shock 38392.ppt

7/29/2019 shock 38392.ppt

1/50

SHOCK

NGA B. PHAM, MD, FAAPCRITICAL CARE MEDICINE

CHILDRENS HEALTHCARE OF ATLANTA

EGLESTON2006

7/29/2019 shock 38392.ppt

2/50

Objectives

Review basic physiologic aspects of shock

Define shock and its different categories Describe management of shock

7/29/2019 shock 38392.ppt

3/50

What is Shock?

Pathophysiology of shock

Oxygen

Demand > Supply

7/29/2019 shock 38392.ppt

4/50

Definition of Shock

Inadequate tissue perfusion to meet tissuedemands

Usually result of inadequate blood flowand/or oxygen delivery

Shock is not a blood pressurediagnosis

7/29/2019 shock 38392.ppt

5/50

Determinants of Oxygen Delivery

Oxygen

Delivery = Content x Cardiac output

7/29/2019 shock 38392.ppt

6/50


Oxygen content = 1.34 (Hgb x SaO2) + (PaO2 x0.003)

SaO2: Oxygen saturation

Hgb: Hemoglobin concentration PaO2: partial pressure Oxygen in plasma

To improve Oxygen content

Increase Hemoglobin concentration

Increase saturation

7/29/2019 shock 38392.ppt

7/50


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

7/29/2019 shock 38392.ppt

8/50

Secondary Organ Dysfunction

Respiratory failure

Tachypnea

Decreased compliance

Pulm edema, pulm infiltrate, etc.

Increased resistance

Diaphragm fatigue

Central vs peripheral

Demand >> supply

Inadequate O2 delivery

7/29/2019 shock 38392.ppt

9/50

Secondary Organ Dysfunction

CNS altered mental status

Renal insufficiency pre-renal

Coagulation abnormalities DIC Hepatic/GI dysfunction bowel ischemia

Endocrine Calcium, hypo-adrenalism,

vasopressin

7/29/2019 shock 38392.ppt

10/50

Classification of Shock

Hypovolemic Shock (#1 cause world wide)

Dehydration, hemorrhagic

Cardiogenic Shock Pump failure, obstructive, L-R shunt

Distributive Shock

NeurogenicAnaphylaxis

Septic Shock All of the above

7/29/2019 shock 38392.ppt

11/50

Classification of Shock

Compensated Organ perfusion is maintained

Uncompensated Circulatory failure with end organ dysfunction

Irreverisble

Irreparable loss of essential organs

7/29/2019 shock 38392.ppt

12/50

7/29/2019 shock 38392.ppt

13/50

Hypovolemic Shock

#1 cause of death world wide

Gastroenteritis

Hemorrhagic Trauma, GI bleed

7/29/2019 shock 38392.ppt

14/50

Diagnosis of Hypovolemic Shock

Early Increase HR

Decrease perfusion

Normal BP, decrease pulse pressure

Late Sign increase HR

Sign decrease perfusion Decrease BP

End organ dysfunction

7/29/2019 shock 38392.ppt

15/50

Pathophysiology of

Hypovolemic Shock

Decrease intravascular volume

Compensation increase endogenouscatecholamines

Increase HR increase C.O., O2 delivery

Increase SVR increase BP (esp diastolic)

Compensation for

7/29/2019 shock 38392.ppt

16/50

Cardiogenic Shock

Pump failure/malfunction(decreased contractility)

7/29/2019 shock 38392.ppt

17/50

Cardiogenic Shock

Electrical Failure

Arrhythmias

Mechanical failure

Cardiomyopathy

Metabolic acidosis

Anatomic

Hypoxia/ischemia

Obstruction

7/29/2019 shock 38392.ppt

18/50

Cardiogenic Shock

Symptoms

Tachycardia

Tachypnea

Respiratory distress Mental status change

Cool extremities

Poor perfusion Signs of dehydration

7/29/2019 shock 38392.ppt

19/50

Cardiogenic Shock

Obstruction of Flow

Causes

Pericardial tamponade

Pulmonary embolism

Pulmonary hypertension

7/29/2019 shock 38392.ppt

20/50

Cardiogenic Shock

Obstruction of FlowCardiac tamponade

Causes Pericarditis Post-traumatic Post-cardiac surgery Complication of central line placement

