DR. Neeraj Kumar Jain

Assistant Professor

Deptt. Of Surgery

Define shock and its different categories

Review basic physiologic and pathophysiologic aspects of shock

Inadequate tissue perfusion to meet tissue

demands. Usually result of inadequate blood

flow and/or oxygen delivery

Circulatory failure is a life-threatening medical

condition that occurs due to inadequate substrate

for aerobic cellular respiration. In the early stages

this is generally an inadequate tissue level of

oxygen.

Shock is not a blood pressure diagnosis

In Adults:◦ systolic BP 90 mm Hg

◦ mean arterial pressure 60 mm Hg

◦ systolic BP > 40 mm Hg from the patient’s

baseline pressure

Oxygen

Demand > Supply

• THE HEART (pump)

• THE BLOOD (circulating fluid)

• THE VASCULAR CAPACITY

(veins and arteries)

• THE MICRO- CIRCULATION

Fluid

Pump

Vessels

Flow

ATP + H2O ADP + Pi + H+ + Energy

Acidosis results from the accumulation of acid

when during anaerobic metabolism the creation

of ATP from ADP is slowed.

H+ shift extracellularly and a metabolic acidosis

develops

• Cellular responses to decreased systemic oxygen delivery•ATP depletion → ion pump dysfunction•Cellular edema•Hydrolysis of cellular membranes and cellular

death• Goal is to maintain cerebral and cardiac perfusion

•Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow

• Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms

DO2O2

CASECADESHEMO

DYNAMICS

VENTILATION

PULMONARY O2

EXCHANGE

O2 TRANSPORT

TISSUE EXCHANGE

QT

HB CONTENT

MICR

CIRCULATION

QT x HB x 10 x 1.36 X SO2 + PO2 x0.003

TISSUE PERFUSION

CONSTANT FLOW

CONSTANT DO2

TARGET FUNCTION OF CVS

REGIONAL PERFUSION PRESSURE

P = F X R

Autorgulation is controlled by;

*** Myogenic *NO

*** Metabolic *H Ione

*ADENOSINE *CO2

*PG *O2

F

P

RP R

F

FCONSTANT

TISSUEPERFUSION

MAP=60mmHg

Tissue perfusion

Large arteries Resistant arteriole

Precapillary arteriole

CapillaryPost capillary venule

Collecting vein

Capacitance vein

MAPR

F

BP Constriction Dilatation Constant Constriction

Constriction Dilatation Constant ConstrictionBP

MAP<60 Constriction no more Flow Constriction

=

x

REGIONAL PERFUSION PRESSURE MAP

QT

SVR

MAP = QT X SVR

BODY RESPONSE TO SHOCK

Neuro endocrinal

Auto regulation

Aortic arch, carotid body, cerebral ischemia, renal ischemia

Catecholamine

ADH, RAAS, STEROIDS

Vasoconstriction

Salt and water retention

To keep regional perfusion pressure

Vasodilatation

To keep organ flow constant

P = F X R

MAP 60 mmHg

TISSUE PERFUSION

P = F X R

Oxygen content = 1.34 (Hgb x SaO2) + (PaO2 x 0.003)

SaO2: Oxygen saturation

Hgb: Hemoglobin concentration

PaO2: partial pressure Oxygen in plasma

To improve Oxygen content◦ Increase Hemoglobin concentration

◦ Increase saturation

Cardiac output◦ C.O. = Heart rate x stroke volume

To improve Cardiac output◦ Increase Heart rate

◦ Increase Stroke Volume

Preload – volume of blood in the ventricle

Afterload – resistance to contraction

Contractility – force applied

Compensatory mechanisms for shock

1** S.V.R.

vascular capacity

Spasm of large and resistant arteries

Catecholamine

Vasopressin

Angiotensin 2

Cortisol

Aldosterone

2** QT

Effective blood volume

x =BP (MAP> 60mmHg)

*Venous spasm to V.R.

