Hemodynamic monitoring and Shock

Dr. Mohammad Aljawadi PharmD, Msc, PhD

PHCL 477

Clinical Pharmacy Department

College of Pharmacy

King Saud University

April 2015

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What is Shock?

Inadequate tissue

perfusion

Cellular Injury

Organ Dysfunction

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To understand the hemodynamics of shock we need:

To understand the basics of hemodynamics

What is a pulmonary artery catheter and how it is used

Let us start with the latter and go back to the former later

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Pulmonary Artery Catheter

Swan-Ganz Catheter 110 cm long Up to 5 ports Tip encloses a

balloon 1.5 mL Ports at 19cm and

30cm for the infusion of drugs.

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Pulmonary Artery Catheter

Indications Myocardial infarction with

shock/hypotension. Intraoperative cardiac or

vascular surgery patients. Severe trauma.

Relative Indications CHF Pulmonary hypertension Neurosurgical procedures Sepsis/septic shock Respiratory failure

• Uses– Establish Diagnosis– Guide therapies– Monitor Treatment– Assess O2 delivery

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Central Venous Access Complications

Line sepsisThrombosisPneumothoraxHemothoraxArrhythmias (Swan-Ganz)Air EmbolusInfarctionCatheter Knotting (Swan-Ganz)

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How it is inserted?

During diastole while mitral valve is open, left ventricle, left atrium and pulmonary capillary become one chamber.

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The Basics of Hemodynamics

Blood Pressure

Cardiac Output

Systemic vascular resistance

Stroke Volume

Heart rate

Pre-load

After-load

Contractility

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The Basics of Hemodynamics

BLOODPRESSURE

CO= X SVR

SV X HR

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The Basics of Hemodynamics

Cardiac Output (CO) Amount of blood that is pumped out of the heart in one

minute. 5.6 L/min for a human male and 4.9 L/min for a female

Stroke Volume The quantity of blood pumped out of the ventricles with

every heart beat. ~ 70 mL in a healthy 70-kg man

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Determinants of stroke volume

PRELOAD

AFTERLOAD

CONTRACTILITY

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DEFINITIONS

Pre-Load Force on ventricles

during relaxation phase (diastole)

Measured at end-diastole (just before ejection)

SV

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DEFINITIONS

Afterload Load on the

ventricle during ejection (in systolic phase)

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DEFINITIONS

Contractility Force of ejection

INOTROPE

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MEASURES OF PRE-LOAD

Right ventricular pre-load Central Venous Pressure (CVP)

0-4 mmHg

Left ventricular pre-load Pulmonary Artery Occlusion Pressure (PAOP)

(8-12 mmHg) Measured during diastole when the MV is open

When mitral valve is open we assume

PAEDP ~ PVEDP ~ LAEDP ~ LVEDP

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Normally, PAOP approximates left atrial pressure, which in turn approximates left ventricular end-diastolic pressure (LVEDP).

LVEDP reflects left ventricular end-diastolic volume (LVEDV).

LVEDV is the actual target

MEASURES OF PRE-LOAD

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MEASURES OF AFTERLOAD

Afterload on Right Ventricle Pulmonary Vascular Resistance

PVR =MPAP – PAWP x 80 (20-120 dyne x sec / cm-5)

CO

Afterload on Left Ventricle Systemic Vascular Resistance SVR = MAP – CVP x 80 (800-1200 dyne x sec / cm-

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CO

MAP = SBP + 2(DBP)

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CONTRACTILITY

CO = SV x HR

CARDIAC OUTPUT (4-7 L/min) Thermodilution: a thermistor near the end of the

catheter injects cold saline into the bloodstream and the temperature change determines CO

CARDIAC INDEX = CO/BSA (2.8-3.6 L/min/m2)

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OXYGEN DEMANDOXYGEN SUPPLY

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OXYGEN SUPPLY

DO2 = CO X CaO2 (arterial O2 content)

CO = SV x HR CaO2 determined by:

HgB SaO2

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OXYGEN DEMAND

Determined by metabolic activity of tissues

O2 extraction Usually about 25% for the entire body CvO2 determined by:

HgB SvO2 (60-75%)

SvO2 = increased oxygen consumption• Either decreased delivery, or increased demands• Examples???

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A word about O2 monitoring

Oxygen Saturation(SpO2)

normal > 90% Non-invasive

Mixed venous oxygen saturation(SvO2)

Normal 65%-75%invasive

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RECAP

PA catheter measurements RA or CVP (0-4 mmHg) PAP (25/10 mmHg) PAOP (8-12 mmHg) CO / CI (4-7 L/min, 2.8-3.6 L/min/m2) SVR (800-1200 dyne x sec / cm-5)

SvO2 (65-75%)

RIGHT HEART PRE-LOAD

BLOOD FLOW / PUMP PERFORMANCE

LEFT HEART AFTERLOAD

OXYGEN SUPPLY /DEMAND

LEFT HEART PRE-LOAD

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SHOCK IN THE ICU

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What is Shock?

Inadequate tissue perfusion resulting in cellular injury.

This causes the release of inflammatory mediators that further compromise tissue perfusion, resulting in organ failure and death unless quickly corrected

Circulating volume must be identified and expanded quickly, and the underlying pathological process must be controlled.

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Classification of Shock

Hypovolemic Shock

Cardiogenic Shock

Distributive Shock

Extra-cardiac Obstructive Shock

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Organ dysfunction is the threat of shock

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Hypovolemic Shock

Results fromLoss of blood or fluid.

