in  severe cases

Cardiac massage , defibrillation