*Salt retention Aldosterone

* Water retention ADH

*Stimulation of thirst Ag.2

*Decrease hydrostatic cap .P.

Tissue fluid reabsorption at rate 15 ml/ kg /h

Target point

Mediators

Weil and Shubin in 1972 classification

Four major categories◦ Hypovolemic

◦ Cardiogenic

◦ Extracardiac Obstructive

◦ Distributive

Overlap exists, and also concomitant categories exist

TYPES OFSHOCK

Compensated Organ perfusion is maintained

Uncompensated Circulatory failure with end organ dysfunction

Irreverisble◦ Irreparable loss of essential organs

#1 cause of death world wide◦ Gastroenteritis

◦ Hemorrhagic – Trauma, GI bleed

THE BLOOD

WHOLEBLOOD

EXTERNALHG.

INTERNALHG.

PLASMA

GUT

*VOMITING

*NGT. DRAIN

*DIARRHOEA

* FISTULA

SKIN

•SWEAT

•* BURN

KIDNEY

*DM

*DI

*DIURETIC

3rd SPACE

* ASCITES

Class I Class II Class III Class IV

Blood Loss < 750 750-1500 1500-2000 > 2000

% Blood Vol. < 15% 15 – 30% 30 – 40% > 40%

Pulse < 100 > 100 > 120 > 140

Blood Pressure Normal Normal Decreased Decreased

Pulse Pressure Normal Decreased Decreased Decreased

Resp. Rate 14 – 20 20 – 30 30 – 40 > 40

UOP > 30 20 – 30 5 – 15 negligible

Mental Status sl. Anxious mildly anx confused lethargic

Fluid crystalloid crystalloid blood blood

Early◦ Increase HR◦ Decrease perfusion◦ Normal BP, decrease pulse pressure

Late◦ Sign increase HR◦ Sign decrease perfusion ◦ Decrease BP◦ End organ dysfunction

Pump failure/malfunction

(decreased contractility)

Myocardial◦ Infarction, contusion, myocarditis,

cardiomyopathy, pharmacologic, depressant factors

Mechanical◦ Valvular stenosis, regrurgitation

◦ Septal Defects

Arrhythmogenic

CARDIACCAUSESAFTERLOAD

PRELOAD

VALVES

MUSCLE POWER

RATE& RHYTHEM

Tachycardia

Tachypnea

Respiratory distress

Mental status change

Cool extremities

Poor perfusion

Signs of dehydration

Extrinsic Vascular Compression◦ tumors, fibrosis

Increased Intrathoracic Pressure◦ Tension pneumo; high autopeep in PPV

Flow obstruction◦ PE, Air embolism, tumors, Ao dissection, Ao

coarctation, acute pulmonary HTN, tamponade.

•Tension pneumothorax•Air trapped in pleural space with 1 way valve,

air/pressure builds up

•Mediastinum shifted impeding venous return

•Chest pain, SOB, decreased breath sounds

•No tests needed!

•Rx: Needle decompression, chest tube

•Cardiac tamponade•Blood in pericardial sac prevents venous return to

and contraction of heart

•Related to trauma, pericarditis, MI

•Beck’s triad: hypotension, muffled heart sounds, JVD

•Diagnosis: large heart CXR, echo

•Rx: Pericardiocentisis

•Pulmonary embolism•Virscow triad: hypercoaguable, venous injury,

venostasis

•Signs: Tachypnea, tachycardia, hypoxia

•Low risk: D-dimer

•Higher risk: CT chest or VQ scan

•Rx: Heparin, consider thrombolytics

SIRS-related As sepsis (infectious); pancreatitis; trauma; burns.

Anaphylactic/anaphylactoid

Spinal Trauma (low pulse, SVR low)

Toxic, pharmacologic (B-blockers overdose)

Endocrine (thyroid, adrenal crisis)

Abnormal vessel tone

(decreased afterload)

Vasodilitation Venous Pooling

Decreased Afterload

Maldistribution of regional blood flow

Neurogenic or Anaphylactic Shock

Diminished or absent sympathetic tone

Reduce peripheral vascular tone

Peripheral pooling of blood volume

Inadequate venous return

Decreased perfusion, acidosis, hypotension

•Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement •IgE mediated

•Anaphylactoid reaction – clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure•Not IgE mediated

•What are some symptoms of anaphylaxis?

