SHOCK

DR D.HURRY
Definition

CIRCULATORY SHOCK IS
A pathophysiological state
characterized by
a significant, systemic
reduction in tissue perfusion
resulting in decreased tissue
oxygen delivery &
insufficient removal of cellular
metabolic products
resulting in tissue injury.
 Classification of Shock

• HYPOVOLEMIC

• CARDIOGENIC

• OBSTRUCTIVE

• DISTRIBUTIVE
NEXT COMES
A TABLE
SHOWING

THE AETIOLOGIC FACTORS

IN THE 4 CLASSES
Hypovolaemic
Hypovolemic
IT IS DUE TO LOSS OF
INTRAVASCULAR VOLUME BY
• HAEMORRHAGE
• PLASMA LOSS OR
• LOSS OF FLUID &
ELECTROLYTES

LOSS MAY BE
OBVIOUS
(external haemorrhage)
OR SUBTLE
(sequestration in a third
 Compensatory Mechanism
• UNTIL 10-15%BLOOD
VOLUME IS LOST BLOOD
PRESSURE IS MAINTAINED
BY TACHYCARDIA AND
VASOCONSTRICTION

• IF UNREPLACED,
HYPOTENSION AND
PROGRESSIVE TISSUE
HYPOXIA RESULTS
THE NEXT SLIDE SHOWS
AS THE COMPENSATORY
MECHANISMS FAIL, SHOCK
BECOMES INCURABLE
COMPENSATORY MECHANISM
NO TIME FOR COMPESATORY
MECHANISM

• ABDOMINAL AORTIC
ANEURYSM
PATHOPHYSIOLOGY
• LOSS OF CIRCULATORY VOLUME LEADS TO
VENOUS RETURN

FILLING OF CARDIAC CHAMBERS

CARDIAC OUTPUT

IN SYSTEMIC VASCULAR RESISTANCE

SYSTEMIC HYPOPERFUSION
 HOW TO ASSESS THE
VOLUME LOSS ?

AS THE LOSS OF VOLUME PROGRESSES

THE CLINCAL PICTURE EVOLVES.
NOW I COME TO

OBSTRUCTIVE SHOCK
OBSTRUCTIVE SHOCK
THERE IS ACUTE
DECREASE IN CARDIAC
OUTPUT SECONDARY
TO OUTFLOW
OBSTRUCTION

CAUSES ARE
• CARDIAC TAMPONADE
• MASSIVE PERICARDIAL
EFFUSION AND
• TENSION
PNEUMOTHORAX • TENSION
PNEUMOTHORAX
Obstructive

• CT scan
• MASSIVE P.E
• CARDIAC
TEMPONADE

CONTRACTILE
FUNCTION OF
HEART IS
RESTRICTED
BY
SURROUNDING
PERICARDIAL.
EFFUSION
DISTRIBUTIVE SHOCK
• There is reduction in systemic vascular
resistance
• Resulting in inadequate cardiac output
despite normal circulatory volume
• Most common varieties are
1.septic shock
2.Neurogenic shock
 Neurogenic shock
• Caused by traumatic
or pharmacological
blockade of
sympathetic nervous
system producing
dilatation of
resistance arterioles
and capacitance veins

• ORTHOPAEDICS WILL GO
INTO MORE DETAIL
SEPTIC SHOCK
• MOST COMMON CAUSE OF DISTRIBUTIVE
SHOCK
• CARRIES MORTALITY 40-80%
• USUALLY PRESENTS WITH FEVER CHILLS
HYPOTENSION & ALTERED MENTAL
STATUS
• MOSTLY DUE TO GRAM -VE BACTEREMIA

TOPIC WILL BE
TAKEN BY SURGERY
AND PAEDIATRICS
 ANAPHYLACTIC SHOCK
GENERALISED IMMUNOLOGICAL REACTION OF
SUDDEN ONSET THAT DEVELOPS AFTER
EXPOSURE TO FOREIGN SUBSTANCE

CLINICAL FEATURES
1.UPPER & LOWER AIRWAY OBSTRUCTION
LEADING TO WHEEZING AND
BRONCHOSPASM

2. PRURITUS,URTICARIA

3.NAUSEA VOMITING ABD. CRAMPS

4. HYPOTENSION AND REDUCED C.O. DUE TO

PLASMA LEAKAGE &
DECREASE INTRAVASCULAR VOLUME
MANAGEMENT OF SHOCK
IT IS A TEAM WORK

MULTIDISCIPLINARY
EFFORTS ARE
NEEDED.
• Treat patients, not parameters.
Treat whole body, not organ.
Treat dynamic course, not stage.
 General management of patient in shock