Recognition Tachycardia Low C.O., narrow pulse pressure (inc. diastole) Inc. CVP, JVD PULSUS PARADOXUS (>10mmHg) Muffled heart sounds (??rub) NO RALES

7/29/2019 shock 38392.ppt

21/50

Distributive Shock

Abnormal vessel tone

(decreased afterload)

7/29/2019 shock 38392.ppt

22/50

Distributive Shock

Vasodilitation Venous Pooling

Decreased Afterload

Maldistribution of regional blood flow

7/29/2019 shock 38392.ppt

23/50

Distributive Shock

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

7/29/2019 shock 38392.ppt

24/50

Septic Shock

Terminology in Sepsis

Infection = response to micro organism

Bacteremia = bug in blood

Systemic Inflammatory Response Syndrome(SIRS)

T>38,

7/29/2019 shock 38392.ppt

25/50

Septic Shock

Terminology in Sepsis

Sepsis = SIRS as response to a knowninfection

Severe sepsis = Sepsis + organ dysfunction

Septic Shock = Sepsis + inadequate oxygendelivery

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

7/29/2019 shock 38392.ppt

26/50

Septic Shock

Components of Septic shock

Decreased volume

Decreased pump function

Abnormal vessel tone

7/29/2019 shock 38392.ppt

27/50

Septic Shock

Therapy for Caridovascular Support

Preload Volume

Contractility Inotropes

Afterload Vasodilators

7/29/2019 shock 38392.ppt

28/50

Septic Shock

Etiologies

Inflammatory: too much, too little

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

Multiple organ system failure

7/29/2019 shock 38392.ppt

29/50

Recognition of Septic Shock

Earlywarm shock similar toneurogenic shock

LateCold shock similar tocardiogenic shock

7/29/2019 shock 38392.ppt

30/50

Diagnosis of Septic Shock

Establish presence of infection

Inc. HR, normal or dec. BP & perfusion

Latic acidosis Muti-organ dysfunction

7/29/2019 shock 38392.ppt

31/50

Early vs Late Septic Shock

Early Late

Heart rate Tachycardia Tachycardia/

bradycardia

Blood pressure Normal decreased

Peripheral

Perfusion

Warm/cool

Dec./inc. pulses

Cool

Dec. pulses

7/29/2019 shock 38392.ppt

32/50

Early vs Late Septic Shock

Early Late

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

Refill

Brain Irritable,restless

Lethargic,unresponsive

Kidneys Oliguria Oliguria, anuria

7/29/2019 shock 38392.ppt

33/50

Treatment Strategies in

Shock

7/29/2019 shock 38392.ppt

34/50

Principles of Resuscitation

Increase Oxygen Delivery\

Increase Oxygen content

Increase Cardiac output

Increase blood pressure

Decrease Demand

Sedation/analgesia

Intubation

7/29/2019 shock 38392.ppt

35/50

Initial Treatment in Shock

Airway

Supplemental oxygen, intubation

Carefull with cardiovascular collapse post intubation due topositive thoracic pressure decrease venous return

Breathing

Circulation

Intravenous access go early, go IO

Volume expansion (40cc/kg NS, repeat prn) Carefull with cardiogenic shock (5cc/kg then reassess)

Optimize cardiac function, oxygenation

7/29/2019 shock 38392.ppt

36/50

Restoration of Circulation

Volume

Fluids, fluids, fluidsCrystalloids vs Colloids

7/29/2019 shock 38392.ppt

37/50


Volume

Crystalloids

NS is the fluid of choice, availability

Rapid redistribution out of intravascular space

capillary leak

7/29/2019 shock 38392.ppt

38/50


Volume

Colloids: albumin, bloodAlbumin

Worsening of edema due to cap leak in early

sepsis Blood

Great volume expanders

Side effects: with massive transfusion >1.5 blood

volumes Risk of infection Dilutional thrombocytopenia and factors V & VIII

Calcium binding hemodynamic instability (citrate)

