Definition Offf Shock2

8/8/2019 Definition Offf Shock2

http://slidepdf.com/reader/full/definition-offf-shock2 1/81

SHOCK SHOCK

DR D.HURRY DR D.HURRY



DefinitionDefinition

CIRCULATORY SHOCK ISCIRCULATORY SHOCK IS

A A pathophysiologicalpathophysiological statestatecharacterized bycharacterized by

a significant, systemica significant, systemicreduction in tissue perfusionreduction in tissue perfusion

resulting in decreased tissueresulting in decreased tissueoxygen delivery &oxygen delivery &

insufficient removal of cellularinsufficient removal of cellularmetabolic productsmetabolic products

resulting in tissue injury.resulting in tissue injury.



Classification of ShockClassification of Shock

HYPOVOLEMICHYPOVOLEMIC

CARDIOGENICCARDIOGENIC

OBSTRUCTIVEOBSTRUCTIVE

DISTRIBUTIVEDISTRIBUTIVE



NEXT COMESNEXT COMES A TABLE A TABLE

SHOWINGSHOWING

THE AETIOLOGIC FACTORSTHE AETIOLOGIC FACTORS

IN THE 4 CLASSESIN THE 4 CLASSES



Hypovolaemic



HypovolemicHypovolemicIT IS DUE TO LOSS OFIT IS DUE TO LOSS OF

INTRAVASCULAR VOLUME BY INTRAVASCULAR VOLUME BY

HAEMORRHAGEHAEMORRHAGE

PLASMA LOSS ORPLASMA LOSS OR

LOSS OF FLUID &LOSS OF FLUID &

ELECTROLYTESELECTROLYTES

LOSS MAY BELOSS MAY BE

OBVIOUSOBVIOUS

(external(external haemorrhagehaemorrhage))

OROR SUBTLESUBTLE

((sequestration in a thirdsequestration in a thirds aces ace))



Compensatory MechanismCompensatory Mechanism

UNTIL 10UNTIL 10--15%BLOOD15%BLOOD VOLUME IS LOST BLOOD VOLUME IS LOST BLOODPRESSURE IS MAINTAINEDPRESSURE IS MAINTAINEDBY TACHYCARDIA ANDBY TACHYCARDIA AND VASOCONSTRICTION VASOCONSTRICTION

IF UNREPLACED,IF UNREPLACED,HYPOTENSION ANDHYPOTENSION AND

PROGRESSIVE TISSUEPROGRESSIVE TISSUEHYPOXIA RESULTSHYPOXIA RESULTS



THE NEXT SLIDE SHOWSTHE NEXT SLIDE SHOWS

AS THE COMPENSATORY AS THE COMPENSATORY MECHANISMS FAIL, SHOCK MECHANISMS FAIL, SHOCK

BECOMES INCURABLEBECOMES INCURABLE



COMPENSATORY MECHANISMCOMPENSATORY MECHANISM



NO TIME FOR COMPESATORY NO TIME FOR COMPESATORY

MECHANISMMECHANISM

ABDOMINAL AORTIC ABDOMINAL AORTIC

ANEURYSM ANEURYSM



PATHOPHYSIOLOGY PATHOPHYSIOLOGY

LOSS OF CIRCULATORY VOLUME LEADS TOLOSS OF CIRCULATORY VOLUME LEADS TO VENOUS RETURN VENOUS RETURN

FILLING OF CARDIAC CHAMBERSFILLING OF CARDIAC CHAMBERS

CARDIAC OUTPUTCARDIAC OUTPUT

IN SYSTEMIC VASCULAR RESISTANCEIN SYSTEMIC VASCULAR RESISTANCE

SYSTEMIC HYPOPERFUSIONSYSTEMIC HYPOPERFUSION



HOW TO ASSESS THEHOW TO ASSESS THE

VOLUME LOSS ? VOLUME LOSS ?

AS THE LOSS OF VOLUME PROGRESSES AS THE LOSS OF VOLUME PROGRESSES

THE CLINCAL PICTURE EVOLVES.THE CLINCAL PICTURE EVOLVES.



