8. PRESENTATION OF SHOCK
A patient with a history of having had any one of the causative
events listed under Shock syndrome presents with:
* Pallor best seen on the face
* Cold moist skin of the extremities(vasoconstriction of skin
vessels)
* Rapid weak pulse (>90/min) and a collapse of superficial veins
because of compensatory peripheral vasconstriction
* Cyanosis and rapid shallow breathing (air hunger)
* Patient may have tendency to vomit and is restless,
later there may be diminishing sensibility, drowsiness and
coma
** On examination there is a declining pulse pressure
followed latter by a drop in blood pressure (systolic < 90 mm
of Hg)
9. MONITORING
In an average hospital or Nursing home, the patient with any of the shock syndromes, is observed, and progress assessed, recording the following
parameters:
* Blood pressure
* Central Venous pressure
* Haematocrit
* Arterial blood gases
* Urine output
All these values, if altered, are the late manifestations of shock.
Thus it is difficult to assess the treatment of shock.
Normal values may not reflect reversal of shock and give no indication of tissue perfusion or O2 debt. Thus silent hypoxia remains undetected.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for access and review
Wednesday, September 1, 2010
Wednesday, August 25, 2010
SHOCK INTERNAL EVENTS
7. PATH PHYSIOLOGY OF SHOCK
Hypo-perfusion, and O2 lack, are common to all types of shock
syndromes.
Shock syndromes, may vary in severity, from silent tissue hypoxia,
to multiple organ failure.
In cases of septic shock, hyper-dynamic circulatory state, is
accompanied by a high O2 debt, due to excessive O2 demand in the presence of infection resulting in hypoxia.
Any Impaired tissue perfusion, leads to low delivery of oxygen in
relation to tissue needs,this is the basic cause of shock state.
The precise role of hypoxia, in pathogenesis of shock, is not clear as yet.
With improved techniques, it is hoped this role will be better
understood. However the events that follow shock states are;
7.1 Acidosis
As the oxygen delivery is deficient to meet O2 demand of tissues,
anaerobic glycolysis (breakdown) starts.
In the absence of O2 pyruvate is converted to lactate, and two molecules of adenosine troposphere (ATP) are made available.
In cases of adequate O2 3 molecules of ATP are released per one molecule of glucose utilized.
As the O2 diminishes, lactate increases and pyruvate diminishes.
This high Lactate level has been correlated with survival in
studies where lactate concentration increase beyond O-2m mol per
liter.
The effects of metabolic acidosis are;
-bradycardia,
-vasodilatation,
-decreased cardiac output and
-ventricular fibrillation.
7.2 Circulatory Redistribution
As a result of hypoxia, the homeostatic response is to preserve
oxygen delivery, to heart and the brain.
This is achieved by diverting blood flow, from other organs (skin, GI tract).
This is achieved through vasoconstriction of skin and visceral
circulation.
The agents responsible for this vasoconstriction
are :
* Catecholamine
* Angiotensin-II
* Vasopressin
* Endothelin
* Thromboxane A2
The changes in microcirculation in redistribution of blood flow
leads to slowing of flow, high viscosity of blood and sludging,
leading to intravascular coagulation and occlusion of capillary
channels.
As a consequence, intestinal mucosal injury occurs, gut
permeabilty may increase, and enteric bacteria and toxins move
across the gut wall, and invade the circulation via lymphatics and
portal venous system.
This is known as bacterial translocation.
Thus, the end effect of vasoconstriction in gut circulation can
lead to ischaemia and irreveresable shock, SIRS and MODS.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for access and review
Hypo-perfusion, and O2 lack, are common to all types of shock
syndromes.
Shock syndromes, may vary in severity, from silent tissue hypoxia,
to multiple organ failure.
In cases of septic shock, hyper-dynamic circulatory state, is
accompanied by a high O2 debt, due to excessive O2 demand in the presence of infection resulting in hypoxia.
