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SHOCKPRESENTED BY Dr. Ketaki H. Pawar
Contents
IntroductionPathophysiologyClassification Severity of shockConsequencesLimitationResuscitation
Introduction
Shock is a systemic state of low tissue perfusion which is inadequate for normal cellular respiration.
Inadequate perfusion and oxygenation of cells leads to: Cellular dysfunction and damage Organ dysfunction and damage
In the presence of oxygen, glucose is metabolized to pyruvate, water and carbondioxide with production of high energy in form of ATP
As perfusion is reduced, cells are deprived of o2
cells switch from aerobic to anaerobic metabolism.
Pathophysiology
CELLULAR- Product of anaerobic respiration- lactic
acid Systemic metabolic acidosis As glucose is exhausted Failure
of sodium / potassium pumps in the cell membrane
Intracellular lysosomes cell lysis potassium released into blood stream
MICROVASCULAR-
Activation of the immune and coagulation systems
generation of O2 free radicals and cytokine release
Injury of capillary endothelial cells Further activates immune and coagulation systems Damaged leaky endothelium Tissue oedema
Systemic- cardiovascular
Preload and after load decreases
Compensatory baroreceptor response
sympathetic activity and release of
catecholaminesResults in tachycardia
and systemic vasoconstriction
Respiratory Increased sympathetic response leads to
increased respiratory rate to increase the excretion of carbon dioxide
Renal Decreased urinary output Renin-angiotensin axis is stimulated
resulting in furthur vasoconstriction and increased sodium and water reabsorption by kidneys
Endocrine
Decreased preload
Vasopressin (ADH)
released from hypothalamus
Vasoconstriction and
resorption of water in renal
collecting system
Cortisol released from adrenal cortex –sodium and water resorption
Classification
Hypovolaemic shock Cardiogenic shock Obstructive shock Distributive shock
Tissue perfusion is determined by Mean Arterial Pressure (MAP)Normal- 70-110 mmHg
MAP = CO x SVR
Heart rate
Stroke volume
Hypovolaemic shock
Loss of blood volume or loss of fluid from the vascular space
Causes:• Haemorrhage• Trauma • Surgery• Burns• Fluid loss due to vomiting or
diarrhoea,urinary loss
HYPOVOLAEMIC SHOCK
Clinical features of hypovolaemic shock
Cold, pale skin Rapid thready pulse Intense thirst Tachycardia Hypotension Dyspnoea Diaphoresis Poor urine output
Management
Control of ongoing haemorrhage-Direct pressure over the site of haemorrhage
In actively bleeding patients, high volume fluid therapy should not be started without controlling the site of haemorrhage
It will increase BP and increase bleeding Fluid therapy cools the patient and dilutes
available coagulation factors So, operative haemorrhage control should
not be delayed
Management
rapid infusion of isotonic saline or a balanced salt solution such as Ringer's lactate through large-bore intravenous lines.
2–3 L of salt solution over 20–30 min Continuing blood loss, with hemoglobin
concentrations declining to 10 g/dL, should initiate blood transfusion
.
severe and/or prolonged hypovolemia, inotropic support with dopamine, vasopressin, or dobutamine may be required to maintain adequate ventricular performance after blood volume has been restored
In a 70 kg male the reduction in intravascular volume may be classified as:
Class 1: reduction by 500-750mL(10-15%) , no clinical features
Class 2: reduction by 750-1500mL(15-30%) venous and arterial constriction and postural hypotension
Class 3: reduction by 1500-2000mL(30-40%) hypotension and tachycardia
Class 4: reduction by greater than 2000mL(40% or more) severe shock. Profound tachycardia and hypotension. Urine output falls to zero , pt is unconscious with laboured respiration
Traumatic shock
Muscle and bone are severely damaged
Eg. Battle casualties and automobile accident victims
Breakdown of skeletal muscle- when shock is accompanied by extensive muscle crushing
Kidney damage due to accumulated myoglobin
Management
"ABCs" of resuscitation
Control of ongoing hemorrhage Early stabilization of fractures debridement of devitalized or
contaminated tissues evacuation of hematoma
Cardiogenic shock
Due to primary failure of heart to pump the blood to tissues
Causes Myocardial infarction Cardiac dysrhythmias valvular heart disease blunt myocardial injury cardiomyopathy
Clinical features of cardiogenic shock
Oliguria Drowsiness or agitation Peripheral cyanosis Tachycardia Hypotension Dyspneoa Diaphoresis
Management
Immediate administration of digitalis is often used for strengthening the heart if the ventricular muscle shows signs of deterioration. Also, infusion of whole blood, plasma, or a blood pressure-raising drug is used to sustain the arterial pressure.
Some success has also been achieved in saving the lives of patients in cardiogenic shock by using one of the following procedures:
(1)surgically removing the clot in the coronary artery, often in combination with coronary bypass graft, or
(2)catheterizing the blocked coronary artery and infusing either streptokinase or tissue-type plasminogen activator enzymes that cause dissolution of the clot.
