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!