NOW I COME TONOW I COME TO

OBSTRUCTIVE SHOCK OBSTRUCTIVE SHOCK



OBSTRUCTIVE SHOCK OBSTRUCTIVE SHOCK THERE ISTHERE IS ACUTEACUTE

DECREASE IN CARDIACDECREASE IN CARDIAC

OUTPUT SECONDARYOUTPUT SECONDARY

TO OUTFLOWTO OUTFLOW

OBSTRUCTIONOBSTRUCTION

CAUSES ARECAUSES ARE

CARDIAC TAMPONADECARDIAC TAMPONADE

MASSIVE PERICARDIALMASSIVE PERICARDIALEFFUSION ANDEFFUSION AND

TENSIONTENSIONPNEUMOTHORAX PNEUMOTHORAX TENSION

PNEUMOTHORAX



Obstructive

CT scan

MASSIVE P.E



CARDIACTEMPONADE

CONTRACTILE

FUNCTION OFHEART IS

RESTRICTED

BY

SURROUNDING

PERICARDIAL.

EFFUSION



DISTRIBUTIVE SHOCK DISTRIBUTIVE SHOCK

There is reduction in systemic vascularThere is reduction in systemic vascularresistanceresistance

Resulting in inadequate cardiac output Resulting in inadequate cardiac output despite normal circulatory volumedespite normal circulatory volume

Most common varieties areMost common varieties are

1.septic shock1.septic shock

2.Neurogenic shock2.Neurogenic shock



Neurogenic shockNeurogenic shock

ORTHOPAEDICS WILL GOORTHOPAEDICS WILL GO

INTO MORE DETAILINTO MORE DETAIL

Caused by traumaticCaused by traumaticor pharmacologicalor pharmacologicalblockade of blockade of

sympathetic nervoussympathetic nervoussystem producingsystem producingdilatation of dilatation of resistance arteriolesresistance arterioles

and capacitance veinsand capacitance veins



SEPTIC SHOCK SEPTIC SHOCK MOST COMMON CAUSE OF DISTRIBUTIVEMOST COMMON CAUSE OF DISTRIBUTIVE

SHOCK SHOCK CARRIES MORTALITY 40CARRIES MORTALITY 40--80%80%

USUALLY PRESENTS WITH FEVER CHILLSUSUALLY PRESENTS WITH FEVER CHILLS

HYPOTENSION & ALTERED MENTALHYPOTENSION & ALTERED MENTALSTATUSSTATUS

MOSTLY DUE TO GRAMMOSTLY DUE TO GRAM --VE BACTEREMIA VE BACTEREMIA

TOPIC WILL BETOPIC WILL BE

TAKEN BY SURGERY TAKEN BY SURGERY AND PAEDIATRICS AND PAEDIATRICS



ANAPHYLACTIC SHOCK ANAPHYLACTIC SHOCK

GENERALISED IMMUNOLOGICAL REACTION OFGENERALISED IMMUNOLOGICAL REACTION OF

SUDDEN ONSET THAT DEVELOPS AFTERSUDDEN ONSET THAT DEVELOPS AFTEREXPOSURE TO FOREIGN SUBSTANCEEXPOSURE TO FOREIGN SUBSTANCE

CLINICAL FEATURESCLINICAL FEATURES

1.UPPER & LOWER AIRWAY OBSTRUCTION1.UPPER & LOWER AIRWAY OBSTRUCTION

LEADING TO WHEEZING ANDLEADING TO WHEEZING ANDBRONCHOSPASMBRONCHOSPASM

2. PRURITUS,URTICARIA2. PRURITUS,URTICARIA

3.NAUSEA VOMITING ABD. CRAMPS3.NAUSEA VOMITING ABD. CRAMPS

4. HYPOTENSION AND REDUCED C.O. DUE TO4. HYPOTENSION AND REDUCED C.O. DUE TOPLASMA LEAKAGE &PLASMA LEAKAGE &

DECREASE INTRAVASCULAR VOLUMEDECREASE INTRAVASCULAR VOLUME



MANAGEMENT OF SHOCK MANAGEMENT OF SHOCK



IT IS A TEAM WORK IT IS A TEAM WORK

MULTIDISCIPLINARY MULTIDISCIPLINARY EFFORTS AREEFFORTS ARENEEDED.NEEDED.



Tr eat patients, not par ameter s.Tr eat patients, not par ameter s.

Tr eat whole body, not organ.Tr eat whole body, not organ.