Obstructive shock
Reduction in preload due to mechanical obstruction in cardiac filling
Heart pumps well, but the output is decreased due to an obstruction (in or out of the heart)
Causes: Cardiac tamponade Tension pneumothorax Massive pulmonary embolism
Distributive shock
Blood volume is normal but the capacity of circulation is increased by marked vasodilatation
Warm shock1. Anaphylactic shock- rapidly
developing severe allergic reaction when an individual who has been previously sensitized to an antigen is reexposed to it.
C/F of Anaphylactic shock
include choking sensation, wheezing, cough, urticaria, oedema,
loss of consciousness, severe hypotension and faint pulse.
There may be pruritus.
Management
Anaphylaxis is a medical emergency that may require resuscitation measures such as airway management, supplemental oxygen, large volumes of intravenous fluids, and close monitoring
Epinephrine 0.5-1.0mg i.m in mid anterolateral thigh
Bronchospasm not relieved by epinephrine-inhaled beta 2 adrenergic agonists- albuterol
antihistamine diphenhydramine, 50 to 100 mg IM or IV for urticaria-angioedema
aminophylline, 0.25 to 0.5 g IV for bronchospasm
2. Septic shock Sepsis with hypotension (arterial blood
pressure <90 mmHg systolic, or 40 mmHg less than patient's normal blood pressure) for at least 1 h despite adequate fluid resuscitation
Tissue hypoperfusion that occurs in the presence of a systemic inflammatory response to infection
Release of bacterial products (endotoxins,LPS) cause vasodilatation and increased capillary permiability,loss of plasma
Clinical features of septic shock In the early stages of septic shock that is
not associated with hypovolaemia; The patient starts with shivering and
malaise and has warm, dry , flushed skin, moderate hypotension, hyperventilation,rapid but bounding pulse
fever ranging from 38.3°to 41 °C. Sudden circulatory collapse or
restlessness, apprehension and confusion may be the initial manifestation.
As the condition progresses, the patient may become comatose with cold clammy skin.
collapsed superficial veins, pale mucosa with a tinge of cyanosis, rapid and feeble
pulse, severe hypotension and oliguria. With pre-existing hypovolaemia, the
clinical features are those of hypovolemic shock with superimposed sepsis
Management
initiate empirical antimicrobial therapy that is effective against both gram-positive and gram-negative bacteria .Maximal recommended doses of antimicrobial drugs should be given intravenously
rapid administration of fluids
(1) ceftriaxone (2 g q24h) or ticarcillin-clavulanate (3.1 g q4–6h) or piperacillin-tazobactam (3.375 g q4–6h); (2) imipenem-cilastatin (0.5 g q6h) or meropenem (1 g q8h) or cefepime (2 g q12h).
If the patient is allergic to -lactam agents, use ciprofloxacin (400 mg q12h) or levofloxacin (500–750 mg q12h) plus clindamycin (600 mg q8h).
3. Neurogenic shock
It occurs as a result sudden loss of sympathetic tone to the arterioles and venules resulting in vasodilation of arterioles and venules of muscles
This occurs following high spinal cord injury, head injury, spinal anaesthesia
In addition to arteriolar dilatation, venodilation causes pooling in the venous system, which decreases venous return and cardiac output.
The extremities are often warm, in contrast to the usual vasoconstriction-induced coolness in hypovolemic or cardiogenic shock
Management
Excessive volumes of fluid may be required to restore normal hemodynamics if given alone. Once hemorrhage has been ruled out, norepinephrine or phenylephrine may be necessary to augment vascular resistance and maintain an adequate mean arterial pressure.
Hypoadrenal shock
Hypoadrenal shock occurs in settings in which unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery.
chronic administration of high doses of exogenous glucocorticoids.
critical illness, including trauma and sepsis, may also induce a relative hypoadrenal state.
adrenal insufficiency
The shock produced by adrenal insufficiency is characterized by loss of homeostasis with reductions in systemic vascular resistance, hypovolemia, and reduced cardiac output. The diagnosis of adrenal insufficiency may be established by means of an ACTH stimulation test.
Management
In the persistently hemodynamically unstable patient, dexamethasone sodium phosphate, 4 mg, should be given intravenously.
If the diagnosis of absolute or relative adrenal insufficiency is established, the patient has a reduced risk of death if treated with hydrocortisone, 100 mg every 6–8 h, and tapered as the patient achieves hemodynamic stability. Simultaneous volume resuscitation and pressor support are required.
Severity of shock
COMPENSATED SHOCK- There is adequate compensation to maintain central blood volume and preserve flow to the kidneys,lungs and brain Reduced perfusion to skin, muscles, and GIT Systemic metabolic acidosis and activation of humoral
and cellular elements within the underperfused organs. c/f- tachycardia and cool peripheries
Decompensation
Loss of around 15% of the circulating blood volume is within normal compensatory mechanisms.
