dr vijayendra kumar

8/7/2019 DR VIJAYENDRA KUMAR

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Shock

Dr. vijayendra kumar

presented by

Associate Prof

Dept of anaesthesiology

G G H kakinada


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INTRO

DUCTION

. Respiratory failure and shock

. Controversies

. Comprehensive understanding of patho physiology

. Aggressive therapy

. Inadequate and delayed treatment


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DEFINATION

. Shock is primary metabolic defect which circulatory

manifestations

. The central role of a defective tissue perfusion.

. Shock as an acute clinical syndrome characterized by hypo

perfusion and severe dysfunction of vital organs.


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APPLIED CARDIO VASCULOR PHYSIOLOGY

HYPO PERFUSIONOF VITAL ORGANS OCCURS

Decreased cardiac output

Mal distribution with adequate cardiac output

STROKE VOLUME

Preload

Myocardial contractility

After load


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THE CATAPULT ANALOGUE


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CARDIAC PUMP

PRELOAD

The left ventricular and diastolic fiber length represent the

preload of the left ventricle


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PRELOAD


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LEFT ATRIAL PRESSURE


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Myo cardial contractility

The ability of ventricular myocardial

Fibres to shorten during systole.

Myocardial contractibility can be quantified in terms

of ejection fraction (EF) .

Ejection fraction = Stroke volume / E.D.V


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AFTER LOAD

The after load of the left ventricular is the impedance to its ejection .

After load is the load that it has to overcome after ventricle

starts contracting

Systemic vascular resistance (SVR) constitutes the after load

of the left ventricle

VENTRICLE FUNCTION CURVES

Which relates preload and contractility the stroke volume

and cardiac output

Which relates afterload and contractility the stroke volume

and cardiac output


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Preload and contractility / the stroke volume cardiac output

. Replace ventricular preload with LVEDP / LAP / PCWP / CVP


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THE STARING CURVES OF THE TWO

VENTRCLES ARE ROUGHLY PARALLEL AND DIVERGE

ATTHEIR UPPER ENDS


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After load and contractility stroke

volume - cardiac output

. This curve relates the after load of the ventriclehas

to overcome to output it generates


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PATHOPHYSIOLOGY AND CLINICAL

PRESENTATIONOF SHOCK

Cellular injury

Neuro humoral respones

Metabolic respones

Organ Dysfunction


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CELLULARINJURY

Hypo perfusion

NEURO HUMARAL RESPONSES

Hypotension

Sympathetic hyper activity leads direct cardiac stimulationand pheripheral vascular constriction

Increased ACTH and ADH hormones from pituitary

Increased release of adrenaline from adrenaline medulla

Stimulation of renin- Angio tensin aldosterone mechanism


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METOBOLIC RESPONSES

Catecholamine response

INCREASED CATABOLISM OF PROTINES

Hypo albomenimia

GI bleeding

Delayed wound healing

ORGAN DYSFUNCTION

VITAL ORGANS

Brain

Heart

K

idney


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BRAIN

. Cerebal perfusion pressure

. Symptoms of cerebral dysfunction

. Confusion

. Anxiety

. Restlessness

. Frank coma


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HEART

Coronary perfusion pressure

Left ventricle end diastolic pressure(LVEDP)

ELEVATIONOF PULMONARY CAPPILLORY

HYDROSTOLIC PRESSURE

Pulmonary Oedema

Respiratory failure

Heart failure

JVP raised

Third heart sound

Dyskinetic apical impulse

Pulmonary rales


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RENAL

Renal hypo perfusion :

Decrease --

GFR

Results oluguria

AzotoemiaSEVERITY OF ORGAN

Pre-existing organ function

Compensatory mechanism

Ateological factor


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PULMONORY OEDEMA AND RESPIRATORY FAILURE

. Hypo tension

. Metabolic acidosis

Metabolic acidosis is the result of anaerobic

metabolism in O2 deprived tissue

Inadequate removal by inefficient perfusion pressure

Hepatic function inadequate to metabolisethe increased lactate

MANI

FESTATION

IN

SHO

CK


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MANAGEMENTOF SHOCK

Airway and breathing

Arterial blood pressure

History

Physical examination

Heart rate and rhythm

Quality of pulse


Pallor

Temperature

Cyanosis


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Signs of ventricular failure

Oedema

Signs of dehydration

Pulmonary rales

Insertion of Lines

Peripheral cannula 14 or 16

Central venous Catheter

Bladder catheterization

Arterial cannula


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MONOTORING

Cardiac rate rhythm


Filling pressures (pcwp or cvp)

Urine output

Temperature

Arterial blood glucose concentration

Arterial O2 saturation by pulse oximetre

End tidal carbon dioxide concentration

Cardiac output by thermo dilution


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INVESTIGATIONS

ECG coronary artery diseases and dysrhythms

Haemoglobine and haematocrit

blood grouping and cross matching

anterial blood gas analysis

plasma electrolyte creatinine

liver function test


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SEPTIC SHOCK

Septic shock in clinical syndrome produced by micro

organism and their toxins

It is single most important cause of death in intensive

care unit

Cancer, heart decease are known to the public

Sepsis is characterized by

Fever increased Temperature

Tachy cardia increased heat rate

Tachypnoea

Respiratory alkalosis


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in septic shock cardio vascular failure

symptoms are initially

hyper dynamic circulation with high cardiac output

low cardiac filling pressure

systemic vascular resistance decreased

in septic shock hypo perfusion is the resultof combination factors are

hypo volemia

myocardial depression

abnormal distribution of blood flow


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HEART

E.F = stroke volume / LV E D V

LUNGS

Myocardial depressant factor

Pulmonary hypoxic

vasoconstriction


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MANAGEMENTOF SEPTIC SHOCK

Maximization of o2 delivery to tissue

Identification and removal of septic nidus

Administration of agents neutralise or reverse

cellular effects of end toxins

Identification and removal of septic nidus by

Clinical examination

Investigation

Radiographs

Imagines

Maximization of o2 delivery to tissue

Increased cardiac output

Increased arterial pressure

Increased arterial O2 by mechanical ventilation


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Administration of agents neutralise or reverse

Endo toxins

Glucocorticoids

Human anti serum

X lipid- anti endo toxin property

CULTURE

Blood, urine , tracheal aspiration body fluids

Nature of micro organisms etc

. Administration broads spectrum anti

biotics


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CONTROVERSIES

Howmuch of which fluid ?

Howmuch of which inotrope or vasopressure ?

How much of which vasodilator ?

What in the current status of cartico steroids ?

CONCLUSION


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dr vijayendra kumar

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