Approach and Hemodynamic Evaluation of Shocks

Mazen Kherallah, MD, FCCPMazen Kherallah, MD, FCCPKing Faisal Specialist Hospital & Research CenterKing Faisal Specialist Hospital & Research Center

Approach and Hemodynamic Evaluation of Shocks

Shock Definition

Question #0

Which of the following is necessary in the definition of shock?

• (a) A drop in the systolic blood pressure of less than 90 mm Hg

• (b) A drop in the mean arterial pressure of less than 60 mm Hg

• (c) A drop in the SBP of 40 mm Hg or 20% from baseline

• (d) An elevated lactic acid of ≥ 4 mmoL/L• (e) Any of the above

Question #1

• Which of the following is necessary in the definition of shock?

• (a) Hypotension

• (b) Tissue hypoxia

• (c) Use of pressors

• (d) Multiple organ dysfunction

Shock

• Profound and widespread reduction in the effective delivery of oxygen leading to first to reversible, and then if prolonged, to irreversible cellular hypoxia and organ dysfunction” Kumar and Parrillo

• Leads to Multiple Organ Dysfunction Syndrome (MODS)

Pathophysiology

Pathophysiology

VO2

DO2Oxygen delivery

Oxygen uptake Oxygen extraction ratio

Mizock BA. Crit Care Med. 1992;20:80-93.

Oxy

gen

Co

nsu

mp

tio

n

Oxygen Delivery

Critical DeliveryThreshold

Lactic

Aci

dosis

Physiologic Oxygen Supply Dependency

sepsissepsisSepsissepsis

Mizock BA. Crit Care Med. 1992;20:80-93.

Oxy

gen

Co

nsu

mp

tio

n

Oxygen Delivery

Pathologic

Physiologic

Pathologic Oxygen Supply Dependency

Pathophysiology

• Most forms of shock – Low cardiac output state

– Supply-dependency of systemic VO2

• Septic shock– Systemic DO2 and VO2 are both supranormal, but an

oxygen deficit remains

– Peripheral oxygen extraction may be deranged and VO2 is pathologically supply-dependent

– Possible microvascular maldistribution of perfusion

Question #2

• Which is not an important determinant of oxygen delivery?

• (a) Hemoglobin level

• (b) Cardiac output

• (c) pO2

• (d) SaO2

Oxygen Delivery (DO2)

Cardiac Output x Oxygen Content

CO x [(1.3 x Hgb x SaO2) + (0.003 x PaO2)]– Hemoglobin concentration– SaO2

– Cardiac output– PaO2 (minimal)

HR SV CO

PreloadContractility

Cardiac Output

Afterload

Preload

• Determined by end-diastolic volume

• Pressure and volume related by compliance of the ventricle

Left ventricular end-diastolic pressure versus left ventricular end-diastolic

volume

0

5

10

15

20

25

30

35

25 50 75 100 125 150 175 200

LVEDV (ml/m2)

LV

ED

P (

mm

HG

)

Decreased compliance Normal compliance

Cardiac Output

• Sterling relationship

Volume loading

Card

iac

outp

ut

0

10

20

30

40

50

60

70

80

5 10 15 20 25 30

PAOP (mmHg)

LV

SW

I (g

.m/m

2)

Hypodynamic Normal Hyperdynamic

Clinical Adaptation of the Sterling Myocardial Function

Curves

SVR CO MAP

SV HR

Global Hemodynamic Relationships

PreloadContractility

Afterload

Question #3

• Which can cause low preload?

• (a) High PEEP

• (b) Tension pneumothorax

• (c) Third spacing

• (d) Positive pressure ventilation

• (e) All of the above

Pathophysiology

• Inadequate/ineffective DO2 leads to anaerobic metabolism

• Large/prolonged oxygen deficit causes decrease of high-energy phosphates stores

• Membrane depolarization, intracellular edema, loss of membrane integrity and ultimately cell death

Effects of Shock at Cellular Level

Common Histopathology Associated with

Tissue Hypoperfusion and Shock?

