SHOCK

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SHOCK

Dr.Mehul JaniMAXILLOFACIAL SURGEON

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ShockShock

DIFINITION

Shock is a physiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased

tissue oxygen delivery.

It is a condition in which circulation fails to meet the nutritional needs of the cells &

at the same time fails to remove the metabolic waste products.

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ETIOLOGIES

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Basic Physiology• Unit of life = cell

• Cells get energy (ATP) from cellular respiration:

O2 + Glucose ATP + water + CO2

No O2 = no energy

No energy = no lifeRemember:

Cell Tissues Organ

Body Organ System

Damage to Damage to Damage to

Damage to Damage to

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Review of the Cardiovascular System

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Cardiovascular System

• Transports oxygen (fuel) to cells

• Removes carbon dioxide and other waste products

• Cardiovascular system must be able to maintain sufficient flow through capillary beds to meet cell’s oxygen and fuel needs

Flow = Perfusion

Inadequate Flow = Inadequate Perfusion = Hypoperfusion

Adequate flow = Adequate Perfusion

SHOCK

Types of shock

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Shock

CardiogenicHypovolaemic

Anaphylactic Septic

Distributive

Neurogenic

Classification of Shock

Hypovolaemic shock

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Clinical featuresClinical features

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Mild shock

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Clinical features are due to adrenergic constriction of blood vessels.•Pale and cool extremities because of collapse of s.c veins.•May be sweat in forehead,hand and feet.•U.O, B.P, pulse may remain normal at this stage.

Moderate shock

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oliguriaMild shock features +

In the initial stage B.P remains normal and falls in later stage.SO PULSE AND B.P ARE NEVER THE MAIN SIGNS OF SHOCK.

SHOCK MAY BE PRESENT EVEN WITH NORMAL PULSE AND B.P

Sever shock

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•Rapid pulse•Low urinary output•Pallor of extremities•Low B.P

Clinical monitoring

• Blood pressure::

It is essential to monitor B.P though it is normal in mild shock.

• Respiration::

Increase in rate & depth of respiration is an important indicator of shock.

• Urine output::

It is a good indication of severity of shock and good index of adequacy of replacement therapy. 18

• Central venous pressure (CVP)::

It is important in assessing shock.

CVP decreases in hypovoleamic shock

Where remain constant in cardiogenic shock.*

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SWAN-GANZ CATHETER

• It is used to get valuable information about the precise diagnosis and circulatory derangement of shock.

• It provides 3 types of information:

1:flow in CVS

2:sampling of blood from pumonary artery to measure the accurate amount of blood gases in venous bllod.

3:filling pressure of rt.&lt. Side of heart 20

Management Management ofof

hypovolaemic shock hypovolaemic shock

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General Treatment of Shock– Remember your ABC’s– Administer airway– 100% O2– Assist ventilations if necessary– Position patient to assist perfusion(in tredelenburg position )– Keep patient warm– Perform focused assessment – Monitor and adjust O2,– gain IV access, cardiac monitor, pulse oximetry– Fluid replacement of LR or NS– Need 3 liter of fluid to replace 1 liter of blood loss– Apply pressure to IV or blood to facilitate faster infusion

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MX

• Resuscitation.

• Control of bleeding

• Extracellular fluid replacement

• Drugs.

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Resuscitation

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Goal of treatment

So,

• Maintain airway

• If require intubate the patient

• Maintain adequate ventilation and oxygenation.

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Bleeding control

• Find out the cause of bleeding and control the bleeding either by raising the foot end of the bed or compression bandage or by surgical intervention if require.

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ECF replacement

• Most important point in Mx ..

• Non sugar,non protein,crystalloid solution with Na concentration that of plasma is best fluid for replacement.

• Normal saline

• Ringer’s lactate* NaHCo3 **

• Ringer’s acetate*

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• 3 litres of fluid given over 45 minutes should resuscitate any pt.with arrested haemrrhage.

• Resuscitation should always start with crystalloid solution even if blood is available.*

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Drugs • Sedatives:Morphine:use to alleviate pain.

:should adminnistrate I.V

should not be use in children,in head injury pt.,pt.with acute abdomen

Berbiturate are preferred in children.

• Vasoconstrictors:help full in hypovolaemic shock.

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Drug Indication Dose MOA Principal actionsDopamine Renal perfusion 2-5 mcg/kg/min Dopaminergic Renal a. dilation

hypotension 5-10 mcg/kg/min 1 &dopaminergic

+ inotrope

Hypotension >10 mcg/kg/min 1 vasoconstrictionDobutamine Cardiogenic shock 2.5-25 mcg/kg/min Selective 1 + inotropeNorepinephrine Hypotension 2-4 mcg/min 1 & 1 VasoconstrictionPhenylephrine Hypotension 40-180 mcg/min Selective 1 Vasoconstriction

• Cardiogenic shock

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Etiology

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,Chronic congestive heart failure

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Clinical features:• In beginning : skin is pale,cool & U.O is

low.

