Shock

Scott G. Sagraves, MD, FACS

Assistant Professor

Trauma & Surgical Critical Care

Associate Director of Trauma

UHS of Eastern Carolina

Objectives

• Define & classify shock

• Outline management principles

• Discuss goals of fluid resuscitation

• Understand the concepts of oxygen supply and demand in managing shock.

• Describe the physiologic effects of vasopressors and inotropic agents

Goals

• Review hemodynamic techniques in the ICU• Introduce the concept of the cardiac cycle• Review of the pulmonary artery catheter

parameters

• Utilize the presentation to analyze clinical cases and to feel comfortable with pa-c parameters.

Shock:

“A momentary pause in the act of death.”

-John Collins Warren, 1800s

Hypotension

• In Adults:– systolic BP 90 mm Hg

– mean arterial pressure 60 mm Hg

systolic BP > 40 mm Hg from the patient’s baseline pressure

Definition

SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation

demand.

“Hypoperfusion can be present in the absence of significant hypotension.”

-fccs course

Pathophysiology

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

Pathophysiology

• ATP production fails, the Na+/K+ pump fails resulting in the inability to correct the cell electronic potential.

• Cell swelling occurs leading to rupture and death.

• Oxidative Phosphorylation stops & anaerobic metabolism begins leading to lactic acid production.

Why Monitor?

• Essential to understanding their disease

• Describe the patient’s physiologic status

• Facilitates diagnosis and treatment of shock

History

• 1960’s– low BP = shock; MSOF resulted after BP

restored

• 1970’s– Swan & Ganz - flow-directed catheter– thermistor cardiac output

• 1980’s– resuscitation based on oxygen delivery,

consumption & oxygen transport balance.

Pulmonary Artery Catheter

Pulmonary Artery Catheter

• INDICATIONS– volume status– cardiac status

• COMPLICATIONS– technical– anatomic– physiologic

PLACEMENT

West’s Lung Zones

• Zone I - PA > Pa > Pv

• Zone II - Pa > PA > Pv

• Zone III - Pa > Pv > PA

• PA = alveolar

• Pa = pulmonary artery

• Pv = pulmonary vein

Correct PA-C Position

Standard Parameters

• Measured– Blood pressure– Pulmonary A.

pressure– Heart rate– Cardiac Output– Stroke volume– Wedge pressure– CVP

• Calculated– Mean BP– Mean PAP– Cardiac Index– Stroke volume

index– SVRI– LVSWI– BSA

Why Index?

• Body habitus and size is individual

• Inter-patient variability does not allow “normal” ranges

• “Indexing” to patient with BSA allows for reproducible standard

Index Example

PATIENT A• 60 yo male• 50 kg• CO = 4.0 L/min• BSA = 1.86

CI = 2.4 L/min/m2

PATIENT B• 60 yo male• 150 kg• CO = 4.0 L/min• BSA = 2.64

CI = 1.5 L/min/m2

PA Insertion

0

5

10

15

20

RA = 5 RV = 22/4 PA 19/10 PAOP = 9

CVP• CVP of SVC at level of right atrium• pre-load “assessment”• normal 4 - 10 mm Hg• limited value

PAOP

• End expiration• Reflection changes with positive pressure• Waveforms change every 20 cm

Waveform Analysis

• A wave - atrial systole• C wave - tricuspid valve closure @

ventricular systole• V wave - venous filling of right atrium

Cardiac Cycle

pulmonary

Left ventricle

systemic

Right ventricleRVSWI

PVRI

LVSWI

SVRI

CVP

MPAPPCWP

MAP

Hemodynamic Calculations

Parameter Normal

Cardiac Index (CI) 2.8 - 4.2

Stroke Volume Index (SVI) 30 - 65

Sys Vasc Resistance Index (SVRI)1600 - 2400

Left Vent Stroke Work Index (LVSWI) 43 - 62

Cardiac Index

C.I. = HR x SVI

SVI measures the amount of blood ejected by the ventricle with each cardiac contraction.

Total blood flow = beats per minute x blood volume ejected per beat

Vascular Resistance Index

SYSTEMIC (SVRI)

MAP - CVP

CI

SVR = vasoconstriction

SVR = vasodilation

PULMONARY (PVRI)

MPAP - PAOP

CI

PVR = constriction

PE, hypoxia

x 80 x 80

Vascular resistance = change in pressure/blood flow

Stroke Work

LVSWI = (MAP-PAOP) x SVI x 0.0136

normal = 43 - 62

VSWI describe how well the ventricles are contracting and can be used to

identify patients who have poor cardiac function.

ventricular stroke work = pressure x vol. ejected

Too Many Numbers

Definitions

• O2 Delivery - volume of gaseous O2

delivered to the LV/min.

• O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min.

