Shock
Is a clinical condition that occurs as a result of in adequate tissue perfusion.It results in metabolic dysfunction of cellular activities and is reversible when treated aggressively in the early state , but when allowed to continue results in cellular death, organ damage and death of the patient.
Types of shock :
1. Hypovolemic 2. Septic 3. Cardiogenic 4. Neurogenic 5. Anaphylactic shock
Other classification of shock
1.Hypovolemic
2. Cardiogenic
3. Obstructive (cardiac tamponade, tension pneumothorax, massive pulmonary embolus and air embolus).
4. Distributive (include septic shock, anaphylaxis neurogenicand spinal cord injury ).
5. Endocrine (include hypo- and hyperthyroidism and adrenal insufficiency).
Pathophysiology :
Increase (() catecholamine by adrenal glandThe juxtaglomerular apparatus of the kidney detects the decreased(() blood pressure, stimulating the release of renin which is converted the angiotensin causing peripheral vasoconstriction, as well as the release of aldosterone.
Increase (()secretion of antidiuretic hormone ( ADH) from the pituitary.
Cellular
As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. The product of anaerobic respiration is not carbon dioxide but lactic acid. When enough tissue is under perfused, the accumulation of
lactic acid in the blood produces systemic metabolic acidosis. As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of the sodium/potassium pumps in the cell membrane and intracellular organelles. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents, including potassium, are released into the bloodstream.
Microvascular
As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and coagulation systems. Hypoxia and acidosis activate complement and prime neutrophils, resulting in the generation of oxygen free radicals and cytokine release.These mechanisms lead to injury of the capillary endothelial cells. These in turn further activate the immune and coagulation systems. Damaged endothelium loses its integrity and becomes leaky. Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, exacerbating cellular hypoxia.
Systemic
CardiovascularAs preload and afterload decrease there is a compensatory baroreceptor response resulting in increased sympathetic activity and release of catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis ).
Respiratory
The metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of carbon dioxide (and so produce a compensatory respiratory alkalosis).Renal - Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The reninangiotensinaldosterone axis is stimulated resulting in further vasoconstriction and increased sodium and water
reabsorption by the kidney.
Endocrine -As well as activation of the adrenal and reninangiotensin systems, vasopressin (antidiuretic hormone) is released from the hypothalamus in response to decreased preload and results in vasoconstriction and reabsorption of water in the renal collecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water reabsorption and sensitizing the cells to catecholamines.
Ischaemiareperfusion syndrome
During the period of systemic hypoperfusion, cellular and organ damage progresses because of the direct effects of tissue hypoxia and local activation of inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypotension.
The cellular and humoral elements activated by the hypoxia (complement,
neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.
Multiple organ failure
Multiple organ failure is defined as two or more failed organ systems (Table 2.3). There is no specific treatment for multiple organ failure. Management is by supporting organ systems with ventilation, cardiovascular support and haemofiltration/dialysis until there is recovery of organ function. Multiple organ failure currently carries a mortality rate of 60%. Thus, prevention is vital by early aggressive identification and reversal of shock.
Table 2.3 Effects of organ failure
Lung Acute respiratory distress syndrome
Kidney Acute renal insufficiency
Liver Acute liver insufficiency
Clotting Coagulopathy
Cardiac Cardiovascular failure
RESUSCITATION
Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway and adequate oxygenation and ventilation. Once airway and breathing are assessed and controlled, attention is directed to cardiovascular resuscitation.
Fluid therapy
First-line therapy, is intravenous access and administration of intravenous fluids. Access should be through short, wide-bore catheters that allow rapid infusion of fluids as necessary. Long, narrow lines such as central venous catheters have too high a resistance to allow rapid infusion and are more appropriate for monitoring than fluid replacement therapy.Type of fluids
(normal saline, Hartmanns solution, Ringers lactate) and colloids(albumin or commercially available products).
Monitoring for patients in shock
Minimum■ Electrocardiogram
■ Pulse oximetry
■ Blood pressure
■ Urine output
Additional modalities
■ Central venous pressure
■ Invasive blood pressure
■ Cardiac output
■ Base deficit and serum lactate
1. Hypovolemic shock :
Is characterized by a loss of circulating volume.
(d.t decrease pre load.)
The type of fluid loss includes ,blood, plasma, fluid.
C.F
Pallor
Peripheral cooling
Prepheral venous constriction
Poor capillary filling
P.R
R.R
B.P ( Hypotension)
U.O.P , Oliguria
Thirst
Acidotic breathing
Later- Loss of consciousness
Treatment
2 cannulaOxygen
Lower the head and elevate the feet to ( VR
IVF
Blood replacement in case blood loss
check Vital sign , UOP
Rx underlying cause.
2. Cardiogenic shock :
Is due to in adequate heart pump.
Etiology
Intrinsic - as MI, Myocardial contusion.
extrinsic - cardiac tamponade
Clinical F .
palecool skin
slow capillary refill
low C.O.P
high PVR
Treatment
IVF, Oxygen
Diuretics and vasodilators to decrease the after load
Increase contractility of the heart by dobutamine, dopamine, isoproterenol.
(In cardiac tamponade treated by pericardiocentesis)
3. Septic shock
It is G ve septicemia & toxemia, mostly seen in surgical conditions like peritonitis, liver abscess-----Predisposing factors
DM, Alcoholism, steroid & cytotoxic therapy.
C.P
Early septic shock (High cardiac out put)
( PVR because of endotoxin
Warm and dry extremities
( capillary permeability
( C.O.P
( R.R
(PR
Intermittent pyrexia and rigor
B- Low cardiac out put
As the shock progresses, there is ( compensation by the heart as the myocardium function resulting ( , resulting in ( C.O.P------
(B.P
Vasoconstriction, occurs creating cool extremities
( U.O.P ( Oliguria)
ATN of the kidney
Jaundice d.t liver damage
Confusion
Treatment
Ventilation
Fluid and electrolyte balance
Urinary cath.
Blood culture
Antibiotics
Inotropic agents to support heart
Steroid
Treatment underlying cause as drainage of abscesses or debridement of any necrotic tissue.
4.Neurogenic shock
D.t sympathetic tone interruptiongeneralized vasodilation , (B.P, (SVR, (PR, warm, dry skin. Pink e.g spinal cord transactionTreatment
Trendelenburg position
IVF
Vasoconstrictor drugs
Vasovagal shock
d.t sudden sever pain or sever emotional reaction.
It is d.t ( tone of Vagus nerve ---( HR and vasodilatation--- (B.P--- (VR and (C.O.P
Rx : lower the head & elevate the limbs to ( blood flow to the brain.
5. Anaphylactic shock
Mainly d.t pencillins, others Dextran, Serum, Stings.
Ag combined with Ig E on the mast cells & basophil---release histamine ---bronchospasm,laryngeal oedema,hypotension, massive vasodilatation---shock
Rx:
Steroids - H.C
Antihistamine- chlorpheniramine
Bronchodilator Adrenaline
Cardiovascular and metabolic characteristics of shock
Hypovolaemia Cardiogenic Obstructive Distributive
Cardiac output Low Low Low High
Vascular resistance High High High Low
Venous pressure Low High High Low
Mixed venous saturation Low Low Low High
Base deficit High High High High
Clinical features of shock
Compensated Mild Moderate SevereLactic acidosis
Urine output Normal Normal Reduced Anuric
Level of consciousness Normal Mild anxiety Drowsy Comatose
Respiratory rate Normal Increased Increased Laboured
Pulse rate Mild increase Increased Increased
Bloodpressure Normal Normal Mild hypotension Severe hypotension