Histopathology of Tissue Hypoperfusion Associated with

Shock

Coagulative necrosisCoagulative necrosis

Contraction bandsContraction bands

EdemaEdema

Neutrophil infiltrateNeutrophil infiltrate

Myocardium

Diffuse alveolar damageDiffuse alveolar damage

Exudate, atelectasisExudate, atelectasis

EdemaEdema

Hyaline membraneHyaline membrane

Lung

Robbins & Cotran Pathologic Basis of Disease: 2005Robbins & Cotran Pathologic Basis of Disease: 2005

Mucosal infarctionMucosal infarction

Hemorrhagic mucosaHemorrhagic mucosa

Epithelium absentEpithelium absent

Small Intestine Liver

Centrilobular hemorrhagic necrosisCentrilobular hemorrhagic necrosis

Nutmeg appearance Nutmeg appearance



Shock


Shock

Brain

Eosinophilia and shrinkage of Eosinophilia and shrinkage of neuronsneurons

Neutrophil infiltrationNeutrophil infiltration

Bland infarct Bland infarct

Punctate hemorrhagesPunctate hemorrhages

Brain



Shock

Kidney

Tubular cells, necroticTubular cells, necrotic

Detached from basement membraneDetached from basement membrane

Swollen, vacuolatedSwollen, vacuolated

Pancreas

Fat necrosisFat necrosis

Parenchymal necrosisParenchymal necrosis


Incidence of Ischemic Histopathology in Patients Dying with Shock

Hypovolemicn = 102 (%)

Septic n = 93 (%)

Cardiogenicn = 197 (%)

Heart 37 17 100

Lung 55 65 10

Kidney 25 18 11

Liver 46 30 56

Intestine 9 26 16

Pancreas 7 6 3

Brain 6 3 4McGovern VJ, Pathol Annu 1984;19:15McGovern VJ, Pathol Annu 1984;19:15

Shock Syndromes

ShockCardiogenic shock - a major component of the the mortality associated with cardiovascular disease (the #1 cause of U.S. deaths)

Hypovolemic shock - the major contributor to early mortality from trauma (the #1 cause of death in those < 45 years of age)

Septic shock - the most common cause of death in American ICUs (the 13th leading cause of death overall in US)

Preload

Afterload

Contractility

Arterialpressure

Cardiacoutput

Peripheralresistance

Heartrate

Strokevolume

Leftventricular

size

Myocardialfiber

shortening

Cardiac Performance

Compensatory Mechanisms

Case 1

• 34 year old involved in a motor vehicle accident arrived to emergency room with blood pressure of 70/30 and heart rate of 140/min

Question #5

• Which is typical of hypovolemic shock?

• (a) High SVR

• (b) High cardiac output

• (c) High oxygen delivery

• (d) Normal wedge pressure

Preload

Afterload

Contractility

Arterialpressure

Cardiacoutput


Heartrate

Strokevolume

Leftventricular

size

Myocardialfiber

shortening

Hypovolemic Shock

Compensatory MechanismAdrenaline

CO SVR PWP EDV

Hypovolemic

Cardiogenic

Obstructiveafterloadpreload

Distributivepre-resuscpost-resusc

Hypovolemic Shock Hemodynamics

Hemorrhagic • Trauma• Gastrointestinal• Retroperitoneal

Fluid depletion (nonhemorrhagic)• External fluid loss

- Dehydration- Vomiting- Diarrhea- Polyuria

• Interstitial fluid redistribution- Thermal injury- Trauma- Anaphylaxis

Increased vascular capacitance (venodilatation)• Sepsis• Anaphylaxis• Toxins/drugs

Kumar and Parrillo, 2001

Hypovolemic Shock

Case 2

• 54 year old with acute onset chest pain arrived to emergency room with blood pressure of 70/30 and heart rate of 140/min

Question #5

• Which is typical of cardiogenic shock?

• (a) Low SVR


• (c) Low oxygen delivery

• (d) Low wedge pressure

Preload

Afterload

Contractility

Arterialpressure

Cardiacoutput


Heartrate

Strokevolume

Leftventricular

size

Myocardialfiber

shortening

Cardiogenic Shock


CO SVR PWP EDV

Hypovolemic

Cardiogenic



Cardiogenic Shock Hemodynamics


Myopathic• Myocardial infarction (hibernating myocardium)• Left ventricle

Right ventricleMyocardial contusion (trauma)MyocarditisCardiomyopathyPost-ischemic myocardial stunningSeptic myocardial depressionPharmacologic

• Anthracycline cardiotoxicity• Calcium channel blockers

Mechanical• Valvular failure (stenotic or regurgitant)• Hypertropic cardiomyopathy• Ventricular septal defect

Arrhythmic• Bradycardia• Tachycardia

Cardiogenic Shock

Case 3

• 67 year old with fever, chills, SOB, and ugly looking abdominal wound arrived to emergency room with blood pressure of 70/30 and heart rate of 140/min

Question #6

• Which is not typical of sepsis?