• Gradually pulse become rapid & B.P becomes low.

• In the case of rt.ventricular dysfunction the neck veins become distended & liver may also be enlarged.

• In case of lt.ventricular dysfunction third heart sound is heard.

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Mx

• Airway must be clear with adequate oxygenation.

• In a case of rt.sided failure caused by pulmonary embolism should be treated by large dose of heparine I.V.

• Diuretics can be help full in cardiogenic shock by reducing volume and decrease filling pressure.

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• Neurogenic shock

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Spinal cord trauma causes a loss of blood

vessel tone and results in widespread vasodilation.

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•is one type of distributive shock.•injury may damage the sympathetic nerve fibers that control vessel tone.*

Clinical features:

• Skin remains WARM, PINK, WELL PERFUSED.*

• U.O normal.

• Heart rate is rapid

• B.P is LOW.

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Mx• Protect and stabilize c-spine.*

• Maintain airway.

• Keep pt.in trendelenburg position.

• Administrate fluid but it is not much important as in hypovolaemic shock.

• Vasoconstrictor drugs by which this shock can be treated safely.

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•Septic shock

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Most frquent organisms are,Gm +ve ,Gm-ve bacteria,And any agent capable of producing infection like viruses,parasites,fungi

Clinical features:• Recognized Initially by chills and temp.>1000F.*• 2 types: early warm shock & late cold shock.

• Early warm shock:Toxins from infected tissue increase body temperature.to bring this down vasodilatation occurs which decrease systemic vascular resistance.

• LV has minimal resistance + adrenergic discharge again increase CO.

• So skin will become WARM-PINK-WELL PERFUSED.

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• LATE COLD SHOCK: due to vasodilatation hypovolaemia takes place which reduces cardiac output .

Clinically it is difficult to differentiate it from hypovolaemic or traumatic shock.

Only guide remains is the knowledge of existence of a septic focus.

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Mx

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• Use of steroids is questionable because it impaires the immunity responce of body. It also improves the cardiac,pumonary,renal functions which is life saving.

• If steroids given SHORT TERM –HIGH DOSE is recommended.

• 15-30 mg /kg- methyl prednisolone or equivalent dexamethasone.(I.V in 5-10 min)

• Same dose repeat at 4 hours if benificial effect have been not achieved.

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Systemic Inflammatory Response Syndrome (SIRS)

• Defined as when generalized inflammation occurs and threatens vital organs

• Causes: multiply transfusions, massive tissue injury, burns, and pancreatitis, severe infections or sepsis

• Effects: endothelium is damaged and allows fluid to leak into the body tissues, results in poor perfusion of blood to organs

• Body is in a hypermetabolic state

• Diagnosis made when 2 or more of the following are seen:– Temperature less than 97 or greater than 100.4– Heart rate more than 90– Respiratory rate more than 20 or PaCO2 less

than 32mm Hg– WBC count less than 4000 cells or more than

12,000– Sepsis is used if patient has SIRS with and

infection

Treatment for SIRS/MODS

• Critical care nursing

• Goals– Prevent and treat infections– Maintain tissue oxygenation– Provide nutritional and metabolic response– Support failing organs

• Anaphylactic shock

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Vasodilation moves blood from the central core to the periphery, causing distributive

shock.

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• Mass release of histamine and slow release substance of anaphylaxis due to allergic hypersensitivity reaction (foods, insect bites, blood transfusion, drugs).

• Causes bronchospasm,laryngeal edema,and respiratory distress which leads to hypoxia.

• Increased capillary permeability with vasodilation reduces venous return and BP.

•HypoAdrenal shock

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• Now that we have an understanding of what shock is and the different types, lets look at the physiology behind shock.

• To understand the physiology of shock we need to understand the following formula:

Blood Cardiac Systemic

Pressure = Output x Vascular Resistance

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• By applying a mathematical aspect to the formula we can start to identify how blood pressure can be maintained.

BP = CO x SVR

• We need to keep both sides balanced.

• If one side of the formula changes, the other side needs to change in the opposite direction to balance this out.

• i.e. If BP increases, we need to decrease CO, SVR or both to bring it back down again

If BP decreases, we need to increase CO, SVR or both to bring it back up again

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What happens if you get a drop in BP?

BP = CO x SVR

• We need to maintain homeostasis so need to increase BP.

• We can increase BP by increasing:

- CO

- SVR

- CO & SVR

to increase BP back up again.

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What happens if you get a rise in BP?

BP = CO x SVR

• We need to maintain homeostasis so need to decrease BP.

• We can decrease BP by decreasing:

- CO

- SVR

- CO & SVR

to bring BP back down again.

