SWAMI DEVI DYAL HOSPITAL AND DENTAL COLLEGE

DEPARTMENT OF ORAL MEDICINE, DIAGNOSIS AND RADIOLOGY

SEMINAR TOPIC

“HAEMORRHAGE AND SHOCK”

GUIDED BY:- SUBMITTED BY:-

DR.GAGAN PURI MANDAKINI

DR.SANJEEV ROLL NO:-7044

DR.MAMTA BDS INTERN

DR.TAJINDER BANSAL

DR.SANDEEP

CONTENTS

HAEMORRHAGE

-DEFINATION-CLASSIFICATION-PATHOPHYSIOLOGY-ASSESMENT OF HAEMORRHAGE-MANAGEMENT-DAMAGE AT INDIVIDUAL ORGANS

SHOCK

-DEFINATION-TYPES OF SHOCK-STAGES OF SHOCK AT CELLULAR LEVEL-GENERALIZED ANAPHYLAXIS-MANAGEMENT OF SHOCK

GENERAL MEASURES SPECIFIC MEASURES OTHER MEASURES

-DAMAGE OF INDIVIDUAL ORGANS

SUMMARY REFERNCES

HAEMORRHAGE AND SHOCKHAEMORRHAGE

DEFINATION:-

Escape of blood from the circulation(arteries,veins,capillaries)to the internal or external tissues is called the haemorrhage.The term is usually applied to loss of blood that is copious enough to threaten health or life.Slow bleeding may lead to anaemia while sudden loss of large amount of blood may cause shock.

CLASSIFICATION OF HAEMORRHAGE

1.Depending upon the nature of vessel

A. Arterial haemorrhage:- Bright red colour;it jets out.Pulsation of the artery can be seen.It can be easily controlled as it is visible

B.Venous haemorrhage:-Dark red colour;it never jets out but oozes out.difficult to control because veins get retracted.Non pulsatile.

C. Capillary haemorrhage:- Red colour;never jets out,slowly oozes out.It becomes significant if there are bleeding tendencies.

2.Depending upon the timing of haemorrhage

A. Primary haemorrhage:-occurs at the time of surgery

B.Reactionary haemorrhage:-occurs after 6-12 hrs of surgery

Causes:1.Hypertension in postoperative period

2.Sneezing

3.Coughing

4.Retching

Example:Superior thyroid artery can bleed postoperatively.hence it is better to ligate it twice.

C.Secondary haemorrhage:-occurs after 5-7 days of surgery

It is due to infection which eats away the suture material,cause sloughing of vessel Bleeding after haemorrhoidectomy,after 5-7 days of surgery.

3.Depending upon the duration of haemorrhage

A.Acute haemorrhage:- occurs suddenly

Example:oesophageal variceal bleeding due to portal hypertension

B.Chronic haemorrhage

Examples:haemorrhoids /piles or chronic duodenal ulcer,tuberculous ulcer of the ileum,diverticular disease of the colon

4.Depending upon the nature of bleeding

A.External haemorrhage/Revealed haemorrhage:- Accounts for nearly 10 million emergency department visits in the United States each year.

The seriousness of the injury is dependent on:

Anatomical source of the hemorrhage (arterial, venous, capillary)

Degree of vascular disruption

Amount of blood loss that can be tolerated by the patient

Examples:Epistaxis,haematemesis.

B.Internal haemorrhage/Concealed haemorrhage:- Internal hemorrhage is associated with higher morbidity and mortality than external hemorrhage.

Examples:splenic rupture following injury,ruptured ectopic gestation,liver laceration following injury

PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK

IT CAN BE CLASSIFIED INTO 3 STAGES:

1.MILD HAEMORRHAGE

When blood loss is less than 500ml in adult,it can be called mild haemorrhage 60-70% of blood volume is present in the lower limb,mainly in the low pressure

veins and venules.These vessels are called capacitance vessels. 10%of blood volume is present in the splanchnic circulation. When there is blood loss of 500 ml,peripheral venoconstriction takes place.It

compensates for the loss of blood volume by shifting some blood into the central circulation

Some amount of blood volume is corrected by withdrawl of fluid from interstitial spaces.