B.P is well maintained and only falls after 30-40% loss of circulating blood volume.
Mild Moderate Severe
Cool extremities Same plus: Same plus:
Capillary refill time
Tachycardia Hypotension
Diaphoresis Tachypnea Marked tachycardia
Mild reduction in urinary output
Oliguria Urinary output falls to zero
Anxiety Drowsy,mildly confused
Mental status deterioration
Limitations
It is important to recognise patients who are in shock despit the absence of clinical signs.
Capillary refill- Not a specific marker Patients with short capillary refill times may
be in the early stages of shock In distributive (septic) shock the
peripheries are warm and capillary refill will be brisk , despite profound shock
Tachycardia Patients who are on b-blockers or
who have implanted pacemakers don’t show tachycardia.
Blood pressure Hypotension is one of the last signs of
shock. Children and fit young adults ate able to
maintain blood pressure until the final stages of shock by dramatic increase in stroke volume and peripheral vasoconstiction
Elderly who are normally hypertensive may present with a presumably normal BP for the general population.
Consequences
Unresuscitable shock Pt with profound shock for a
prolonged period of time Ability of body to compensate is lost Cell death follows from cellular
ischaemia Myocardial depression and loss of
responsiveness to fluid or inotropic therapy
Minimal response to maximal therapy
Multiple organ failure- Result of prolonged systemic
ischemia – end organ damage and multiple organ failure
(2 or more failed organ systems) Ventilation,cardiovascular support
and haemofiltration/dialysis until recovery of organ function.
60% mortality
Monitoring
Minimum ECG Pulse oximetry Blood pressure Urine output
Additional modalities CVP Invasive blood pressure Cardiac output Base deficit and serum lactate
Central venous pressure
There is no ‘normal’ CVP for a shocked patients and we cannot rely on an individual pressure measurement
CVP is a poor reflection of preload(end diastolic volume)
A fluid bolus (250– 500 mL) is infused rapidly over 5–10 minutes.
The normal CVP response is a rise of 2–5 cmH2O which
gradually drifts back to the original level over 10–20 minutes.
Patients with no change in their CVP require further fluid resuscitation.
Cardiac output
Cardiac output monitoring allows assessment of systemic vascular resistance, end diastolic volume and blood volume.
It can help distinguish the type of shock.
Guides the fluid and vasopressor therapy
Systemic and organ perfusion Goal of t/t is to restore cellular and
organ perfusion Best measures of organ perfusion and
best monitor of the adequacy of shock therapy is urine output
Level of consciousness is an important marker of the cerebral perfusion,but brain perfusion is maintained until very late stages of shock, so is a poor marker of adequacy of therapy.
The only clinical indicators of perfusion of the GIT and muscular beds are the global measures of lactic acidosis(lactate and base deficit) and the mixed venous oxygen saturation
Base deficit and lactate
Degree of lactic acidosis, as measured by serum lactate level and/or base deificit, is sensitive for diagnosis and monitoring the response to therapy.
Pts with base deficit over 6 mmol/L have a much higher morbidity than those with metabolic acidosis.
Mixed venous oxygen saturation The % saturation of O2 returning to the
heart from the body is a measure of the O2 delivery and extraction by the tissues.
Accurate measurement is via analysis of blood drawn from a long central line placed in the right atrium.
Normal mixed O2 saturation levels are 50-70%
Levels below 50% indicate inadequate O2 delivery and increased O2 extraction by cells
High mixed venous saturations (>70%) is seen in sepsis and some other forms of distributive shock.
In sepsis, there is disordered O2 utilization at the cellular level.
Less O2 presented to the cells. Cells cannot utilize it. Thus venous blood has a higher O2 concentration than normal.
Patients who are septic should have mixed venous O2 saturation above 70%. Below this level they are not only in septic shock but also in hypovolaemic or cardiogenic shock.
End points of resuscitation Traditionally pts have been resuscitated
until they have a normal pulse,BP and urine output.
But these parameters monitor the organ systems whose blood flow is preserved until the late stages of shock.
Therefore, a pt may be resuscitated to restore central perfusion to the brain, lungs and kidneys and yet continue to underperfuse the gut and muscle beds.
Thus the activation of inflammation and coagulation may be ongoing and lead to reperfusion injury when these organs are finally perfused, and ultimately organ failure
This state of normal vital signs and continued underperfusion is called “occult hypoperfusion”
Resuscitation algorithms directed at correcting global perfusion end points( base deficit, lactate, mixed venous O2 saturation) rather than traditional end points have been shown to reduce mortality and morbidity in high-risk surgical patients.
References
Bailey and Love’s short practice of surgery, 26th edition
Harrison’s principles of internal medicine,17th edition
Guyton and hall textbook of medical physiology-12th edition
Thank You!