Tr eat dynamic cour se, not stage.Tr eat dynamic cour se, not stage.



G ener al management of patient in shock G ener al management of patient in shock

MobiliseMobilise team/call for helpteam/call for help

Dont hesitate to ask help from seniorsDont hesitate to ask help from seniors

Address the priorities(ABC) Address the priorities(ABC)

Look for the cause of shock Look for the cause of shock



GENERAL MEASURESGENERAL MEASURES

Frequent Frequent BP,pulseBP,pulse checkschecks

Continuous cardiac monitorContinuous cardiac monitor

O2 saturation monitoringO2 saturation monitoring

Secure adequate venous accessSecure adequate venous access

High Flow O2 by maskHigh Flow O2 by mask

CatheteriseCatheterise & monitor urine output hourly& monitor urine output hourly

Pulmonary capillary wedge pressure /CVP for hemodynamicPulmonary capillary wedge pressure /CVP for hemodynamicassessment assessment



INVESTIGATIONSINVESTIGATIONS

LAB TESTSLAB TESTS FBCFBC R.B.S.R.B.S. Bl.UreaBl.Urea

S.CREATINE &S.CREATINE & S. ELECTROLYTESS. ELECTROLYTES LFTLFT Coagulation profileCoagulation profile Fluid/ blood culture ,Fluid/ blood culture ,

BlBl grouping and Crossgrouping and Crossmatchingmatching

ABG ABG

OTHERSOTHERS

ECGECG

CXRCXR SONOGRAPHY SONOGRAPHY

CT SCANCT SCAN

MRIMRI



VOLUME REPLACEMENT VOLUME REPLACEMENT

CRYSTALLOIDS : NACL , RINGERS LACTATECRYSTALLOIDS : NACL , RINGERS LACTATE

COLLOIDS/PLASMA SUBSTITUTECOLLOIDS/PLASMA SUBSTITUTE BLOOD PRODUCTSBLOOD PRODUCTS

If evidence of decreased circulatory volumeIf evidence of decreased circulatory volume--20ml/kg NACL BOLUS20ml/kg NACL BOLUS

++

give fluid according to etiologygive fluid according to etiology

Blood products are indicated forBlood products are indicated for haemorrhagichaemorrhagicshockshock

URINE OUTPUT+CVP/PCWPURINE OUTPUT+CVP/PCWP to monitor fluid requirement &to monitor fluid requirement &

responseresponse



Management of Anaphylactic ShockManagement of Anaphylactic Shock

ALONG WITH GENERAL MANAGEMENT ALONG WITH GENERAL MANAGEMENT

I/V adrenaline 5I/V adrenaline 5--10 ml 1:10000 or through10 ml 1:10000 or throughendotrachealendotracheal tube.tube.

FluidsFluids

I/I/VHydrocortisone VHydrocortisone 300 bolus & 100 6300 bolus & 100 6 hrlyhrly

DiphenhydramineDiphenhydramine 1mg/kg iv slowly1mg/kg iv slowly

Aminophylline Aminophylline 250 mg bolus over 10 min. to250 mg bolus over 10 min. to

relieverelieve bronchospasmbronchospasm.. Dopamine if hypotensionDopamine if hypotension

Ventilatory Ventilatory support if patient critical.support if patient critical.



NOW I COME TO CARDIOGENICNOW I COME TO CARDIOGENIC

SHOCK SHOCK



Cardiogenic shockCardiogenic shock



Cardiogenic ShockCardiogenic Shock

DEFINITIONDEFINITION

INCIDENCEINCIDENCE

Etiologies Etiologies

Pathophysiology Pathophysiology

Clinical/Hemodynamic Characteristics Clinical/Hemodynamic Characteristics

Treatment Options Treatment Options



Cardiogenic ShockCardiogenic Shock

Systemic hypoperfusion secondary toSystemic hypoperfusion secondary tosevere depression of cardiac outputsevere depression of cardiac output

and sustained systolic arterial and sustained systolic arterial hypotensionhypotension despite elevated fillingdespite elevated fillingpressures.pressures.