2.MODERATE HEMORRHAGE Loss of 500-1000 ml of blood results in moderate haemorrhage Peripheral venoconstriction may not be sufficient to maintain the circulation Hence adrenaline and noradrenaline are released from the sympathoadrenal system

causing powerful vasoconstriction Increased secretion of ADH causes retention of water and salt Clinically it results in cold ,clammy extremities,feeble or absent peripheral pulses

and a temporary increase in BP due to increase in peripheral resistance resulting in peripheral vasoconstriction.This is followed by persistent hypotension due to hypovolaemia

Renal vessels undergo vasoconstriction resulting in oliguria.Untreated cases may develop into acute renal tubular necrosis with renal failure.

At this stage myocardium and brain usually do not suffer

3.SEVERE HAEMORRHAGE

Loss of blood volume >1 litre All the signs and symptons of the 2nd stage become worse. Pulse 130-140/min ,feeble,low volume,hypotension.Oliguria,anuria and brain stem

hypoxia result in change in the rate and depth of respiration

As a result of anoxia,anaerobic metabolism dominates.It results in release of lactic acid ,which accumulates causing intracellular acidosis.

The cells also get swollen due to influx of Na+ and water from extracellular compartment

Due to the change in the intracellular pressure,lysosomal enzymes leak which help in production of kinins that produce arteriolar dilation hence fluid loss occurs due to increase in capillary permeability

In an attempt to maintain circulation of the body,the myocardial contractility increases.The systemic vascular resistance increases because of arteriolar vasoconstriction in the skin,kidney,skeletal muscles and splanchanic circulation.

ASSESMENT OF HAEMORRHAGE

Initial Assessment

General Impression Obvious Bleeding Mental Status

Interventions Manage as you go: O2

Bleeding control Treatment Shock

Fracture and blood loss Pelvic fracture: 2,000 mL

Femur fracture: 1,500 mL

Tibia/fibula fracture: 500–750 mL

Hematomas and contusions: 500 mL

Ongoing Assessment:- Reassess vitals and mental status:

  Q 5 min: UNSTABLE patients

  Q 15 min: STABLE patients

Reassess interventions:

  Oxygen

  ET

  IV

  Medication actions

Trending: improvement vs. deterioration

  Pulse oximetry

  End-tidal CO2 levels

MANAGEMENT OF HAEMORRHAGE

1.TREATMENT OF THE SHOCK

1.HOSPITALISATION

2.INTRAVENOUS LINE:Urgent intravenous administration of ringer lactate /plasma or plasma expanders e.g.Hetastarch or gelatin.This is to optimize the ventricular preload.Occasionally a venous cut down may be necessary.

3.As soon as blood is available,transfusion is started with careful monitoring of pulse rate,BP,urine output,Hb%pcv,etc.Dopamine improves cardiac output too.

4.Oxygen:If po2 is less than 70 mmhg,O2 should be given by face mask or nasal cathethers.blood gas analysis,if the shock is severe ,to rule out acidosis and hypoxia.

2.Specific methods to control splanchnic haemorrhage

1.PRESSURE AND PACKING

To control bleeding from nose,scalp.

Packing using roller gauze with or without adrenaline to control bleeding from nose.Bleeding from vein-middle thyroid vein in thyroidectomy,lumbar veins after lumber sympathectomy can be controlled by pressure pack for few minutes

Sengstaken tube is used to control bleeding from oesophageal varices-internal tamponade

2.POSITION AND REST

Elevation of the legs controls bleeding from the varicose veins Elevation of the head end reduces venous bleeding in thyroidectomy-Anti-

Trendelenberg position. Sedation to relieve anxiety-injection morphine 8-12 mg LM

3.TOURNIQUETS:

TORNIQUET

Apply band above injury site, tighten to stop bleeding

Indications:

Reconstruction of hand Repair of tendons Repair of tendons When a bloodless field is desired

Contraindication:

Patient with peripheral vascular disease as the arterial disease may be aggrevated due to thrombosis resulting in gangreneTypes:i)Pneumatic ordinary BP cuffii)rubber bandagePrecautions:

Too loose a tourniquet doesnot serve the purpose Too tight :arterial thrombosis and can result in gangrene Too long(duration):gangrene of the limb.Hence,when a tourniquet is being

tied ,tourniquet time should be noted down and at the end of 45 min.it has to be deflated for about 10 minutesComplication:

-Ischaemia and gangrene-Tourniquet nerve palsy

4.SURGICAL METHODS TO CONTROL HAEMORRHAGE:

Application of artery forceps (spencer well’s forceps)to control bleeding from veins,arteries and capillaries.

Application of ligatures,for bleeding vessels Cauterisation Application of bone wax used to control bleeding from the bones. Silver clips are used to control bleeding from cerebral vessels(Cushing’s clip) Surgical procedures such as Splenectomy done for splenic rupture and Laparotomy

for control of bleeding from ruptured ectopic,etc.

DAMAGE AT INDIVIDUAL ORGANS

1.GIT-Mucosal ulcerations-upper GI bleeding increases absorption of toxins and bacteria leading to bacteraemia

2.Liver-Decreases clearance of endotoxins leading to bacteraemia

3.Kidney-Persistent arteriolar constriction leading to renal failure

4.Heart-Fall in BP,tachycardia,increased left ventricular end diastolic pressure

5.Lungs-Loss of surfactant ,interstitial oedema,increasing arteriovenous shunting results in MULTIORGAN FAILURE

DENTAL MANAGMENT

Dental management required for patients with bleeding disorder depends on both the type and invasiveness of the dental procedure and the type and severity of the bleeding disorder.Thus,less modification is needed for patients with mild coagulopathies in preparation for dental procedure anticipated to have limited bleeding consequences.When significant bleeding is expected,the goal of managment is to preoperatively restore the

hemostatic system to an acceptable range,while supporting coagulation with adjunctive and local measures.For reversible coagulopathies(e.g coumarin anticoagulation),it may be best to remove the causative agent or treat the primary illness or defect in order to allow the patient to return to a manageable bleeding risk for the dental treatment period.For irrereversible coagulopathies ,the missing or defective element may need to be replaced from an exogenous source to allow control of bleeding(eg. Coagulation factor concentrate therapy for hemophilia).Assessment of the coagulopathy and delivery of appropriate therapy prior to dental procedures is best accomplished in consultation with a hematologist.

SHOCK

DEFINATION:-

Shock is an acute clinical syndrome characterized by hypoperfusion and severe dysfunction of vital organs.There is a failure of the circulatory system to supply blood in sufficient quantities or under sufficient pressure necessary for the optimal function of organs vital to survival.STAGES OF SHOCK

Compensated – vital organ function maintained, BP remains normal

Uncompensated – microvascular perfusion becomes marginal – organ and cellular function deteriorate– hypotension develops

• Shock is a clinical syndrome of circulatory dysfunction – resulting in inadequate oxygen and nutrient delivery– inability to meet the metabolic demands of the tissues• results in a cascade of events resulting in altered cellular metabolism, function, structure,

and ultimately death• Shock is NOT necessarily hypotension– begins with a normal blood pressure and progresses over time

Types• Hypovolemic shock – dehydration -

- loss of plasma as in burns shock and loss of fluid or dehydration as in gastroenteritis

– deprivation 3rd degree burnsrd degree/full thickness burn– heat stroke 3rd degree/full thicknes3rd degree/full thickness burn s burn– hemorrhage – burns

• Distributive shock– anaphylaxis - traumatic – neurogenic - infectious – drug toxicity -

–

Urtricaria/anaphylaxis

Septic shock actually has components of several groups including distributive and cardiogenic.It is produced by microorganism ,toxins or both.May be produced by bacteria,virus,fungi or even protozoa

• Cardiogenic shock– congenital heart disease– ischemic heart disease– anoxia– Kawasaki's– cardiomyopathies

– tamponade

Stages of ShockCellular Level:-

Four Stages:-

Stage 1: Vasoconstriction

Stage 2: Capillary and venule opening

Stage 3: Disseminated intravascular coagulation Stage 4: Multiple organ failure

Stage 1: Vasoconstriction

Vasoconstriction begins as minimal perfusion to capillaries continues.