Any Impaired tissue perfusion, leads to low delivery of oxygen in
relation to tissue needs,this is the basic cause of shock state.
The precise role of hypoxia, in pathogenesis of shock, is not clear as yet.
With improved techniques, it is hoped this role will be better
understood. However the events that follow shock states are;
7.1 Acidosis
As the oxygen delivery is deficient to meet O2 demand of tissues,
anaerobic glycolysis (breakdown) starts.
In the absence of O2 pyruvate is converted to lactate, and two molecules of adenosine troposphere (ATP) are made available.
In cases of adequate O2 3 molecules of ATP are released per one molecule of glucose utilized.
As the O2 diminishes, lactate increases and pyruvate diminishes.
This high Lactate level has been correlated with survival in
studies where lactate concentration increase beyond O-2m mol per
liter.
The effects of metabolic acidosis are;
-bradycardia,
-vasodilatation,
-decreased cardiac output and
-ventricular fibrillation.
7.2 Circulatory Redistribution
As a result of hypoxia, the homeostatic response is to preserve
oxygen delivery, to heart and the brain.
This is achieved by diverting blood flow, from other organs (skin, GI tract).
This is achieved through vasoconstriction of skin and visceral
circulation.
The agents responsible for this vasoconstriction
are :
* Catecholamine
* Angiotensin-II
* Vasopressin
* Endothelin
* Thromboxane A2
The changes in microcirculation in redistribution of blood flow
leads to slowing of flow, high viscosity of blood and sludging,
leading to intravascular coagulation and occlusion of capillary
channels.
As a consequence, intestinal mucosal injury occurs, gut
permeabilty may increase, and enteric bacteria and toxins move
across the gut wall, and invade the circulation via lymphatics and
portal venous system.
This is known as bacterial translocation.
Thus, the end effect of vasoconstriction in gut circulation can
lead to ischaemia and irreveresable shock, SIRS and MODS.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for access and review
Wednesday, August 18, 2010
SHOCK COMPENSATORY CASCADE
6. COMPENSATORY MECHANISM
6.1 The baroreceptors in the aortic arch and carotid sinus receive the signal of falling BP and send less afferent stimuli to the vasomotor centre in the medulla.
This results in enhanced sympathetic tone ending in arteriorlar and venous constriction.
There is increase in the after load and increase in venous
return to the heart (increase pre-load).
The vascular constriction is least in cardiac and cerebral circulation.
The enhanced adrenal medullary output of catacholamines results in
increased heart rate and mycardial contractility.
All these mechanisms improve cardiac output.
6.2 Antidiuretic hormone (ADH) is also released from the
posterior pituitary in response to the hypovolemia.
This ADH produces vaso-constriction in the visceral circulation and
increased re-absorbtion of water from the distal tubules of the
kidney.
6.3 Renin secretion is also stimulated by the hypo-perfusion of
juxta-glomerular apparatus in the kidney.
This leads to formation of angiotensin-I in the liver and later to angiotensin-II in the lungs.
This angiotensin-II is a powerful vasoconstrictor. This
is also a signal for release of aldersterone from the adrenal
cortex.
6.4 The aldersterone is a valuable restorer of circulating volume
by re-absorbtion of sodium from the renal tubules.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
6.1 The baroreceptors in the aortic arch and carotid sinus receive the signal of falling BP and send less afferent stimuli to the vasomotor centre in the medulla.
This results in enhanced sympathetic tone ending in arteriorlar and venous constriction.
There is increase in the after load and increase in venous
return to the heart (increase pre-load).
The vascular constriction is least in cardiac and cerebral circulation.
The enhanced adrenal medullary output of catacholamines results in
increased heart rate and mycardial contractility.
All these mechanisms improve cardiac output.
6.2 Antidiuretic hormone (ADH) is also released from the
posterior pituitary in response to the hypovolemia.
