Shock

SHOCK

Dr.sugunakar

DEFINITION

Shock is simply

defined as perfusion

that is inadequate to

meet the body's

metabolic needs.

EFFECTIVE TISSUE

PERFUSION

Cardiac Performance

Vascular performance

Cellular function

Oxygen unloading and diffusion

Energy generation

Respiratory failure

ARDS

Ischemic hepatitis

Cholestasis

Ileus

Erosive gastritis

Pancreatitis

Cholecystitis

Transluminal bacterialtranslocation

Encephalopathy

Arrhythmias

Ischemia

DIC

Thrombocytopenia

Hyperglycemia

Hypoglycemia

Electrolyte abnormalities

Cold extremities

Thready pulse

CLINICAL RECOGNITION

Mean arterial pressure < 65 mm Hg (in

previously normotensive individual

TYPES OF SHOCK

Hypovolemic

Cardiogenic

Obstructive

Distributive

CAUSES

Hemorrhagic

Non-hemorrhagic

(Fluid depletion)

Venodilation

Fluid depletion:

Dehydration

Vomiting

Diarrhea

BurnsAnaphylaxis

Hemorrhagic:

Don’t forget concealed

bleeds:

Abdomen

Pelvis / FemoralRetroperitoneal

Venodilation:

Sepsis

Anaphylaxis

Toxins / drugs

Common withdistributive shock

small bowel obstruction, hypovolemic shock

can develop as a result of shift of fluid into

the bowel lumen.

Patients with peritonitis after perforation of a

duodenal ulcer accumulate several liters of

inflammatory fluid in their peritoneal cavity,

A reduction in intravascular volume is often

a contributing factor to hypotension in

patients with septic shock.

Hemorrhagic shock can be categorized into three

grades of severity based on the magnitude of blood

loss:

compensated shock,

uncompensated shock,

and lethal exsanguination

Patients with

less than a 20%

deficit in blood

volume

Can maintain

Or restore

blood

pressurewith iv

fluids

20% to 40% of

their blood

volume

cannot sustain

mean aortic

pressure by

vasoconstriction

, have low

cardiac output,

are subject to

anaerobic

stress, and

have acidemia

BLOOD

TRANSFUSION

more than 40%

of their blood

volume and

profound

hypotension

develops. With

severely

reduced blood

flow to their

brain, these

patients

become

comatose within

minutes and die

of cardiac

arrest.

Hypovolemia

! Preload

! Diastolic Filling

! Cardiac Output

! MAP

Shock

MODS

CARDIOGENIC

SHOCK

causes

1.infarction 1.bradycardia

2.tachycadia

Pump (CHF

1.Cardiomyopathy

2.Valve failure

3.Endocarditis

4.Acute massive pumonary embolism

Ischemia

Hypovolemia

! Preload

! Diastolic Filling!

Cardiac Output

! MAP

Shock

MODS

Cardiogenic

! Cardiac Output

! MAP

Shock

MODS

DISTRIBUTIVE

SHOCK

CAUSES

Septic

Toxic Shock Syndrome

Anaphylactic /

Anaphylactoid

Neurogenic (Spinal

Shock)Endocrinologic

Adrenal Crisis

Thyroid Storm

Toxins

Humans respond to invasive infection with an

immune response that involves multiple mediators.

These mediators enable the patient's inflammatory

processes to destroy the organisms at the site of

infection. These same mediators can damage the

individual's organs if they produce an exaggerated

systemic inflammatory response syndrome

PATHO PHYSIOLOGY OF SEPTIC

SHOCK

Endo toxins

Complement activation+macrophage aaaaaaactivation

Tnf, IL1, IL6

NEUTROPHIL ACTIVATION+ENDOTHELIAL CELL UPGRADATION

BRADYKININ,COAGULATION CASCADE ACTIVATION,ARACHIDONIC ACIDMETABOLITES,NITRI ACID,O2 FREE RADICALS

CAPILLARY LEAKAGE,MICROTHROMBUS FORMATION,VASODILATATION,TISSUE DESTRUCTION

ORGAN INJURY

Distributive Shock

! Systemic Vascular

Resistance

Maldistribution of flow

! Cardiac Output

! MAP

Shock

MODS

Myocardial Suppression

SYSTEMIC INFLAMMATORY

RESPONSE SYNDROME

36C < Fever > 38C

Tachycardia > 90

Hypocapnia (PaCO2 > 32 mm Hg) / RR > 20 or

use of mechanical ventilation

4000 < WBC > 12000 (or left shift)

Sepsis

Same criteria as for SIRS but with a clearly established focus of infection

Severe sepsis - SIRS + Organ dysfunction…Indicators of hypoperfusion:

▪ Systolic blood pressure <90 mm Hg ▪

>40 mm Hg fall from normal systolic blood pressure

▪ Lacticacidemia

▪ Oliguria

▪ Acute mental status changes

Septic Shock - Severe sepsis + refractory

hypotension despite adequate fluid &

resuscitation

TREATMENT

Management of a patient in shock is focused on the

following:

1. Identifying the presence of shock

2. Searching for and treating immediately life-

threatening conditions

3. Treating shock based on the underlying

pathophysiology

THINK ABOUT...