• (a) Low SVR


• (c) Low oxygen delivery

• (d) Low wedge pressure

Preload

Afterload

Contractility

Arterialpressure

Cardiacoutput


Heartrate

Strokevolume

Leftventricular

size

Myocardialfiber

shortening

Distributive Shock


CO SVR PWP EDV

Hypovolemic

Cardiogenic



Distributive Hemodynamics


Septic (bacterial, fungal, viral, rickettsial)

Toxic shock syndrome

Anaphylactic, anaphylactoid

Neurogenic (spinal shock)

Endocrinologic• Adrenal crisis• Thyroid storm

Toxic (e.g., nitroprusside, bretylium)

Distributive Shock

Preload

Afterload

Contractility

Arterialpressure

Cardiacoutput


Heartrate

Strokevolume

Leftventricular

size

Myocardialfiber

shortening

Obstructive Shock


CO SVR PWP EDV

Hypovolemic

Cardiogenic



Obstructive Shock Hemodynamics


Impaired diastolic filling (decreased ventricular preload)• Direct venous obstruction (vena cava)

- Intrathoracic obstructive tumors

• Increased intrathoracic pressure- Tension pneumothorax

- Mechanical ventilation (with excessive pressure or volume depletion)

- Asthma

• Decreased cardiac compliance- Constrictive pericarditis

- Cardiac tamponade

Impaired systolic contraction (increased ventricular afterload)• Right ventricle

- Pulmonary embolus (massive)

- Acute pulmonary hypertension

• Left ventricle- Saddle embolus

- Aortic dissection

Extracardiac Obstructive Shock

Clinical Features

Symptoms of Shock

• Anxiety /Nervousness• Dizziness• Weakness• Faintness• Nausea & Vomiting• Thirst• Confusion• Decreased UO

• Hx of Trauma / other illness

• Vomiting & Diarrhoea

• Chest Pain• Fevers / Rigors• SOB

General Symptoms Specific Symptoms

Signs of ShockPale

Cold & ClammySweatingCyanosis

TachycardiaTachypnoea

Confused / AggiatatedUnconscious

Hypotensive/OliguricStridor / SOB

Capillary Refill

Skin Mottling

Skin Mottling

Diagnosis and Evaluation

• Primary diagnosis - tachycardia, tachypnea, oliguria, encephalopathy (confusion), peripheral hypoperfusion (mottled, poor capillary refill vs. hyperemic and warm), hypotension

• Differential DX: – JVP - hypovolemic vs. cardiogenic– Left S3, S4, new murmurs – cardiogenic– Right heart failure - PE, tamponade– Pulsus paradoxus, Kussmaul’s sign – tamponade– Fever, rigors, infection focus - septic – Poor skin turgor and dry mucous membranes: hypovolemic

Unable to produce Tachycardia

• Limited cardiac response to catecholamine stimulation: elderly

• Autonomic dysfunction: DM

• Concurrent use of beta-adrenergic blocking agents

• The presence of a pacemaker

Severity of Hemorrhage

Comparison of Adult vs Child

Classification of Hemorrhagic Shock

Class I Class II Class III Class IV

Blood loss (ml) Up to 750 750-1500 1500-2000 >2000

Blood loss (%) Up to 15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Pulse pressure Normal Decreased Decreased Decreased

Respiratory rate

14-20 20-30 30-40 >35

Urine output (ml/h)

>30 20-30 5-15 Negligible

CNS/mental status

Slightly anxious

Mildly anxious

Anxious/ confused

Confused/ lethargic

Fluid replacement

Crystalloid Crystalloid Crystalloid/ blood

Crystalloid/ Blood

Shock Evaluation and Monitoring

Initial Therapeutic Steps

A Clinical Approach to Shock Diagnosis and Management

Admit to intensive care unit (ICU)

Venous access (1 or 2 large-bore catheters)

Central venous catheter

Arterial catheter

EKG monitoring

Pulse oximetry

Urine output monitoring

Hemodynamic support (MAP < 60 mmHg)

• Fluid challenge• Vasopressors for severe shock unresponsive to fluids

Diagnosis and Evaluation

• Hgb, WBC, platelets

• PT/PTT

• Electrolytes, arterial blood gases

• BUN, Cr

• Ca, Mg

• Serum lactate• ECG

Laboratory


• CXR

• Abdominal views*

• CT scan abdomen or chest*

• Echocardiogram*

• Pulmonary perfusion scan*

* When indicated

Initial Diagnostic Steps

Diagnosis Remains Undefined orHemodynamic Status Requires Repeated Fluid Challenges or

Vasopressors


Pulmonary Artery Catheterization

• Cardiac output• Oxygen delivery– MVO2– DO and VO• Filling pressures

Echocardiography

• Pericardial fluid• Cardiac function• Valve or shunt abnormalities

Hemodynamic MonitoringMeasurement of PCWP

Components of the Atrial Waves

The difference between CVP and PCWP waves

The mean of the A wave approximates ventricular end-

diastolic pressure

Reading CVP

V A

c

Reading PCWP

A

V

VA

Reading the mean of an A wave

22+10/2=16

Question #7

• Which is true about the “wedge”?