7/29/2019 shock 38392.ppt

39/50


Volume Fluid Choices

Based on:

Type of deficit

Urgency of repletion

Pathophysiology of shock

7/29/2019 shock 38392.ppt

40/50


Volume Fluid Choices

Crystalloids for initial resuscitation

Colloids/PRBCs to replace blood loss

7/29/2019 shock 38392.ppt

41/50

Treatment of Shock

Cardiac Support

Alpha Dopamine Beta

Epinephrine

Norepinephrine DobutamineNeosynephrine

I t

7/29/2019 shock 38392.ppt

42/50

Inotropes

Agent Site of Action Dose

Mcg/kg/min

Effects

Dopamine Dopaminergic

Beta

Alpha > Beta

1-3

5-10

11-20

Renal vasodilation

Inotrope/vasoconstriction

Increase perip. Vasc. resistance

Dobutamine Beta 1 & 2 1-20 Inotrope

Vasodilation

Epineprhine Beta > alpha 0.05 1.0 Inotrope, vasoconstriction

Tachycardia

Norepinephrine Alpha > beta 0.05 1.0 Profound vasoconstriction

inotrope

Nitroprusside Vasodilator

(art > venous)

0.5 1.0 Vasodilation

Milranone Phosphodiesteraseinhibitor

0.5 0.75 Inotrope

vasodilation

7/29/2019 shock 38392.ppt

43/50

New Therapies in Septic Shock

Vasopressin

Steroids

Activated protein C (Xigris) in Septic Shock

7/29/2019 shock 38392.ppt

44/50


Vasopressin

Unclear mechanism of action

Bridging vascular instability in highexogenous catecholamines requirementseptic shock, therefore decrease sideeffects of toxic dosage of catecholamines

Also shows greater blood flow diversion

from non-vital to vital organs

S S

7/29/2019 shock 38392.ppt

45/50


Vasopressin

Dosage 0.01 0.04U/min up to 0.08U/min

N Th i i S i Sh k

7/29/2019 shock 38392.ppt

46/50


Steroids

Hypo-adrenalism: abnormalhypothalamus-pituitary-adrenal axis

At risk of adrenal insufficiency in the

presence of catecholamine requirement Fluid refractory shock

Normal BP, cold shock

Low BP, cold shock Dosage stress dose

Hydrocortisone 150 mg/m2 ivp

N Th i i S ti Sh k

7/29/2019 shock 38392.ppt

47/50


Steroids

Glucocorticoid function immune response

Fall in circulating lymphocytes

Inhibits neutrophils migration to theinflammatory sites

Inhibits macrophages secretion

Promotes eosinophilic apoptosis Modulates cytokines production

N Th i i S ti Sh k

7/29/2019 shock 38392.ppt

48/50


Steroids

Glucocorticoid function Cardiovascular

Modulate vascular reactivity to angiotensinII and to catecholamines -Not fullyunderstood mechanism

Modulate vascular permeability andproduction of NO and other vasodilator

factor

INCREASE IN BLOOD PRESSURE

N Th i i S ti Sh k

7/29/2019 shock 38392.ppt

49/50


Steroids

Glucocorticoid production in stress

Maintain homeostasis

Normalize vascular reactivity

Modulate inflammatory response

N Th i i S ti Sh k

7/29/2019 shock 38392.ppt

50/50


Activated Protein C (Xigris)

Recombinant Human Activated Protein C Prevent DIC cascade with antithrombotic

activity by inhibiting factors Va & VIIIa

May exerts anti-inflammatory effects byinhibiting TNF and by blocking leukocytesadhesions

Side effects Bleeding Pediatric trial terminated early (03/04) due to

no benefit to known risk of bleeding

shock 38392.ppt

Documents