INCIDENCEINCIDENCE LEADING CAUSE OF DEATH OF PTLEADING CAUSE OF DEATH OF PT

HOSPITALIZED WITH MIHOSPITALIZED WITH MI

RATE OF CS COMPLICATING MI ABOUT 8%RATE OF CS COMPLICATING MI ABOUT 8%

TYPICALLY ASSOCIATED WITH STEMITYPICALLY ASSOCIATED WITH STEMI OF THE 8% CS COMPLICATING MIOF THE 8% CS COMPLICATING MI

¼ ARE ON ADMISSION¼ ARE ON ADMISSION

¼¼ DEVELOP WITHIN 6HRDEVELOP WITHIN 6HR ANOTHER ¼ LATER ON THE FIRST DAY ANOTHER ¼ LATER ON THE FIRST DAY



ETIOLOGY ETIOLOGY

PRIMARY MYOCARDIAL DYSFUNCTIONPRIMARY MYOCARDIAL DYSFUNCTION;;

MOST COMMONLY SECONDARY TO ACUTE MIMOST COMMONLY SECONDARY TO ACUTE MI

LESS COMMON CAUSESLESS COMMON CAUSES

CARDIOMYOPATHY/CARDIOMYOPATHY/ MYOCARDITISMYOCARDITIS

ACUTE VALVULAR DYSFUNCTION ACUTE VALVULAR DYSFUNCTION

SECONDARY TO OBSTRUCTIONSECONDARY TO OBSTRUCTION

CARDIAC TAMPONADECARDIAC TAMPONADE

P.EMBOLISMP.EMBOLISM

TENSION PNEUMOTHORAX TENSION PNEUMOTHORAX



PATHOPHYSIOLOGYPATHOPHYSIOLOGYTHE VICIOUS CYCLETHE VICIOUS CYCLE

DEPRESSION OF MYOCARDIUMDEPRESSION OF MYOCARDIUM REDUCED C O & BPREDUCED C O & BP

MORE MYOCARDIAL HYPOPERFUSION &MORE MYOCARDIAL HYPOPERFUSION &

FURTHER ISCHAEMIAFURTHER ISCHAEMIA MORE DEPRESSION OF CO WITH ANOXIAMORE DEPRESSION OF CO WITH ANOXIALEADING TO LACTIC ACIDOSISLEADING TO LACTIC ACIDOSIS

WITH MASSIVE INFARCTS A SYSTEMICWITH MASSIVE INFARCTS A SYSTEMICINFLAMMATORY RESPONSE MAY OCCURINFLAMMATORY RESPONSE MAY OCCURDUE TO RELEASE OF INFLAMMATORY DUE TO RELEASE OF INFLAMMATORY MEDIATORS WHICH CONTRIBUTE TOMEDIATORS WHICH CONTRIBUTE TO

GENESIS OF SHOCK GENESIS OF SHOCK




SYMPTOMSSYMPTOMS

CONTINUING CHEST PAINCONTINUING CHEST PAIN

DYSPNOEADYSPNOEAPALLORPALLOR

APPREHENSION APPREHENSION

DIAPHORESISDIAPHORESIS ALTERED MENTATION; ALTERED MENTATION;

(CONFUSION,AGITATION)(CONFUSION,AGITATION)




SIGNSSIGNS

SBP<90mmhgSBP<90mmhg PULSE RAPID THREADYPULSE RAPID THREADY

NARROW PULSE PRESSURE<30mmhgNARROW PULSE PRESSURE<30mmhg

Elevated JVPElevated JVP

S1 SOFT ,S3 GALLOP, murmurs in acuteS1 SOFT ,S3 GALLOP, murmurs in acuteregurgitation (M.R. due to P.M.D./Ruptureregurgitation (M.R. due to P.M.D./Rupture ChordaeChordaeand A.R. in S.B.E.)and A.R. in S.B.E.)

