Shock: Quick Review and Management.

SHOCK

DEFINITION:-

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

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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


4 Comments
  1. June 22, 2010
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  3. March 26, 2014
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