Oxygen and substrate delivery to the cells supplied by these capillaries decreases.

Anaerobic metabolism replaces aerobic metabolism.

Production of lactate and hydrogen ions increases.

The lining of the capillaries may begin to lose the ability to retain large molecular structures within its walls.

Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).

Sympathetic stimulation produces:

Pale, sweaty skin

Rapid, thready pulse

Elevated blood glucose levels

The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles.

Blood is shunted to the heart, brain, skeletal muscle, and capillary flow to kidney

Stage 2: Capillary and Venule Opening

Stage 2 occurs with a 15% to 25% decrease in intravascular blood volume. Heart rate, respiratory rate, and capillary refill are increased, and pulse pressure is decreased at this stage. Blood pressure may still be normal.

As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space.

Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.

As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly.

Even normal blood volume may be inadequate to fill the container.

The capillary and venule capacity may become great enough to reduce the volume of available blood for the great veins and vena cava.

Resulting in decreased venous return and a fall in cardiac output

Low arterial blood pressure and many open capillaries result in stagnant capillary flow.

Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid.

The respiratory system attempts to compensate for the acidosis by increasing ventilation to blow off carbon dioxide.

As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation).

Halts perfusion

Affects nutritional flow and prevents removal of cellular metabolites

Clotting mechanisms are also affected, leading to hypercoagulability.

This stage of shock often progresses to the third stage if fluid resuscitation is inadequate or delayed, or if the shock state is complicated by trauma or sepsis.

Stage 3: Disseminated Intravascular Coagulation (DIC)

Time of onset will depend on degree of shock, patient age, and pre-existing medical conditions.

Stage 3 occurs with 25% to 35% decrease in intravascular blood volume. At this stage, hypotension occurs. This stage of shock usually requires blood replacement.

Stage 3 is resistant to treatment (refractory shock), but is still reversible.

Blood begins to coagulate in the microcirculation, clogging capillaries.

Capillaries become occluded by clumps of RBCs.

Decreases capillary perfusion and prevents removal of metabolites

Distal tissue cells use anaerobic metabolism, and lactic acid production increases.

Lactic acid accumulates around the cell.

Cell membranes no longer have the energy needed to maintain homeostasis.

Water and sodium leak in, potassium leaks out, and the cells swell and die.

Pulmonary capillaries become permeable, leading to pulmonary edema.

Decreases the absorption of oxygen and results in possible alterations in carbon dioxide elimination

May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS)

If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.

Stage 4: Multiple Organ Failure

The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ.

Usually hepatic failure occurs, followed by renal failure, and then heart failure.

If capillary occlusion persists for more than 1 to 2 hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.

In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less).

Cells can no longer use oxygen, and metabolism stops.

ANAPHYLACTIC SHOCKGeneralized anaphylaxis is an allergic emergency .The mechanism of generalized anaphylaxis is the reaction of IgE antibodies to an allergen that causes the release of histamine,bradykinin,and SRS-A.These chemical mediator cause the contraction of smooth muscles of the respiratory and intestinal tracts as well as increased vascular permeability.

The following factors increase the patient’s risk for anaphylaxis:

History of allergy to other drugs History of asthma Family history of allergy Parentral administration of the drug Administration of high-risk allergens such as penicillin

Anaphylactic reactions may occur within seconds of drug administration or may occur 30-40 minutes later ,complicating the diagnosis.The symptons of generalized anaphylaxis should be known so that prompt treatment may be initiated.for e.g.patients have been diagnosed as allergic to local anaesthetics when a psychic reaction to an injection or reaction to epinephrine have occurred.Such an erroneous diagnosis will make future dental management difficult.