TACHYPNOEA,CHEYNETACHYPNOEA,CHEYNE--STOKES RESP,STOKES RESP,

Rales Rales oliguriaoliguria

QuietQuiet precordiumprecordium



LAB FINDINGSLAB FINDINGS

WBC TYPICALLY ELEVATEDWBC TYPICALLY ELEVATED

PROGRESSIVE RENAL AND HEPATICPROGRESSIVE RENAL AND HEPATICDYSFUNCTION SECONDARY TODYSFUNCTION SECONDARY TOHYPOPERFUSIONHYPOPERFUSION

ABG SHOWS HYPOXAEMIA & METABOLIC ABG SHOWS HYPOXAEMIA & METABOLIC ACIDOSIS ACIDOSIS

INCREASE ANION GAP ACIDOSISINCREASE ANION GAP ACIDOSIS



ECG-MAY SHOW EVIDENCE OF MI/ISCHAEMIA

PULMONARY EMBOLISM ARRHYTHMIASELECTROLYTE DISTURBANCES

CXR MAY SHOW FEATURES OF

PULMONARY OEDEMACARDIOMEGALY PLEURAL EFFUSIONPNEUMOTHORAX

ECHO-HELPS TO FIND ETIOLOGY



ECGECG--

MAY SHOWMAY SHOW

ISCHAEMIAISCHAEMIA INFARCTINFARCT

ARRHYTHMIAS ARRHYTHMIAS



CXR MAY SHOWCXR MAY SHOW

ACUTE PULMONARY ACUTE PULMONARY OEDEMAOEDEMA

CARDIOMEGALY CARDIOMEGALY

PLEURAL EFFUSIONPLEURAL EFFUSION



ECHOCARDIOGRAPHY ECHOCARDIOGRAPHY

HELPS TO FIND ETIOLOGY HELPS TO FIND ETIOLOGY

SHOWS REAL TIMESHOWS REAL TIMEGLOBAL HEART FUNCTIONGLOBAL HEART FUNCTION

PERICARDIAL EFFUSIONPERICARDIAL EFFUSION

VALVULAR LESIONS VALVULAR LESIONS

CHAMBERS SIZECHAMBERS SIZE



PERICARDIALEFFUSION/

TEMPONADE



Potential TherapiesPotential Therapies

INOTROPESINOTROPES

FIBRINOLYTICSFIBRINOLYTICS

IntraIntra--aortic Balloon Pump (IABP)aortic Balloon Pump (IABP)

Revascularization: CABG/PCIRevascularization: CABG/PCI

Refractory shock: ventricular assist device,Refractory shock: ventricular assist device,cardiac transplantationcardiac transplantation



INOTROPESINOTROPES

DOPAMINEDOPAMINE--USUALLY THE 1USUALLY THE 1STST

LINE AGENT BECAUSE OF ITSLINE AGENT BECAUSE OF ITSCOMBINED INOTROPIC & VASOPRESSORS & RENALCOMBINED INOTROPIC & VASOPRESSORS & RENALPERFUSIONPERFUSION

DOBUTAMINEDOBUTAMINE--IN PTS WITH RELATIVELY STABLE BP(>90)IN PTS WITH RELATIVELY STABLE BP(>90)BUT LOW CO & HYPOPERFUSION AS IT CAUSES PERIPHERALBUT LOW CO & HYPOPERFUSION AS IT CAUSES PERIPHERAL VASODILATATION CAUTION NEEDED VASODILATATION CAUTION NEEDED

NORADRENALINENORADRENALINE--IF HYPOTENSION REMAINS REFRACTORY IF HYPOTENSION REMAINS REFRACTORY IT CAN BE ADDEDIT CAN BE ADDED

MILRINONEMILRINONE--POTENTPOTENT INOTROPE BUT CAN CAUSEINOTROPE BUT CAN CAUSE VASODILATATION VASODILATATION--LIKE DOBUTAMINELIKE DOBUTAMINE



INTRAINTRA--AORTIC BALLOON COUNTERPULSATION AORTIC BALLOON COUNTERPULSATION

Introduced in 1968 for promoting coronary bloodIntroduced in 1968 for promoting coronary bloodflow in acute MI withflow in acute MI with cardiogeniccardiogenic shockshock

A sausage A sausage--shaped polyurethane balloon attached toshaped polyurethane balloon attached todistal end of large bore catheter is inserted intodistal end of large bore catheter is inserted intofemoral artery and advanced retrograde.femoral artery and advanced retrograde.

Its tip lies just below the left Its tip lies just below the left subclaviansubclavian artery.artery.