This ADH produces vaso-constriction in the visceral circulation and
increased re-absorbtion of water from the distal tubules of the
kidney.
6.3 Renin secretion is also stimulated by the hypo-perfusion of
juxta-glomerular apparatus in the kidney.
This leads to formation of angiotensin-I in the liver and later to angiotensin-II in the lungs.
This angiotensin-II is a powerful vasoconstrictor. This
is also a signal for release of aldersterone from the adrenal
cortex.
6.4 The aldersterone is a valuable restorer of circulating volume
by re-absorbtion of sodium from the renal tubules.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
Tuesday, August 10, 2010
SHOCK TO RECOGNISE AND MANAGE
5. MANAGEMENT
HYPOVOLEMIC SHOCK is the common form in practice, we use this form as working model.
The signs and symptoms appear only when the loss from
the circulatory system is above a certain volume usually (750 cc)
The compensatory mechanism fail and tissue perfusion suffers as
a result.
A summary of these volume losses and manifestations
in a seventy kilogram man are given below:
-Thus the first sign may be a rise in pulse rate because of increase in catecholamine.
-As the loss of blood or fluid continues the pulse rises and the systolic BP falls.
-The urine production per hour drops.
-The mental state passes through stages of apprehension, anxiety and lethargy to coma
A clinical staging system of hemorrhagic shock based on the percentage of acute blood volume loss has been described
Typically
-Classes I(Loss of 750cc of blood) and II(loss of 750-1500) are referred to as compensated shock states in which the adrenergic response maintains a normal blood pressure.
-Passing from a compensated state of shock to class IV (uncompensated) shock may occur rapidly in children and young adults.
-De-compensation of homeostatic mechanisms and inability to maintain systolic blood pressure above 90 mmHg after trauma induced hypovolemia are associated with a mortality of more than 50%.
However, rapid and adequate restoration of circulating blood volume simultaneous with control of bleeding can reverse even severe hemorrhagic shock.
It is thus crucial to recognize compensated shock early and intervene with speed for good results.
Laboratory evaluation may provide some diagnostic information.
- Non hemorrhagic forms of hypovolemic shock cause hemoconcentration.
- If there is loss of free water, then hemoconcentration will occur with hyponatremia.
- Following acute hemorrhage there may be no alteration in the hemoglobin or hematocrit values when compensatory fluid shifts occur fluids are administered hemoglobin and hematocrit will drop.
In clinical situations in which the cause of underlying shock state is not clear, the most critical decision is to ensure that cardiogenic shock is not cause.
The findings of jugular venous distension, rates, and the presence of an S3 gallop in cardiogenic shock may assist in diagnosis.
Both forms of shock, however, are associated with a reduction in cardiac output and a compensatory sympathetic mediated response.
Further, both types of shock may be treated with, and respond to, volume resuscitation.
If the diagnosis is in doubt or the clinical situation suggests both as a possibility, then invasive monitoring with a pulmonary artery catheter may required to assess effect of therapy.
All questions be posted to drmmkapur@gmail.com
All posts ae stored in archives for your access and review
HYPOVOLEMIC SHOCK is the common form in practice, we use this form as working model.
The signs and symptoms appear only when the loss from
the circulatory system is above a certain volume usually (750 cc)
The compensatory mechanism fail and tissue perfusion suffers as
a result.
A summary of these volume losses and manifestations
in a seventy kilogram man are given below:
-Thus the first sign may be a rise in pulse rate because of increase in catecholamine.
-As the loss of blood or fluid continues the pulse rises and the systolic BP falls.
-The urine production per hour drops.
-The mental state passes through stages of apprehension, anxiety and lethargy to coma
A clinical staging system of hemorrhagic shock based on the percentage of acute blood volume loss has been described
Typically
-Classes I(Loss of 750cc of blood) and II(loss of 750-1500) are referred to as compensated shock states in which the adrenergic response maintains a normal blood pressure.
