SHADES OF SHOCK 4

4.4 Cardiogenic shock occurs most often as result of i) Myocardial infarction (MI) ii) Tamponade (collection of blood in the pericardium due to leak from the myocardium) This shock is due to cardiac muscle being unable to maintain
adequate cardiac output from causes intrinsic to the heart
muscle such as MI, cardiomyopathy, or drug toxicity or causes
extrinsic to heart muscle such as compression i.e. tamponade,tension pneumo- thorax or pulmonary embolus (3.3).

Cardiogenic Shock
The syndrome of cardiogenic shock is defined as the inability of the heart (as a result of reduction of its pumping function) to deliver sufficient blood flow to the tissues to meet resting metabolic needs. Thus, the clinical definition of cardiogenic shock requires a low cardiac out put and evidence of tissue hypoxia in the presence of an adequate intravascular volume. -If hemodynamic monitoring is available, the diagnosis is confirmed by the combination of a low systolic blood pressure and a depressed cardiac index (<2,2 l/min/m2) in the presence of an elevated pulmonary capillary wedge pressure (>15mmHg)
-A reduced blood pressure activates the baroreceptors.
-The adrenergic response leads to an increase in heart rate, myocardial contractility, and arterial and venous vasoconstriction.
-The renin angiotensin system is activated by inadequate renal perfusion and sympathetic stimulation, leading to additional vasoconstriction and salt and water retention.
Finally, hypotension increases the secretion of antidiuretic hormone, which further increase water retention. The reduction in blood pressure in conjunction with an elevated left ventricular end diastolic pressure resulting from fluid retention and low left ventricular function reduces coronary perfusion pressure and thus myocardial oxygen delivery.
Increase in heart rate, systemic vascular resistance, and contractility all increase myocardial oxygen consumption and demand.
-The difference between myocardial oxygen demand and oxygen delivery further reduces left ventricular function and will lead to circulatory collapse.
The clinical picture of cardiogenic shock is remarkably similar to those of hypovolemic shock.
-In making the diagnosis of cardiogenic shock, history of cardiac disease may be of great value. -Physical exam demonstrates inadequate tissue perfusion with an elevated jugular venous pressure, an S3 gallop, and pulmonary edema. -A chest radiograph provides diagnostic information regarding the presence of pulmonary edema, pleural effusion, or cardiac chamber enlargement.
-Cardiac enzymes may provide evidence of acute myocardial infarction.

Arterial blood gas analysis provides information regarding the adequacy of gas exchange. Severe hypoxia in the presence of a normal chest radiograph may support the diagnosis of massive pulmonary embolus rather than a primary cardiac cause of shock.
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SHADES OF SHOCK 3

4.3 Neurogenic shock due to decreased peripheral resistance
resulting from:
I) Increase vagal tone as in case of severe pain,
intense emotion, can lead to slow heart rate.
ii) Spinal anesthesia leading to loss of sympathetic impulse
And enlarged blood vessels-leads to pooling of blood


Neurogenic shock, can occur in severe injury to the spinal cord/
head injury-results in failure of the sympathetic nervous
system resulting in insufficient vascular tone.
The vasodilatation and increased venous capacity results in less
cardiac filling (3.1) and poor vascular resistance-less tissue perfusion and shock .

Neurogenic Shock
Hypotension and bradycardia may occur following acute cervical or high thoracic spinal cord injury.
-This result from blockage of sympathetic outflow in presence of unopposed vagal tone result in clinical features referred to as neurogenic shock,
-The diagnosis should be suspected in any patient with hypotension and bradycardia following injury.
-In some cases, these findings may represent the first suggestion of a spinal cord injury in a comatose patient.
-The patient with neurogenic shock is typically warm and well perfused.
-If a pulmonary artery catheter is in situ, the cardiac index may be elevated while the systemic vascular resistance is markedly reduced.
-Occult hemorrhage should be ruled out before attributing spinal cord injury as the exclusive cause of hypotension.
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SHADES OF SHOCK 2

4.2 Bacteraemia (septic shock)
Also named, Toxic shock, and Distributive shock.
It is diagnosed more often in surgical practice today.
There are more aged, immune-compromised patients in hospital.
There are more implants and interventions.
There are more post trauma admissions.