• Mobilise team/call for help

• Don’t hesitate to ask help from seniors

• Address the priorities(ABC)

• Look for the cause of shock

GENERAL MEASURES
• Frequent BP,pulse checks

• Continuous cardiac monitor

• O2 saturation monitoring

• Secure adequate venous access

• High Flow O2 by mask

• Catheterise & monitor urine output hourly

• Pulmonary capillary wedge pressure /CVP for hemodynamic assessment

 INVESTIGATIONS
LAB TESTS
OTHERS
• FBC
• R.B.S. • ECG
• Bl.Urea
• S.CREATINE & • CXR
• S. ELECTROLYTES • SONOGRAPHY
• LFT
• CT SCAN
• Coagulation profile
• Fluid/ blood culture , • MRI
• Bl grouping and Cross
matching
• ABG
VOLUME REPLACEMENT
• CRYSTALLOIDS : NACL , RINGERS LACTATE
• COLLOIDS/PLASMA SUBSTITUTE
• BLOOD PRODUCTS

• If evidence of decreased circulatory volume-

20ml/kg NACL BOLUS
+
give fluid according to etiology

• Blood products are indicated for haemorrhagic

shock
URINE OUTPUT+CVP/PCWP to monitor fluid requirement &
response
 Management of Anaphylactic Shock
• ALONG WITH GENERAL MANAGEMENT
• I/V adrenaline 5-10 ml 1:10000 or through
endotracheal tube.
• Fluids
• I/VHydrocortisone 300 bolus & 100 6 hrly
• Diphenhydramine 1mg/kg iv slowly
• Aminophylline 250 mg bolus over 10 min. to
relieve bronchospasm.
• Dopamine if hypotension
• Ventilatory support if patient critical.
NOW I COME TO CARDIOGENIC
SHOCK
Cardiogenic shock
Cardiogenic Shock

• DEFINITION

• INCIDENCE

• Etiologies

• Pathophysiology

• Clinical/Hemodynamic Characteristics

• Treatment Options
Cardiogenic Shock

• Systemic hypoperfusion secondary to

severe depression of cardiac output
and sustained systolic arterial
hypotension despite elevated filling
pressures.
INCIDENCE
• LEADING CAUSE OF DEATH OF PT
HOSPITALIZED WITH MI
• RATE OF CS COMPLICATING MI ABOUT 8%
• TYPICALLY ASSOCIATED WITH STEMI
• OF THE 8% CS COMPLICATING MI
• ¼ ARE ON ADMISSION
• ¼ DEVELOP WITHIN 6HR
• ANOTHER ¼ LATER ON THE FIRST DAY
ETIOLOGY
• PRIMARY MYOCARDIAL DYSFUNCTION;
• MOST COMMONLY SECONDARY TO ACUTE MI
LESS COMMON CAUSES
• CARDIOMYOPATHY/
• MYOCARDITIS
• ACUTE VALVULAR DYSFUNCTION

• SECONDARY TO OBSTRUCTION
• CARDIAC TAMPONADE
• P.EMBOLISM
 PATHOPHYSIOLOGY
THE VICIOUS CYCLE
• DEPRESSION OF MYOCARDIUM
• REDUCED C O & BP
• MORE MYOCARDIAL HYPOPERFUSION &
FURTHER ISCHAEMIA
• MORE DEPRESSION OF CO WITH ANOXIA
LEADING TO LACTIC ACIDOSIS
• WITH MASSIVE INFARCTS A SYSTEMIC
INFLAMMATORY RESPONSE MAY OCCUR DUE
TO RELEASE OF INFLAMMATORY
MEDIATORS WHICH CONTRIBUTE TO
GENESIS OF SHOCK
CLINICAL FEATURES
SYMPTOMS
CONTINUING CHEST PAIN
DYSPNOEA
PALLOR
APPREHENSION
DIAPHORESIS
ALTERED MENTATION;
(CONFUSION,AGITATION)
CLINICAL FEATURES
SIGNS
• SBP<90mmhg
• PULSE RAPID THREADY
• NARROW PULSE PRESSURE<30mmhg
• Elevated JVP
• S1 SOFT ,S3 GALLOP, murmurs in acute
regurgitation (M.R. due to P.M.D./Rupture Chordae
and A.R. in S.B.E.)
• TACHYPNOEA,CHEYNE-STOKE’S RESP,
• Rales
• oliguria
• Quiet precordium
LAB FINDINGS
• WBC TYPICALLY ELEVATED