ProperlyProperly placed,it placed,it should extend from just belowshould extend from just below

subclaviansubclavian to just above renal arteryto just above renal artery

H d i ff t f IABPH d i ff t f IABP



Hemodynamic effects of IABPHemodynamic effects of IABP

INFLATION BEGINS AT ONSET OF DIASTOLEINFLATION BEGINS AT ONSET OF DIASTOLEINCREASE MEAN PRESSURE IN AORTA WHICH IS THEINCREASE MEAN PRESSURE IN AORTA WHICH IS THEDRIVING FORCE FOR SYSTEMIC BLOOD FLOW.DRIVING FORCE FOR SYSTEMIC BLOOD FLOW.

IN DIASTOLIC PRESSURE ALSO INCREASESIN DIASTOLIC PRESSURE ALSO INCREASESCORONARY BLOOD FLOWCORONARY BLOOD FLOW

DEFLATION REDUCES THE END DIASTOLICDEFLATION REDUCES THE END DIASTOLICPRESSURE WHICH REDUCES IMPEDENCE TO FLOWPRESSURE WHICH REDUCES IMPEDENCE TO FLOWDURING SYSTOLEDURING SYSTOLE



SO IN SHORT IABP is aSO IN SHORT IABP is a

temporizing measuretemporizing measure Augments coronary blood flow in diastole Augments coronary blood flow in diastole

Balloon collapse in systole creates aBalloon collapse in systole creates avacuum effect vacuum effect decreases afterloaddecreases afterload

Decrease myocardial oxygen demandDecrease myocardial oxygen demand



Intra-Aortic Balloon Pump



Limitation of IABPLimitation of IABP Lack of active circulatory support Lack of active circulatory support

Needs a certain level of left ventricular (LV)Needs a certain level of left ventricular (LV)function.function.

With severely depressed LV function IABP isWith severely depressed LV function IABP isinadequate to revert CS.inadequate to revert CS.

In such cases use of In such cases use of percutaneouspercutaneous LV assist LV assist devices (LVAD) with active circulatory support devices (LVAD) with active circulatory support might be beneficial .might be beneficial .



FIBRINOLYSISFIBRINOLYSIS

RANDOMIZED TRIALS HAVERANDOMIZED TRIALS HAVESHOWN THATSHOWN THAT

IN CARDIOGENIC SHOCK IN CARDIOGENIC SHOCK PHARMACOLOGICPHARMACOLOGICREFERFUSION BY REFERFUSION BY THROMBOLYTIC THERAPY THROMBOLYTIC THERAPY HAS A REDUCED EFFICACY HAS A REDUCED EFFICACY

P.C.I. GIVE SUPERIORP.C.I. GIVE SUPERIOROUTCOMESOUTCOMES

REPERFUSIONREPERFUSION



REPERFUSIONREPERFUSION

RAPID ESTABLISHMENT OF BLOOD FLOW IN INFARCTRAPID ESTABLISHMENT OF BLOOD FLOW IN INFARCT

RELATED ARTERY IS ESSENTIAL IN THE MANAGEMENTRELATED ARTERY IS ESSENTIAL IN THE MANAGEMENTOF C.S.OF C.S.

FOR STEMI OR MI WITH LBBB WITH CS WITHIN 36FOR STEMI OR MI WITH LBBB WITH CS WITHIN 36

HRS ,EARLY P.C.I./C.A.B.G. IS A CLASS IHRS ,EARLY P.C.I./C.A.B.G. IS A CLASS IRECOMMENDATIONRECOMMENDATION

IABP &FIBRINOLYTIC THERAPY IS RECOMMENDEDIABP &FIBRINOLYTIC THERAPY IS RECOMMENDED

ONLY WHEN REVASCULARISATION NOT POSSIBLEONLY WHEN REVASCULARISATION NOT POSSIBLE



P.C.I. (P.C.I. (PER CUTANEOUS INTERVENTIONS)PER CUTANEOUS INTERVENTIONS)

CORONARY BALLOON ANGIOPLASTYCORONARY BALLOON ANGIOPLASTYEXPANDS THE CORONARY LUMEN BY STRETCHINGEXPANDS THE CORONARY LUMEN BY STRETCHING

& TEARING THE ATHEROMATOUS PLAQUE& TEARING THE ATHEROMATOUS PLAQUE

CORONARY STENTS ARECORONARY STENTS ARE USED IN >90% PCIUSED IN >90% PCIPROCEDURESPROCEDURES

IT SCAFFOLDS ARTERIAL DISSECTION FLAP THUSIT SCAFFOLDS ARTERIAL DISSECTION FLAP THUSLOWERS THE INCIDENCE OF VESSEL CLOSURELOWERS THE INCIDENCE OF VESSEL CLOSURE