• O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner

Demand > consumption = anaerobic metabolism

Rationale for Improving O2 Delivery

Insult

Tissue Hypoxia

Increased Delivery

Increased Consumption

Demands are met

Critical O2 Delivery

VO

2I

DO2I

The critical value is variable& is dependent upon the patient, disease, and the metabolic demands of the patient.

Oxygen Calculations

• Arterial Oxygen Content (CaO2)

• Venous Oxygen Content (CvO2)

• Arteriovenous Oxygen Difference (avDO2)

• Delivery (O2AVI)

• Consumption (VO2I)

Efficiency of the

oxygenation of blood and the rates of

oxygen delivery and consumption

Arterial Oxygen Content

CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031)

If low, check hemoglobin or pulmonary gas exchange

Arteriovenous Oxygen Difference

avDO2 = CaO2 - CvO2

Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock

Oxygen Delivery (DO2I)

O2AVI = CI x CaO2 x 10

Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues.

< 400 is bad sign

Oxygen ConsumptionVO2I = CI x (CaO2 - CvO2)

If VO2I < 100 suggest tissues are not getting enough oxygen

SvO2

SvO2 = 1-VO2

DO2

Oxycalculations

Resuscitation Goals

• CI = 4.5 L/min/m2

• DO2I = 600 mL/min/m2

• VO2I = 170 mL/min/m2

NOT ALL PATIENTS CAN ACHIEVE THESE GOALS

Critically ill patients who can respond to their disease states byspontaneously or artificially meeting these goals do show a better survival.

Break Time…

“Shock is a symptom of its cause.”

-fccs course

Signs of Organ Hypoperfusion

• Mental Status Changes

• Oliguria

• Lactic Acidosis

Components

Categories of Shock

• HYPOVOLEMIC

• CARDIOGENIC

• DISTRIBUTIVE

• OBSTRUCTIVE

Goals of Shock Resuscitation

• Restore blood pressure

• Normalize systemic perfusion

• Preserve organ function

In general, treat the cause...

Hypovolemic Shock

• Causes

– hemorrhage

– vomiting

– diarrhea

– dehydration

– third-space loss

– burns

• Signs cardiac

output PAOP SVR

Classes of Hypovolemic Shock

Treatment - Hypovolemic

• Reverse hypovolemia vs. hemorrhage control

• Crystalloid vs. Colloid

• PASG role?

• Pressors?

Resuscitation

• Transport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial.

• Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.

Fluid Administration

• 1 L crystalloid 250 ml colloid• crystalloids are cheaper• blood must supplement either• FFP for coagulopathy, NOT volume

• Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused

• NO survival benefit with colloids

Role of PASG?

• Houston - Higher mortality rate in penetrating thoracic, cardiac trauma

• No benefit in penetrating cardiac trauma

• Role undefined in rural, blunt trauma

• Splinting role

Cardiogenic Shock

• Cause– defect in cardiac function

• Signs cardiac output PAOP SVR left ventricular stroke work (LVSW)

Coronary Perfusion Pressure

Coronary PP = DBP - PAOP

coronary perfusion = P across coronary a.

GOAL - Coronary PP > 50 mm Hg

The Failing Heart

• Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient.

• Fluids first, then cautious pressors

• Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure)

• If inotropes and vasopressors fail, intra-aortic balloon pump

Distributive Shock

• Types– Sepsis– Anaphylactic– Acute adrenal insufficiency– Neurogenic

• Signs– ± cardiac output PAOP SVR

SIRS - Distributive Shock• Prompt volume replacement - fill the tank

• Early antibiotic administration - treat the cause

• Inotropes - first try Dopamine

• If MAP < 60– Dopamine = 2 - 3 g/kg/min– Norepinephrine = titrate (1-100 g/min)

• R/O missed injury

Adrenal Crisis Distributive Shock

• Causes– Autoimmune adrenalitis– Adrenal apoplexy = B hemorrhage or infarct– heparin may predispose

• Steroids may be lifesaving in the patient who is unresponsive to fluids, inotropic, and vasopressor support. Which one?

Obstructive Shock

• Causes– Cardiac Tamponade– Tension Pneumothorax– Massive Pulmonary Embolus

• Signs cardiac output PAOP SVR

Endpoints?

• ACS CoT ATLS - restoration of vital signs and evidence of end-organ perfusion

• Swan-guided resuscitation

– C.I. 4.5, DO2I 670, VO2I 166

• Lactic Acid clearance

• Gastric pH

Summary

Type PAOP C.O. SVR

HYPOVOLEMIC

CARDIOGENIC

DISTRIBUTIVE or N varies

OBSTRUCTIVE

Vasopressor Agents?

• Augments contractility, after preload established, thus improving cardiac output.