• PROGRESSIVE RENAL AND HEPATIC

DYSFUNCTION SECONDARY TO HYPOPERFUSION

• ABG SHOWS HYPOXAEMIA & METABOLIC

ACIDOSIS

• INCREASE ANION GAP ACIDOSIS

 ECG-MAY SHOW EVIDENCE OF MI/ISCHAEMIA
PULMONARY EMBOLISM
ARRHYTHMIAS
ELECTROLYTE DISTURBANCES

CXR MAY SHOW FEATURES OF

PULMONARY OEDEMA
CARDIOMEGALY
PLEURAL EFFUSION
PNEUMOTHORAX

ECHO-HELPS TO FIND ETIOLOGY

ECG-

MAY SHOW

• ISCHAEMIA
• INFARCT
• ARRHYTHMIAS
CXR MAY SHOW

• ACUTE PULMONARY
OEDEMA

• CARDIOMEGALY

• PLEURAL EFFUSION
ECHOCARDIOGRAPHY
• HELPS TO FIND ETIOLOGY

• SHOWS REAL TIME

GLOBAL HEART FUNCTION

• PERICARDIAL EFFUSION

• VALVULAR LESIONS

• CHAMBERS SIZE
• PERICARDIAL
EFFUSION/
• TEMPONADE
 Potential Therapies
• INOTROPES

• FIBRINOLYTICS

• Intra-aortic Balloon Pump (IABP)

• Revascularization: CABG/PCI

• Refractory shock: ventricular assist device, cardiac

transplantation
INOTROPES

• DOPAMINE-USUALLY THE 1ST LINE AGENT BECAUSE OF ITS

COMBINED INOTROPIC & VASOPRESSORS & RENAL
PERFUSION

• DOBUTAMINE-IN PTS WITH RELATIVELY STABLE BP(>90)

BUT LOW CO & HYPOPERFUSION AS IT CAUSES PERIPHERAL
VASODILATATION CAUTION NEEDED

• NORADRENALINE-IF HYPOTENSION REMAINS REFRACTORY

IT CAN BE ADDED

• MILRINONE-POTENT INOTROPE BUT CAN CAUSE

VASODILATATION-LIKE DOBUTAMINE
 INTRA-AORTIC BALLOON COUNTERPULSATION

• Introduced in 1968 for promoting coronary blood flow

in acute MI with cardiogenic shock

• A sausage-shaped polyurethane balloon attached to

distal end of large bore catheter is inserted into femoral
artery and advanced retrograde.

• Its tip lies just below the left subclavian artery.

• Properly placed,it should extend from just below

subclavian to just above renal artery
 Hemodynamic effects of IABP

• INFLATION BEGINS AT ONSET OF DIASTOLE

INCREASE MEAN PRESSURE IN AORTA WHICH IS THE
DRIVING FORCE FOR SYSTEMIC BLOOD FLOW.

• IN DIASTOLIC PRESSURE ALSO INCREASES

CORONARY BLOOD FLOW

• DEFLATION REDUCES THE END DIASTOLIC PRESSURE

WHICH REDUCES IMPEDENCE TO FLOW DURING
SYSTOLE
SO IN SHORT IABP is a
temporizing measure
• Augments coronary blood flow in diastole

• Balloon collapse in systole creates a

vacuum effect  decreases afterload

• Decrease myocardial oxygen demand

Intra-Aortic Balloon Pump
Limitation of IABP
• Lack of active circulatory support
• Needs a certain level of left ventricular (LV)
function.
• With severely depressed LV function IABP is
inadequate to revert CS.

• In such cases use of percutaneous LV assist

devices (LVAD) with active circulatory support
might be beneficial .
FIBRINOLYSIS
RANDOMIZED TRIALS HAVE
SHOWN THAT

• IN CARDIOGENIC SHOCK
PHARMACOLOGIC
REFERFUSION BY
THROMBOLYTIC THERAPY
HAS A REDUCED EFFICACY

• P.C.I. GIVE SUPERIOR

OUTCOMES
REPERFUSION
• RAPID ESTABLISHMENT OF BLOOD FLOW IN INFARCT
RELATED ARTERY IS ESSENTIAL IN THE MANAGEMENT
OF C.S.