The generalized anaphylactic reaction may involve the skin,cardiovascular system,the intestine,and the respiratory system.The first signs often occur on the skin and similar to those are seen in localized anaphylaxis(e.g urticaria,angioedema,erythema and pruritis).Pulmonary symptons include dyspnoea,wheezing and asthma)

GI tract disease (e.g vomiting,cramps and diarrhea)often follows skin symptons.If these are untreated symptons of hypertension appears as the result of loss of intravascular fluid;if untreated this leads to shock.Patients with generalized anaphylaxis may die from respiratory failure,hypotensive shock or larynzeal oedema.

-The most important therapy for generalized anaphylaxis is administration of epinephrine.-All clinicians who administer drugs should have a vial of aqueous epinephrine(at a 1:1000 dilution)and a sterile syringe easily accessible.For adults 0.5 ml of epinephrine should be administered intrvascularly or subcutaneously;smaller doses of from 0.1 to 0.3 ml should be used for children ,depending on their size.If the allergen was administered in an extremity,a tourniquet should be placed above the injection site to minimize further absorption in the blood.The absorption can be further reduced by injecting 0.3 ml of epinephrine(1:1000)directly into the injection site.the tourniquet should be removed every 10 minutes. - Epinephrine will usually reverse all signs of generalized anaphylaxis .If improvement is not observed in 10 minutes,readminister epinephrine. - If the patient continues to deteriorate,several steps can be taken,depending on whether the patient is experiencing bronchospasm or edema. - For bronchospasm slowly inject 250mg of aminophylline intravenously over a period of 10 minutes.To rapid an administration can lead to fatal cardiac arrhythmia. -Don’t give aminophylline if hypotensive shock is a part of the clinical picture .-Inhalation sympathomimetics may be used to treat bronchospasm and oxygen should be given to prevent or manage hypoxia.-For patients with laryngeal oedema establish an airway.This may necessitate endotracheal intubation;in some cases,a cricothyroidotomy may be necessary.

Shock Management

General measures

1) Airwayneeds will vary depending on etiology of shock, from no intervention to aggressive intervention (i.e. anaphylaxis)

2) Breathingconsider O 2 to help with oxygen delivery even though sats may be OK, may need intubation, or other respiratory support, particularly to help compensate for metabolic acidosis

3)Blood pressure:should be kept above 90 mmhg systolic.the treatment depends on the aetiology of shock.Administration of fluids/blood is appropriate in hypovolaemic shock.In addition ,inotropic support may be required.

4) Fluid Resuscitation

Catheter size and length

Large bore

20 mL/kg of NS or LR

Polyhemoglobins

STABILIZE VITALS to SBP of 80 mmHg or 90 mmHg in head injuries.

5) 5) History– a) vomiting, diarrhea, decreased oral intake– b) lethargy, increased sleepiness– c) trauma– d) allergic symptoms / exposure (or rapid change in physiologic status)– e) congenital heart disease

6) Physical findings• a) decreased CNS activity• b) abnormal color pale => gray => mottled• c) decreased urine output (sign of overall tissue hypoperfusion)• d) tachypnea, tachycardia• e) delayed capillary refill

7)Insertion of lines:intravenous lines,either central or peripheral,by percutaneous cut down needs to be inserted for rapid infusion of fluids or drugs

8)The urinary bladder should be catherterised

9)Monitoring:Continous monitoring of heart rate,rhythm,blood pressure,oxygen saturation,urine output and arterial blood gases are mandatory

Monitoring Keys• a) electrolytes• b) glucose• c) blood gases (pH and oxygenation)• d) Central venous pressure• e) hemodynamics• f) coagulation status• g) urine output• h) neurologic status

Electrolytes• Na: can be markedly abnormal as a result of the underlying disease (hypo/hypernatremic dehydration)• can become elevated during process of correcting base deficit

• goal should be to normalize Na to avoid abnormal fluid shifts, this should be done SLOWLY!