*Septic Shock
Septic shock is the second most frequent cause of shock in the surgical patients.
Invasive bacterial infection represents the most common cause of septic shock, with the most likely sites of infection being the lungs, abdomen, and urinary tract.
Bacterial products cause release of cytokines, tumor necrosis factor-alpha (TNF –alpha) and thromboxanes platelet activating factor, prostaglandin’s etc.
The inflammatory milieu induces several circulatory changes
First, myocardial depression is often evident despite an increase in cardiac index. Several factors contribute to cardiac dysfunction, including biventricular dilatation, myocardial hypo-responsiveness to catecholamine, and diastolic dysfunction.
-Together these phenomena result in a significant reduction in ejection fraction and a sub-optimal response to volume infusion that persists for as long as 10 days.
-The increase in cardiac index despite a reduction in myocardial contractility occurs as a result of a profound reduction in vasomotor tone, the principal cause of hypotension in septic shock.
-The reduction in venous tone leads to pooling of blood in large capacitance vessels, effectively reducing circulating blood volume.
-Several microcirculatory changes also occur distinct from change in vasomotor tone.
These also play a role in the manifestations of septic shock.
The mediator environment of sepsis,
-results in activation of the coagulation cascade,
-leading to micro-thrombus formation, leading to capillary plugging.
This micro-vascular occlusive phenomenon induces the opening of arteriovenous shunts, effectively depriving tissues of adequate perfusion.
Several pro-inflammatory mediators also increase neutrophil endothelial adherence and subsequent exit of activated inflammatory cells into the interstitium where they induce tissue injury.
Increased vascular permeability results in edema which effectively increase the distance required to be covered for cellular oxygen delivery and the opening of arterio-venous shunts, induces cellular hypoxia.


Clinical
Early manifestations of severe sepsis, include, tachypnea, tachycardia, oliguria, and changes in mental status.
-Thus, these simple clinical features should be considered evidence of impending shock in those at risk.
-These clinical features may be followed by the onset of fever and leukocytosis.
Early aggressive management is required to minimizing the morbidity and mortality of septic shock.
- The systemic vaso-dilation and increase in micro-vascular permeability result in patients to require large amount of intravenous fluid to restore a normal blood pressure.
- Vasopressors used are dopamine, epinephrine, or nor-epinephrine if there is an inadequate blood pressure response to fluid resuscitation.
- In-patients not responding to fluid infusion or those with underlying cardiac of renal disease, the use of pulmonary artery catheter is indicated.
- The resuscitation process is incomplete without all measures to reverse the infections process as early as possible.
- The correct choice of antibiotic or antibiotic combination is required.
- If the infection source is an abscess or there is a prior soiling of the pleural or peritoneal cavities, then either drainage or control of contamination is mandatory.
- Similarly, necrotic, infected tissue requires aggressive debridement.*
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SHADES OF SHOCK

4. Shock Syndromes

The events of shock may result from:

4.1 Oligemic (Hypo-volemic) shock due to decrease in circulating
blood volume resulting from :
i) Hemorrhage (internal or external)
ii) Loss of fluid as in burns,trauma(Third space) or
dehydration
iii) Decreased extra-cellular fluid because of hypo-natreamia
as in Addison's disease

Hypovolemic shock occurs most often following trauma resulting
in blood loss.
It also occurs following GI bleeds, or a leak from an aneurysm.
Plasma volume losses can occur in trauma, burns, intestinal obstruction, diarrhea and heat stoke.
*Hypovolemic shock
Hypovolemic shock is the most common cause of shock. It may occur as a result of one of two events:
1. hemorrhage, representing intravascular volume decrease through the loss of whole blood or
2. loss of plasma volume through extra-vascular fluid loss or fluid loss from gastrointestinal, urinary tracts, and insensible loss.
-Hemorrhage is the form of volume loss that is common in practice can be measured and studied and thus is the better understood form of shock.
-Extra-vascular internal fluid leak, also referred to as “third space” fluid losses, is frequently unnoticed as a cause of shock.
-Third space fluid losses are the principal cause of volume loss in the early postoperative period and in local inflammatory processes, such as pancreatitis, in which local changes in capillary permeability result in fluid extravasations from the intravascular space into the interstitial space.
-Fluid leak is the principal cause of shock in patients with small bowel obstruction.
In this case, volume loss results from fluid loss into the interstitial space, bowel lumen, and exudation of fluid into the peritoneal cavity.
-The clinical manifestations of nonhemorrhagic forms of hypovolemic shock are the same as with hemorrhage, although they can be more slow in onset.
-The physiological responses of the body to hypovolemic shock are aimed at maintenance of cerebral and coronary perfusion and improving the circulating blood volume. The major compenstory mechanisms include
- An increase in sympathetic activity
- Release of stress hormones and
- Volume improvement through restoration of interstitial fluid, mobilization of intracellular fluid, saving of fluids and electrolytes by the kidney.
The clinical picture reflects this intense adreno-sympathetic response and renal conservation of fluid.
-Micro-vascular low perfusion of some vascular beds of organs results from a combination of low intravascular blood volume, diminished cardiac output resulting from a reduction in venous return and preload, and compensatory vaso-constriction.*
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