• FOR STEMI OR MI WITH LBBB WITH CS WITHIN 36

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

• IABP &FIBRINOLYTIC THERAPY IS RECOMMENDED

ONLY WHEN REVASCULARISATION NOT POSSIBLE
P.C.I. (PER CUTANEOUS INTERVENTIONS)
• CORONARY BALLOON ANGIOPLASTY
EXPANDS THE CORONARY LUMEN BY STRETCHING
& TEARING THE ATHEROMATOUS PLAQUE

• CORONARY STENTS ARE USED IN >90% PCI

PROCEDURES
IT SCAFFOLDS ARTERIAL DISSECTION FLAP THUS
LOWERS THE INCIDENCE OF VESSEL CLOSURE

• DRUG ELUTING STENTS-PROVIDE SUSTAINED

LOCAL DELIVERY OF ANTIPROLIFERATIVE AGENT AT
SITE OF VESSEL WALL INJURY(SIROLIMUS ELUTING
STENTS,PACLITAXEL E.STENTS)
EARLY REVASCULARIZATION
V/S
MEDICAL MANAGEMENT
 The Should We Emergently Revascularize Occluded
Coronaries for Cardiogenic Shock (SHOCK TRIAL)

• randomly assigned 302 patients of MI with

predominant LVF to
1)emergency revascularization(CABG/PCI)within
6 hrs
or
2)initial medical stabilization.

• The primary end point of the study was 30-day

all-cause mortality.
RESULTS OF SHOCK TRIAL
• No significant difference in 30 days survival.
• A significant survival benefit with early
revascularization at 6 and 12 months.
• The benefit was greatest for those <75 years,
• 20 lives were saved at 6 month per 100 patients
treated.
• Therefore the American College of Cardiology now
recommends emergency revascularization for
patients younger than 75 years with cardiogenic
shock
L.V. NEEDS ASSISTANCE
LV ASSIST DEVICE
LVAD

• LVAD, is a mechanical
pump that is
implanted inside a
person's chest to help
a weakened heart
ventricle pump blood
 How Does an LVAD Work?
• the LVAD is a pump. The LVAD is surgically
implanted just below the heart.
• One 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.
 LVAD

• MOST COMMONLY USED AS A

MEANS OF TEMPORARY
SUPPORT TO A PLANNED
DEFINITIVE TREATMENT
SUCH AS HEART
TRANSPLANT

• THERE ARE ONGOING TRIAL

FOR USE OF LVAD AS
DEFINITIVE THERAPY FOR
END STAGE CARDIAC
FAILURE
 • TEACHER & COLLEGUES

THANK YOU

AUDIENCE
 CARDIOGENIC VS NON CARDIOGENIC ACUTE
PULMONARY OEDEMA(DIAGNOSIS)
1.ECHOCARDIOGRAPHY

• 2.ECG MAY SHOW ST

ELEVATION OR Q WAVES-
REPERFUSION THERAPY

• BRAIN NATRIURETIC
PEPTIDE;WHICH WHEN ELEVATED
SUPPORT DIAGNOSIS OF HEART
FAILURE
BRAIN TYPE NATRIURETIC PEPTIDE
• BNP IS A NEUROHORMONE THAT IS RELEASED
BY VENTRICULAR MYOCARDIUM IN RESPONSE
TO VENTRICULAR STRETCHING;VOLUME
OVERLOAD
• PLASMA LEVELS OF BNP INCREASE IN DIRECT
RELATION TO INCREASE IN VENTRICULAR
END-DIASTOLIC VOLUME & END DIASTOLIC
PRESSURE
• A PLASMA BNP >100 PG/ML CAN BE USED AS
AN EVIDENCE OF HEART FAILURE AS A CAUSE
OF DYSPNEA
TREATMENT

• SUPPORT OF OXYGENATION &

VENTILATION
• O2 THERAPY
• POSITIVE PRESSURE VENTILATION

• REDUCTION OF PRELOAD
Classification of shock
• Dopamine usually is administered first in
patients with cardiogenic shock because it
has inotropic and vasopressor properties.
Typically, the dose is titrated to maintain a
mean arterial BP of 60 mm Hg or greater.
Subsequent
VASOVAGAL SHOCK
RESULT FROM
• POOLING OF BLOOD IN LARGER VASCULAR
RESERVOIRS(LIMB MUSCLES) &
• DILATATION OF SPLANCNIC ARTERIOLAR BED
LEADING TO
• C.O; CEREBRAL PERFUSION
&UNCONSCIOUSNESS

• IF PATIENT MAINTAIN IN UPRIGHT POSITION

PERMANENT CEREBRAL DAMAGE RARELY