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Key Issues In Shock

• Recognise and treat early (during compensatory phase)

Increased resp. rate,Restlessness, EarlyAnxiety, signs of

Argumentative shock

• Falling BP = Late sign of shock

• Pallor, tachycardia and slow capillary refill = Shock until proven otherwise

Hallmark symptoms are:Decreased BPIncreased HR

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Inadequate cellular Oxygen Delivery

Inadequate Energy Production

Anaerobic Metabolism Lactic Acid

Production

Metabolic Failure

CELL DEATH

Metabolic Acidosis

• What happens in compensated shock???

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Compensated shock

• Baroreceptors detect fall in BP• Sympathetic nervous system activated

(see diagram 1)

1. Cardiac Effects

- increased force of contractions

- increased rate (tachycardia)

- increased cardiac output

2. Peripheral Effects

- arteriolar constriction

- increased peripheral resistance

- shunting of blood to main core organs (causing cold clammy skin)

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sympathetic innervation of myocardium

sympathetic innervation of arterioles

Baroreceptors on aorta and carotid sinus send information about

changes in BP to cardiovascular centre

cardiovascular centre

sympathetic and parasympathetic innervation

of Sino-atrial node

Control of Blood Pressure via the Baroreceptor Reflex

brain

key parasympathetic nerves sympathetic nerves afferent sensory nerves

arterioles

heart

© Roger McFadden – University of Central England 2003

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3. Respiratory Effects

Tachypnoea is one of the first signs that reflects reduced blood flow and oxygen transport.

the cardiovascular and respiratory systems work together-

If blood flow around the body is compromised in any way, oxygen delivery to tissues is reduced.

To compensate for this, ventilation will increase to attempt to increase oxygen uptake in the lungs.

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So how does this happen ??                                 

respiratorycentres in medulla

chemoreceptorson aorta and carotid

artery

heart

brain

intercostal nerve to externalintercostal muscles

phrenic nerve to diaphragm

ribs

The Baroreceptors not only stimulate the cardiovascular control centre but also the respiratory centre in the medulla, increasing the respiratory rate.

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4.Renal Effects

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Renin – Angiotensin – Aldosterone Pathway                                              

THIRST

ANGIOTENSIN II

ADRENAL CORTEX

KIDNEYS increase Na+ reabsorption from filtrate

 BP

VASOCONSTRICTION

BLOOD PRESSURE

ALDOSTERONE  

BLOOD VOLUME

ANGIOTENSIN CONVERTING ENZYME

JUXTAGLOMERULAR cells in the kidney respond to a REDUCTION

IN BLOOD VOLUME from EXCESS VOMITING,

SWEATING, & HAEMORRHAGE etc.

RENIN released into blood

ANGIOTENSINOGEN ANGIOTENSIN I

. 5.Hypothalamus Effects

- decreased blood flow to hypothalamus- release of ADH from post pituitary (see diag 3)results in retention of salt, waterand peripheral vasoconstriction

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osmoreceptors in hypothalamus detect increase in osmolarity of

bloodand release ADHinto blood stream

ADHFILTRATE

ADH

water

urine blood

nephron capillary

ADH increases the amount of water

reabsorbed from the filtrate to the blood

urine output is reduced as more water is returned to the blood

Role of ADH in dehydrationRole of ADH in dehydration    

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6. Hormonal Effects

- Glucagon (contributes to hyperglycaemia)

- ACTH (stimulates cortisol release and glucose production)

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Progressive Shock

1. Cardiac Effects- decreased RBC oxygenation- decreased coronary blood flow- myocardial ischaemia-decreased ventricular filling- decreased force of contraction

2. Peripheral Effects- peripheral pooling of blood- plasma leakage into interstitial

spaces- cold, grey waxy skin- confusion, slow speech- tachycardia, weak thready pulse- decreased BP- decreased body temperature

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3. Respiratory effects

If oxygen delivery to tissues continues to be inadequate, cells must do anaerobic respiration to continue ATP production.

Anaerobic respiration produces lactic acid as a waste product – this must be removed.

Central chemoreceptors will detect a fall in pH and stimulate the respiratory centre to increase ventilation.

This allows the excess acid to be ‘blown off’ in the form of CO2

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Anaerobic respiration

Lactic acid

PCO2 and

H+ in blood

expiration of PCO2

H+ in CSF

stimulation ofcentral

chemoreceptors

frequency of impulses to medullary rhythm generator

rate and depth of ventilation

Response to acidosis

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Irreversible Shock• Loss of peripheral vascular resistance

• Confusion, slurred speech, unconscious

• Slow, irregular, thready pulse

• Falling BP (diastolic is zero)

• Cold, clammy cyanotic skin

• Slow, shallow, irregular respirations

• Dilated, sluggish pupils

• Severely decreased body temperature

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Irreversible Shock leads to:

• Renal failure

• Hepatic failure

• Multiple organ systems failure

• Adult respiratory distress syndrome

• Death

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THANK YOU