• (a) Measures LVEDV

• (b) Falsely elevated by PEEP

• (c) Increased in pulmonary HTN

• (d) Accurately measured in mitral stenosis

Wedge Pressure

• Correlates well with LA and LVEDP if normal anatomy

• Reliable measure of preload (volume) only with normal/stable ventricular compliance

• Falsely elevated by PEEP (and auto-PEEP)

Shock Management

Management

• Treatment of underlying cause

• Volume

• Vasopressors

A Clinical Approach to ShockDiagnosis and Management

Identify source of blood or fluid loss in hypovolemic shock

Intra-aortic balloon pump (IABP), cardiac angiography, and revascularization for LV infarction

Echocardiography, cardiac cath and corrective surgery for mechanical abnormality

Pericardiocentesis surgical drainage for pericardial tamponade

Thrombolytic therapy, embolectomy for pulmonary embolism

Source control and early broad antibiotics for septic shock

Perfusion Goals in Patients with Septic Shock

HEMODYNAMCS

MAP > 60 mm HgPAOP = 12 - 18 mmHgCardiac Index > 2.2 L/min/m2

ORGAN PERFUSION

CNS - improved sensoriumSkin - warm, well perfusedRenal - UOP > 0.5 cc/kg/hrDecreasing lactate (<2.2 mM/L)Improved renal, liver fucntion

O2 DELIVERY ADEQUACY

Arterial Hgb SpO2 > 92%Hgb concentration > 9 gm/dLSVO2 > 65%Blood Lactate Conc < 2 mM/L

Volume Therapy

Crystalloids

• Lactated Ringer’s solution• Normal saline

Colloids

• Hetastarch• Albumin

Packed red blood cells

Infuse to physiologic endpoints

Rivers E, Nguyen B, Havstad S, et al 2001;345:1368-1377.

Early Goal Directed Therapy89

49.2%

33.3%

0

10

20

30

40

50

60

Standard Therapy N=133

EGDTN=130

P = 0.01*

*Key difference was in sudden CV collapse, not MODS

Early Goal-Directed Therapy Results:28 Day Mortality

Vascular Collapse

21% vs 10%

p=0.02

MODS

22% vs 16%

P=0.27

NEJM 2001;345:1368-77.

Mortality %

Rivers E, Nguyen B, Havstad S, et al. 2001;345:1368-1377.

In-hospital mortality

(all patients)

0

10

20

30

40

50

60 Standard therapyEGDT

28-day mortality

60-day mortality

NNT to prevent 1 event (death) = 6 - 8M

ort

ali

ty (

%)

The Importance of Early Goal-DirectedThe Importance of Early Goal-DirectedTherapy for Sepsis-induced HypoperfusionTherapy for Sepsis-induced Hypoperfusion

92

SepsisSIRS Severe Sepsis Septic ShockInfection

Early Goal Directed Therapy

Early Goal-Directed Therapy (EGDT): involves adjustments of cardiac preload, afterload, and contractility to balance O2 delivery with O2 demand: Fluids, Blood, and Inotropes

Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEJM 2001;345:1368.

CVP > 8-12 mm Hg MAP > 65 mm Hg Urine Output > 0.5 ml/kg/hr ScvO2 > 70% SaO2 > 93% Hct > 30%

*

Therapies Across The Sepsis Continuum

Type of Fluids

Therapy: Resuscitation Fluids

• Crystalloid vs. colloid

• Optimal PWP 10 - 12 vs. 15 - 18 mm Hg

• 20-40 mL/kg fluid challenge in hypovolemic or septic shock with

• Re-challenges of 5 - 10 mL/kg

• 100 - 200 mL challenges in cardiogenic

Vasoactive Agent Receptor Activity

Agent a1 a2 b1 b2 Dopa

Dobutamine + + ++++ ++ 0

Dopamine ++/+++ ? ++++ ++ ++++

Epinephrine ++++ ++++ ++++ +++ 0

Norepinephrine +++ +++ +/++ 0 0

Phenylephrine ++/+++ + ? 0 0

0

Vasopressors/Inotrops

Dopamine Norepinephrine

Take Home Points

• Shock is defined by inadequate tissue oxygenation, not hypotension

• Oxygen delivery depends primarily on CO, Hgb and SaO2 (not pO2)

• Volume expand with crystalloids and blood, if indicated; then add vasoactive drugs to improve vital organ perfusion

• Early treatment of shock is critical

Thank You

Approach and Hemodynamic Evaluation of Shocks

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