• K: in acidotic state potassium can be elevated to the point of cardiac dysrhythmias, as correction of acidosis occurs K can be driven back into cells developing severe hypokalemia in some cases• Ca: in treatment of base deficit calcium can be chelated and dramatically decrease, leading to problems from seizures, hypotension and myocardial dysfunction• CaCl2 can be used acutely to correct hypocalcemia

Glucose• part of response to compensatory mechanisms (epinephrine and corticosteroids) hyperglycemia is a common occurrence in stressed children• can cause problems from osmotic diuresis and glucose intolerance (some studies showed poor neurologic outcome could be best predicted by hyperglycemia in patients with shock

Blood Gases• close monitoring is essential to evaluate correction of base deficit

Hemodynamics• good, reliable blood pressure monitoring and ECG monitoring are important• blood pressure is typically normal in early shock, decreasing blood pressure is a sign of someone who is decompensatingCoagulation Status• as DIC is a common complication even early in shock, close monitoring of coagulation status will allow early correction of deficits

Urine Output• this is representative of organ perfusion, improving urine output can be a sign of improving volume status, while worsening UO suggests more aggressive therapyNeurologic Status• this is also representative of organ perfusion, namely the brain

10) 10) Laboratory findings• a) acidosis on ABG with a base deficit signifying tissue hypoperfusion• b) decreased mixed venous oxygen saturation on a VBG• c) electrolyte abnormalities (related to cause of shock)11)Investigations:To arrive at a diagnosis of the aetiology of the shock e.g.haemogram,urine examination,cardiac injuryenzymes,chest x ray,serum electrolytes etc.

SPECIFIC MEASURES

A.HAEMORRHAGIC SHOCK :VIDE SUPRA

B.SEPTIC SHOCK:empirical antibiotics,treat source of infectionby drainage of pus,resection of gangrene,chest infection,oxygen delivery to the tissues,support in intensive care unit.

TREATMENT

1.Maximisation of oxygen delivery to the tissues:-

Volume expansion with CVP monitoring Inotropes such as dopamine Aggressive respiratory care

2.Identification and removal of the septic nidus

3.Drainage of abscess,removal of gangrenous area

4.Administration of agents that may neutralize or reverse the cellular effects of endotoxins.

C.ANAPHYLACTIC SHOCK

Common agents that cause anaphylaxis are penicillin,streptomycin

TREATMENT

1.Oxygen

2.Airway-endotracheal intubation

3.Injection adrenaline-0.3-0.5mgS/C,I.M or IV.It be given through endotracheal tube

4.Intravenous fluids

5.Vasopressors e.g Mephenteramine,dopamine

6.Cardiopulmonary resuscitation in case of cardiac arrest

7.Diphendydramine-1mg/kg or chlorpheniramine maleate

8.Injection hydrocortisone 1.5mg/kg

9.Injection Aminophylline 5mg/kg over 20 minutes for bronchospasm

OTHER MEASURES FOR TREATMENT OF SHOCK

HYPERBARIC OXYGEN

Here the oxygen is administered one to two atmospheric pressure in a compression chamber

Indications

1.Carbon monoxide poisoning.