2 large bore peripheral lines - iv fluids

Central line - for CVP & vasopressors

Arterial line - BP monitoring and repeated ABG

Foley - urine output

Nasogastric tube - maintain gut integrity

Hypovolemic Fluids---RINGER

LACTATE

BLOOD

HEMOSTASIS

Cardiogenic Cath Lab

Inotropes

IABP

Obstructive Remove obstruction

Distributive Antibiotics

Epinephrine

SURGERY

A surgeon treating a patient in hypovolemic shock

faces two concurrent challenges. First, the surgeon

must restore intravascular volume to normal.

Second, the surgeon must identify the cause of the

patient's hypovolemic shock and decide whether

immediate surgical therapy is needed.

HEMORRHAGIC SHOCK

Acidemia is used as a measure of the severity of

hemorrhagic shock

bicarbonate excess …-10 mEq/L or less in a

hypovolemic patient is an indication that the patient

has uncompensated shock and is at risk for death if

resuscitation not done

HEMORRHAGIC SHOCK

Adult patients who do not respond to 2 to 4 L of balanced electrolyte solution (children are given 20 mL/kg) and remain hypotensive usually require blood transfusions

The surgeon must identify the potential sites of active hemorrhage in an irreversibly hypotensive patient and perform hemostatic interventions

HEMORRHAGIC SHOCK

rapid resuscitation, timely hemostasis, and

postresuscitation support of organ function.

TRETMENT OF CADIOGENIC

SHOCK

The most common cause of cardiogenic shock is occlusion of a coronary artery in which a plaque in the coronary artery ruptures, combined with the formation of an intraluminal thrombus

The key to improving survival of patients in cardiogenic shock is to promptly reestablish blood flow at the site of the coronary artery occlusion.[46]

aspirin and a β-blocker , fibrinolysis, deployment of coronary artery stents, and surgery

SHOCK CAUSED BY CARDIAC

CONTUSION

dobutamine, epinephrine, or dopamine may

improve myocardial contraction in a patient with

cardiac contusion and profound pump dysfunction.

An intra-aortic balloon pump may provide

temporary support while the contused cardiac

muscle recovers

SHOCK CAUSED BY CARDIAC

TAMPONADE

Acute cardiac tamponade is always suspected after

gunshot or stab wounds to the chest in the vicinity

of the sternum. Patients with acute cardiac

tamponade have hypotension, distended neck

veins

pulsus paradoxus,

immediate surgery to decompress the pericardium

pulsus paradoxus,

SEPTIC SHOCK ….TREATMENT


Culture relevant body fluids, including blood.

Infuse a balanced electrolyte solution of 500

mL/15 min. Monitor the systolic blood

pressure response.

Insert a central venous or pulmonary artery

catheter. ▪ If after a 500-mL bolus of

saline the patient remains hypotensive and

CVP is <8-12 mm Hg or PAWP is <8-12 mm

Hg, infuse another 500-mL bolus of fluid


If CVP is >15 or PAWP is 15-20 and the

patient remains hypotensive (<65 mm Hg),

start an infusion of the inotropedobutamine

or dopamine. The goal is a mean systemic

pressure >65 mm Hg and a pulse rate <120

beats/min. Determine the cardiac index and

systemic vascular resistance. ▪ If after

infusion of fluid and inotropes SVR is <600,

infuse avasopressor—either norepinephrine

or vasopressin—to increase SVR


Monitor mixed venous oxygen saturation and urine

output as an indication that therapeutic

interventions have improved perfusion.

CVP, central venous pressure; PAWP, pulmonary

artery wedge pressure; SVR, systemic vascular

resistance.


As a final consideration in the treatment of any

patient in septic shock, resuscitation is often futile

without effective treatment of the source of the

sepsis. A patient's survival from an episode of

sepsis often hinges on prompt and effective

performance of a surgical procedure.

MONITORING & GOALS...

Hemodynamics

1. MAP > 60

2. CVP > 12

3. CI > 2.2 L

4.PCWP

Oxygen

1. Hb > 10

2. Sa O2 > 92

%

3. Mechanical

Ventilation

4.Serial blood

gases

Organ

Dysfunction

1. Urine output

2. Mental

Status

3. Lactate

levels

4. LFT

AVOID

HYPOTHERMIA,

HYPERGLYCEMIA

,HYPERCHLOREMIC ACIDOSIS,

ACTIVATED PROTEIN C, LOW DOSE

STEROIDS IMPROVE SURVIVAL RATES.

New therapeutic agents are still being

tested for sepsis in multicentre trials.

THANK YOU

Shock

Health & Medicine

Transcript of Shock