DRUG ELUTING STENTSDRUG ELUTING STENTS--PROVIDE SUSTAINEDPROVIDE SUSTAINEDLOCAL DELIVERY OF ANTIPROLIFERATIVE AGENTLOCAL DELIVERY OF ANTIPROLIFERATIVE AGENT

AT SITE OF VESSEL WALL INJURY(SIROLIMUS AT SITE OF VESSEL WALL INJURY(SIROLIMUS

ELUTING STENTS,PACLITAXEL E.STENTS)ELUTING STENTS,PACLITAXEL E.STENTS)



EARLY REVASCULARIZATIONEARLY REVASCULARIZATION V/S V/S

MEDICAL MANAGEMENTMEDICAL MANAGEMENT

Th Sh ld W E lTh Sh ld W E l R l iR l i O l d dO l d d



The Should We EmergentlyThe Should We Emergently RevascularizeRevascularize OccludedOccluded

Coronaries forCoronaries for CardiogenicCardiogenic ShockShock (SHOCK TRIAL)(SHOCK TRIAL)

randomly assigned 302 patients of MI withrandomly assigned 302 patients of MI withpredominant LVF topredominant LVF to

1)emergency revascularization(CABG/PCI)within1)emergency revascularization(CABG/PCI)within

6 hrs6 hrs

oror

2)initial medical stabilization.2)initial medical stabilization.

The primary end point of the study was 30The primary end point of the study was 30--daydayallall--cause mortality.cause mortality.



RESULTS OF SHOCK TRIALRESULTS OF SHOCK TRIAL



No significant difference in 30 days survival.No significant difference in 30 days survival.

A significant survival benefit with early A significant survival benefit with earlyrevascularization at 6 and 12 months.revascularization at 6 and 12 months.

The benefit was greatest for those <75 years,The benefit was greatest for those <75 years,

20 lives were saved at 6 month per 100 patients20 lives were saved at 6 month per 100 patientstreated.treated.

Therefore the American College of Cardiology nowTherefore the American College of Cardiology nowrecommends emergency revascularization forrecommends emergency revascularization for

patients younger than 75 years withpatients younger than 75 years with cardiogeniccardiogenicshockshock

RESULTS OF SHOCK TRIALRESULTS OF SHOCK TRIAL



CONCLUSIONS:

Restoration of coronary blood flowis a major predictor of survival incardiogenic shock.

Surgery should be considered insh

ock

patients with severe mitralinsufficiency or multivessel diseasenot amenable to relatively complete

percutaneous revascularization.



L.V. NEEDS ASSISTANCEL.V. NEEDS ASSISTANCE



LV ASSIST DEVICELV ASSIST DEVICE



L V A DL V A D

LVAD, is a mechanicalLVAD, is a mechanicalpump that ispump that is

implanted inside aimplanted inside aperson's chest to helpperson's chest to helpa weakened heart a weakened heart ventricle pump bloodventricle pump blood



How Does an LVAD Work?How Does an LVAD Work?

the LVAD is a pump. The LVAD is surgicallythe LVAD is a pump. The LVAD is surgicallyimplanted just below the heart.implanted just below the heart.

One end is attached to the left ventricleOne end is attached to the left ventricle

The other end is attached to the aorta

Blood flows from the ventricles into the pump

which passively fills up. When the sensors

indicate it is full, the blood is ejected out of the

device to the aorta

A tube called driveline passes from the device

through the skin & connects the pump to the

external controller and power source.