2.Infections such as tetanus and gas gangrene

3.Cancer therapy to potentiate radiotherapy

4.Arterial insufficiency

5.Decompression sickness and air embolism

CENTRAL VENOUS PRESSURE

One of the essential requirement while treating patients in shock includes monitoring of CVP

CVP indicates volume of blood in the central veins,distensibility and contractility in the right heart chamber,intrathoracic pressure and intrapericardial pressure.Thus,in shock,measurement of CVP is essential so as to plan for proper fluid management

USES

1.If CVP is low,venous return should be supplemented by IV infusion as in cases of hypovolaemic shock

2.When CVP is high,infusion of fluids may result in pulmonary oedema

3.In cardiogenic shock,CVP may be normal

COMPLICATIONS:

1.Pneumothorax,haemothorax

2.Accidental carotid artery puncture

3.Haematoma in the neck

4.airembolism

5.Infection

PULMONARY CAPILLARY WEDGE PRESSURE-PCWP

This is a better indicator of the circulatory blood volume and left ventricular function

It is measured by a pulmonary artery ballon flotation cathether-“SWAN GANZ”cathetherUSES OF PCWP

1.To differentiate between left and right ventricular failure

2.Pulmonary embolus

3.Septic shock

4.Accurate administration of fluids,inotropic agents and vasodilators

COMPLICATIONS

Arrhythmias Pulmonary infarction Pulmonary artery rupture

Endogenous Vasoconstrictors • epinephrine and norepinephrine– released from adrenal medulla and sympathetic nerves cause vasoconstriction and increased cardiac output• vasopressin (antidiuretic hormone)– released from posterior pituitary– potent vasoconstrictor• renin (from decreased renal perfusion)– eventually yielding angiotensin

a very potent vasoconstrictor

Renal Conservation of Water• aldosterone release• stimulated by vasopressin• causes Na reabsorption in distal tubules• water follows the sodium Correct Acidosis• acidosis can cause significant problems with cellular function and should be aggressively treated• bicarbonate replacement when deficit is >6mEq/l• formula:– 0.3x(weight in kg)x(base deficit) = mEq NaHCO 3 to replace half of deficit– should be given slowly in 1-2mEq/kg boluses– may need 10-20mEq/kg to correct acidosis– this can be a large Na load leading to hyperosmolarity

Vasoactive Substances• select to optimize desired effect• consider the main effects as follows:– beta effects: increase inotropy and chronotropy - increasing cardiac output (beta-1)– also some pulmonary and peripheral vasodilation (beta-2)

• alpha effects: – increase systemic vascular resistance - maintaining blood pressure• vasodilators: – decrease systemic vascular resistance - decrease afterload, potentially improving cardiac function– also dramatically reducing BP in hypovolemic patient

Choices• epinephrine (beta and alpha, stronger beta)• norepinephrine (alpha and beta, more alpha)• dobutamine (beta-1 alone)• dopamine (dopaminergic at low doses, beta at medium to high and alpha at high doses)• isoproteronol (pure beta effects, both beta-1 and beta-2)• nitroprusside (vasodilator, a nitric oxide donor)• nitroglycerin (vasodilator, a nitric oxide donor)

DAMAGE OF INDIVIDUAL ORGANS

Cardiovascular system-in an attempt to maintain circulation to the body,the sympathoadrenal system is activated releasing catecholamine that leads to increase in myocardial contractility.Increase in blood pressure is there.Thus perfusion of vital organs is maintained till very low perfusion pressure.Later these mechanism fails resulting in fall of blood pressure,tachycardia and cardiac failure.

Lungs-Increased arteriovenous shunting,interstitial oedema,loss of surfactant and ARDS

Liver-Decreased clearance of endotoxins-Bacteremia,endotoxaemia

Kidney-Persistent arteriolar constriction-Renal failure

Gastrointestinal tract-Mucosal ulceration-Upper GI bleeding

-In essence,the end result is multiorgan failure

SUMMARY

Shock = inadequate tissue perfusion

Find shock by looking at tissue perfusion

Categories of shock

Hypovolemic

Septic shock

Distributive

Cardiogenic

Most common source of shock = hemorrhage

Management of shock

Stop the bleeding

Vascular access

Volume

Reassess

REFERENCES BURKETT-11TH EDITION MANIPAL MANUAL OF SURGERY FOR DENTAL STUDENTS BY K.RAJGOPAL SHENOY HUMAN PHYSIOLOGY FOR DENTAL STUDENTS BY A.K JAIN-THIRD EDITION