• First- Pruritus, flushing, urticaria appear

•Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness

•Finally- Altered mental status, respiratory distress and circulatory collapse

• Risk factors for fatal anaphylaxis • Poorly controlled asthma • Previous anaphylaxis

• Reoccurrence rates• 40-60% for insect stings• 20-40% for radiocontrast agents• 10-20% for penicillin

• Most common causes• Antibiotics• Insects• Food

• Mild, localized urticaria can progress to full anaphylaxis

• Symptoms usually begin within 60 minutes of exposure

• Faster the onset of symptoms = more severe reaction

• Biphasic phenomenon occurs in up to 20% of patients• Symptoms return 3-4 hours after initial reaction has cleared

• A “lump in my throat” and “hoarseness” heralds life-threatening laryngeal edema

•Clinical diagnosis

•Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems

•Look for exposure to drug, food, or insect

•Labs have no role

•Occurs after acute spinal cord injury•Sympathetic outflow is disrupted leaving

unopposed vagal tone•Results in hypotension and bradycardia•Spinal shock- temporary loss of spinal

reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)

•Loss of sympathetic tone results in warm and dry skin

•Shock usually lasts from 1 to 3 weeks

•Any injury above T1 can disrupt the entire sympathetic system•Higher injuries = worse paralysis

Terminology in Sepsis◦ Infection = response to micro organism

◦ Bacteremia = bug in blood

◦ Systemic Inflammatory Response Syndrome (SIRS)

T>38, <36

Increase HR

Increase RR, paCO2<32

WBC>12,000, <4,000, >10% bands

Terminology in Sepsis◦ Sepsis = SIRS (systemic inflammatory response

syndrome) as response to a known infection

◦ Severe sepsis = Sepsis + organ dysfunction

◦ Septic Shock = Sepsis + inadequate oxygen delivery

◦ Multiple Organ Dysfunction Syndrome (MODS) –organ dysfunction that requires intervention

Components of Septic shock◦ Decreased volume

◦ Decreased pump function

◦ Abnormal vessel tone

Therapy for Caridovascular Support

Preload Volume

Contractility Inotropes

Afterload Vasodilators

Etiologies

Inflammatory: too much, too little

Coagulation pathway: DIC-bleeding, pro-coagulant, microthombosis

Multiple organ system failure

Early – warm shock – similar to neurogenic shock

Late – Cold shock – similar to cardiogenic shock

Early Late

Heart rate Tachycardia Tachycardia/

bradycardia

Blood pressure Normal decreased

Peripheral

Perfusion

Warm/cool

Dec./inc. pulses

Cool

Dec. pulses

Early Late

End-organ: skin Dec. cap refill Very dec. cap

Refill

Brain Irritable, restless

Lethargic, unresponsive

Kidneys Oliguria Oliguria, anuria

HYPOXICFAILURE

COMPENSATORY

POST CAP.VASO-CON.

STRESS

PRE&POST CAP.V.CON.

PRECAPILLARY SHUNT

FAILURE

OPEN PRECAP

LEAKAGE

RECOVARY

Type PAOP C.O. SVR

(pul. Art.occul. Press.)

HYPOVOLEMIC

CARDIOGENIC

DISTRIBUTIVE or N varies

OBSTRUCTIVE

SEQULEE OF SHOCK

INSULT

MILD Within the adaptive mechanisms

Moderate To severe

Beyond the adaptive mechanisms

Normal physiologicoscillation

Pathologicaloscillation

Failure of compensatory mechanisms

MAP<60Failure of Autorgulation

Tissue flow

DO2

CEF OF O2

Tissue necrosisMSODDeath

THANK YOU