• Risk tachycardia and increased myocardial oxygen consumption if used too soon

• Rationale, increased C.I. improves global perfusion

Vasopressors & Inotropic Agents

• Dopamine

• Dobutamine

• Norepinephrine

• Epinephrine

• Amrinone

Dopamine• Low dose (0.5 - 2 g/kg/min) = dopaminergic

• Moderate dose (3-10 g/kg/min) = -effects

• High dose (> 10 g/kg/min) = -effects

• SIDE EFFECTS– tachycardia– > 20 g/kg/min to norepinephrine

Dobutamine

-agonist

• 5 - 20 g/kg/min

• potent inotrope, variable chronotrope

• caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension

Norepinephrine

• Potent -adrenergic vasopressor

• Some -adrenergic, inotropic, chronotropic

• Dose 1 - 100 g/min

• Unproven effect with low-dose dopamine to protect renal and mesenteric flow.

Epinephrine

- and -adrenergic effects

• potent inotrope and chronotrope

• dose 1 - 10 g/min

• increases myocardial oxygen consumption particularly in coronary heart disease

Amrinone• Phosphodiesterase inhibitor, positive inotropic

and vasodilatory effects

• increased cardiac stroke output without an increase in cardiac stroke work

• most often added with dobutamine as a second agent

• load dose = 0.75 -1.5 mg/kg 5 - 10 g/kg/min drip

• main side-effect - thrombocytopenia

Dilators

+ inotropes- inotropes

Pressors

Summary `pressors & inotropes

- inotrope + inotrope

dilator

pressor

DobutamineMilrinone/Amrinone

-dopamine

IsuprelDigoxinCalcium

epinephrine

-dopamine

neosynephrine

norepinephrine

-blocker

LabetalolCa+2 blocker

ACE inhibitorhydralazine

nitroglycerineNipride

Case Studies

GSW• 24 year old male victim of a

shotgun blast to his right lower quadrant/groin at close range.

• Hemodynamically unstable in the field and his right lower extremity was cool and pulseless upon arrival to the trauma resuscitation area.

Shotgun Blast

Post-op

• Patient received 12 L crystalloid, 15 units of blood, 6 units of FFP, and 2 6 packs of platelets.

• HR 130, BP 96/48, T 34.7° C

• PAWP 8, CVP 6, CI 4.2, SVRI 2700, LVSWI 42.

Diagnosis? Treatment?

SHOCK/HYPOVOLEMIA

• FLUIDS… FLUIDS… FLUIDS…

• BLOOD & PRODUCTS TRANSFUSION

• CORRECT– ACIDOSIS– COAGULOPATHY– HYPOTHERMIA

MVC• 38 year old

female restrained driver who was involved in a high speed MVC.

• She sustained a pulmonary contusion and fractured pelvis.

ICU Course

• Intubated and monitored with PA-C

• PCWP = 22, CI = 3.5, SVRI = 2400, LVSWI = 39.8

• HR = 120, BP = 110/56, SpO2 = 91, UOP = 25 cc/hr

What do you think...

HYPOVOLEMIA

ADJUST YOUR WEDGE FOR THE PEEP

Wedge Adjustment

• Measured PAOP - ½ PEEP = “real PAOP”• PEEP = 28, therefore “real wedge” = 8

Auto-Pedestrian Crash• Thrown from the

rear bed of pick up truck during a MVC at 60 mph.

• Hemodynamically unstable

• Pain to palpation of the pelvis

• Hematuria with Foley® insertion

ICU Course

• Pelvis “closed”• QID Dressings, intubated, PA-C inserted

• PCWP = 20, CI = 5.2, SVRI = 280, LVSWI = 24.5, PEEP = 8

Diagnosis? Treatment?

Sepsis

• Fluids• Correct the cause

• Antibiotics• Debridement

• Vasopressors– Phenylephrine

– Levophed

Initial Resuscitation

• CVP: 8- 12 mm Hg

• MAP 65 mm Hg

• UOP 0.5 cc/kg/hr

• Mixed venous Oxygen Sat 70%

• Consider:– Transfusion to Hgb 10 – Dobutamine up to 20 g/kg/min

Vasopressors• Assure adequate fluid volume• Administer via CVL• Do not use dopamine for renal

protection• Requires arterial line placement• Vasopressin:

– Refractory shock– Infusion rate 0.01 – 0.04 Units/min

Steroid Use in Sepsis

• Refractory shock 200-300 mg/day of hydrocortisone in divided doses for 7 days

• ACTH test

• Once septic shock resolves, taper dose

• Add fludrocortisone 50 g po q day

Geriatric Trauma• 70 year old female

• MVC while talking on her cell phone

• ruptured diaphragm and spleen s/p OR

• Intubated and PA-C

ICU Course

• PCWP = 28, CI = 1.8, SVRI = 3150, LVSWI = 20.7

Diagnosis? Treatment?

Cardiogenic Shock

• Preload augmentation - Consider Fluids

• Contractility– dopamine– dobutamine– phosphodiesterase inhibitor

• Afterload reduction– nitroglycerin– dobutamine

Don’t forget...

-Samuel D. Gross, 1872

Shock: “rude unhinging of the machinery of life.”