-Passing from a compensated state of shock to class IV (uncompensated) shock may occur rapidly in children and young adults.
-De-compensation of homeostatic mechanisms and inability to maintain systolic blood pressure above 90 mmHg after trauma induced hypovolemia are associated with a mortality of more than 50%.
However, rapid and adequate restoration of circulating blood volume simultaneous with control of bleeding can reverse even severe hemorrhagic shock.
It is thus crucial to recognize compensated shock early and intervene with speed for good results.
Laboratory evaluation may provide some diagnostic information.
- Non hemorrhagic forms of hypovolemic shock cause hemoconcentration.
- If there is loss of free water, then hemoconcentration will occur with hyponatremia.
- Following acute hemorrhage there may be no alteration in the hemoglobin or hematocrit values when compensatory fluid shifts occur fluids are administered hemoglobin and hematocrit will drop.
In clinical situations in which the cause of underlying shock state is not clear, the most critical decision is to ensure that cardiogenic shock is not cause.
The findings of jugular venous distension, rates, and the presence of an S3 gallop in cardiogenic shock may assist in diagnosis.
Both forms of shock, however, are associated with a reduction in cardiac output and a compensatory sympathetic mediated response.
Further, both types of shock may be treated with, and respond to, volume resuscitation.
If the diagnosis is in doubt or the clinical situation suggests both as a possibility, then invasive monitoring with a pulmonary artery catheter may required to assess effect of therapy.
All questions be posted to drmmkapur@gmail.com
All posts ae stored in archives for your access and review
Wednesday, August 4, 2010
SHADES OF SHOCK 5
4.5 Decreased respiratory ventilation and SHOCK LUNG
There is a decrease in available O2 in these in all cases as OF:
i) Pneumothorax
ii) Pulmonary embolus
iii) Shock lung or adult respiratory distress syndrome (ARDS).
This is met with in trauma, sepsis, aspiration of
gastric contents, and pneumonia
All these conditions lead to injury to the lung
tissue resulting in damage to the alveolar epithelium/
Capillary bed interface producing leakage of protein
Rich fluid into the interstitial space and later into
The alveolar space leading to respiratory distress.
This impairs gas exchange capacity of the lung The clinical features of ARDS of hypoxia, low lung
compliance and all these conditions interfere with
tissue perfusion with O2 because of impaired gas
exchange.
A diffuse interstitial pattern on X-ray is
visible.
4.1.1+ 2 and 4.3 are due to Pre-load and after-load effects
while 4.4 is due to cardiac muscle fuction impairment (infarct
/compression). All have low available O2 in the
blood.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
There is a decrease in available O2 in these in all cases as OF:
i) Pneumothorax
ii) Pulmonary embolus
iii) Shock lung or adult respiratory distress syndrome (ARDS).
This is met with in trauma, sepsis, aspiration of
gastric contents, and pneumonia
All these conditions lead to injury to the lung
tissue resulting in damage to the alveolar epithelium/
Capillary bed interface producing leakage of protein
Rich fluid into the interstitial space and later into
The alveolar space leading to respiratory distress.
This impairs gas exchange capacity of the lung The clinical features of ARDS of hypoxia, low lung
compliance and all these conditions interfere with
tissue perfusion with O2 because of impaired gas
exchange.
A diffuse interstitial pattern on X-ray is
visible.
4.1.1+ 2 and 4.3 are due to Pre-load and after-load effects
while 4.4 is due to cardiac muscle fuction impairment (infarct
/compression). All have low available O2 in the
blood.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review
Wednesday, July 28, 2010
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.
Any questions be sent to drmmkapur@mail.com
All earlier posts are stored in archives for your access and review
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.
Any questions be sent to drmmkapur@mail.com
All earlier posts are stored in archives for your access and review
Wednesday, July 21, 2010
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.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in the archives for your access and review
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.
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in the archives for your access and review
Subscribe to:
Posts (Atom)