LVADLVAD

MOST COMMONLY USEDMOST COMMONLY USED AS A MEANS OF AS A MEANS OFTEMPORARY SUPPORT TOTEMPORARY SUPPORT TO A PLANNED DEFINITIVE A PLANNED DEFINITIVE

TREATMENT SUCH ASTREATMENT SUCH ASHEART TRANSPLANTHEART TRANSPLANT

THERE ARE ONGOINGTHERE ARE ONGOINGTRIAL FOR USE OF LVADTRIAL FOR USE OF LVAD AS DEFINITIVE THERAPY AS DEFINITIVE THERAPY FOR END STAGE CARDIACFOR END STAGE CARDIAC

FAILUREFAILURE

TEACHER &TEACHER &



THANK YOUTHANK YOU

UDIENCEUDIENCE

TEACHER &TEACHER &COLLEGUESCOLLEGUES



CARDIOGENIC VS NON CARDIOGENIC ACUTECARDIOGENIC VS NON CARDIOGENIC ACUTE



CARDIOGENIC VS NON CARDIOGENIC ACUTECARDIOGENIC VS NON CARDIOGENIC ACUTEPULMONARY OEDEMA(DIAGNOSIS)PULMONARY OEDEMA(DIAGNOSIS)

1.ECHOCARDIOGRAPHY 1.ECHOCARDIOGRAPHY

2.ECG MAY SHOW ST2.ECG MAY SHOW STELEVATION OR Q WAVESELEVATION OR Q WAVES--

REPERFUSION THERAPY REPERFUSION THERAPY

BRAIN NATRIURETICBRAIN NATRIURETICPEPTIDE;PEPTIDE;WHICHWHICH WHEN ELEVATEDWHEN ELEVATED

SUPPORT DIAGNOSIS OF HEARTSUPPORT DIAGNOSIS OF HEARTFAILUREFAILURE



BRAIN TYPE NATRIURETIC PEPTIDEBRAIN TYPE NATRIURETIC PEPTIDE

BNP IS A NEUROHORMONE THAT IS RELEASEDBNP IS A NEUROHORMONE THAT IS RELEASEDBY VENTRICULAR MYOCARDIUM IN RESPONSEBY VENTRICULAR MYOCARDIUM IN RESPONSETO VENTRICULAR STRETCHING;VOLUMETO VENTRICULAR STRETCHING;VOLUMEOVERLOADOVERLOAD

PLASMA LEVELS OF BNP INCREASE IN DIRECTPLASMA LEVELS OF BNP INCREASE IN DIRECTRELATION TO INCREASE IN VENTRICULARRELATION TO INCREASE IN VENTRICULARENDEND--DIASTOLIC VOLUME & END DIASTOLICDIASTOLIC VOLUME & END DIASTOLICPRESSUREPRESSURE

A PLASMA BNP >100 PG/ML CAN BE USED AS A PLASMA BNP >100 PG/ML CAN BE USED AS AN EVIDENCE OF HEART FAILURE AS A CAUSE AN EVIDENCE OF HEART FAILURE AS A CAUSEOF DYSPNEAOF DYSPNEA



TREATMENTTREATMENT

SUPPORT OF OXYGENATION &SUPPORT OF OXYGENATION & VENTILATION VENTILATION

O2 THERAPY O2 THERAPY POSITIVE PRESSURE VENTILATIONPOSITIVE PRESSURE VENTILATION

REDUCTION OF PRELOADREDUCTION OF PRELOAD



Classification of shockClassification of shock



Dopamine usually is administered first inDopamine usually is administered first inpatients with cardiogenic shock because it patients with cardiogenic shock because it

has inotropic and vasopressor properties.has inotropic and vasopressor properties.Typically, the dose is titrated to maintain aTypically, the dose is titrated to maintain amean arterial BP of 60 mm Hg or greater.mean arterial BP of 60 mm Hg or greater.Subsequent Subsequent



VASOVAGAL SHOCK VASOVAGAL SHOCK RESULT FROMRESULT FROM

POOLING OF BLOOD IN LARGER VASCULARPOOLING OF BLOOD IN LARGER VASCULARRESERVOIRS(LIMB MUSCLES) &RESERVOIRS(LIMB MUSCLES) &

DILATATION OF SPLANCNIC ARTERIOLAR BEDDILATATION OF SPLANCNIC ARTERIOLAR BED

LEADING TOLEADING TO C.O; CEREBRAL PERFUSIONC.O; CEREBRAL PERFUSION&UNCONSCIOUSNESS&UNCONSCIOUSNESS

IF PATIENT MAINTAIN IN UPRIGHT POSITIONIF PATIENT MAINTAIN IN UPRIGHT POSITIONPERMANENT CEREBRAL DAMAGE RARELY PERMANENT CEREBRAL DAMAGE RARELY

Definition Offf Shock2

Documents

Transcript of Definition Offf Shock2