Decreased circulating blood volume decrease in diastolic filling pressure and volume

inadequate CO, hypotension, and shock

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Hypovolemic Shock

Causes: dehydration, hemorrhage, gastrointestinal fluid

losses, urinary losses, or decreased vascular permeability from sepsis

hypotension with signs of shock indicating tissue hypo-perfusion, activation of the inflammatory cascade, and widespread cellular damage

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Hypovolemic Shock

Acute Loss in circulating Blood Volume

Consequences

10% Tachycardia, ↑ SVR , ↔ BP

20% to 25% Mild hypotension, ↓CO, ↑lactate

40% Moderate-severe hypotension with signs of shock indicating tissue hypo-perfusion, activation of the inflammatory cascade, and widespread cellular damage

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Cardiogenic Shock

Myocardial damage or cardiac mechanical abnormality

Reduced cardiac functionDecrease in cardiac output and blood

pressure Shock

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Cardiogenic Shock

Causes: Q-wave myocardial infarctions.

Special signs: Patients have signs of heart failure, an S3,

elevated neck veins, and peripheral hypo-perfusion

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Cardiogenic Shock

Q-wave MI

(most frequent in-hospital cause)

↑ Preload

↑PAOP

↑CVP

↑Ventricular volume

↓CI

↓SV

↓MAP

Signs of heart failure:

an S3, elevated neck veins, and peripheral

hypo-perfusion

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Distributive Shock

Loss of peripheral resistance fluid leak to extracellular space

Vasodilation Decrease in preload Hypotension Normal or increased CO

Myocardial depression frequently accompanies distributive shock.

Decrease in SVR inadequate blood pressure shock and multi-organ dysfunction

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Distributive Shock

Causes: Sepsis Anaphylaxis, drug overdose, neurogenic

causes, and Addisonian crisis

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Extra-cardiac obstructive

Obstruction to flow in the cardiovascular circuit. inadequate diastolic filling or decreased systolic function secondary to an increase in afterload and a drop in CO and blood pressure

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Extra-cardiac obstructive

Causes cardiac tamponade, constrictive pericarditis,

pneumothorax, mediastinal tumors and pulmonary embolus

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Tip of the mountain

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Causes:

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Pathophysiology

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Auto-regulation

45Body auto-regulation during shock

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Manifestations of shock

CNS: Alerted level of consciousness from confusion

to coma Ischemia

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Manifestations of shock

CVS: Hypotension

Decreased coronary artery perfusion pressure Ischemia in patients with coronary artery disease

Tachycardia. (which type of shock is not associated with it?)

Contractility will increase in most typesCardiogenic

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Manifestations of shock

Respiratory: Increase in minute ventilation

Hypocapnia

Severe hypo-perfusion Respiratory muscle weakness

Respiratory alkalosis

Respiratory Failure

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Renal: Because of auto-regulation glomerular filtration

is maintained by efferent arteriole constriction Late in shock:

Cortical and medullary ischemia tubular necrosis

↓ urine output followed by ↑ BUN and SCr

Manifestations of shock

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Manifestations of shock

GI: Very sensitive to sympathetic vasoconstriction:

Ileus Gastritis Pancreatitis Acalculous cholecystitis (not due to stone gallbladder inflammation)

Colonic submucosal hemorrhage Ischemia of the gut can lead to translocation of

bacteria from the gut to the circulation

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Liver: LFTs elevations

Hematological: Disseminated intravascular coagulation Dilutional thrombocytopenia due resuscitation

Metabolic: Hyperglycemia due ↓ insulin production Protein catabolism negative nitrogen balance

Manifestations of shock

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Cardiogenic shock: jugular venous distension, an S3 and S4, and regurgitation murmurs.

Pulmonary embolus: patients present with hypoxia, dyspnea, and elevated right heart pressures.

Septic shock patients may have fevers, chills, and usually a nidus of infection ( a source of infection)

Manifestations of shock

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Labs:

Low or high WBC count with a left shift and bands

High or normal hemoglobin levels

High to low platelets

Low serum bicarbonate

High anion gap

High or normal creatinine

High lactate

(unless hemorrhagic shock)

Why?

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Hemodynamic monitoring:

Arterial pressure and CVP monitor vasopressors effect

Mixed venous oxygen saturation (Svo2) Normal 65%-75% Inversely proportional to perfusion level

Pulmonary artery catheter no evidence of decreased mortality

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CO SVR PAOP CVP

Hypovolemic

Cardiogenic

Distributivepre-resusc

post-resusc

Extra-cardiac obstructiveShock (pulmonary embolism)

Shock Hemodynamics

or normal

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Goals of therapy:

Prevent target organ damage Achieve adequate

CO and MAP Treat underlying

cause

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Therapy

Adequate oxygenation (mechanical ventilation) Goal: Oxygen saturation 90% or greater

Volume resuscitation Mainly crystalloids (NaCl 0.9%) Colloids

(Albumin) Good in severe sepsis

Hetastarch Limited use in renal failure

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Therapy

Once volume resuscitation is optimized vasopressors and inotropes

What happened if you start with a vasopressor before fluid resuscitation?

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Vasopressors:

Norepinephrine: Reliable increase in blood pressure and

inotrope

Dopamine: Low dose: mild inotropic effect as well as some

renal effects. high dose: vasoconstriction Higher incidence of mesenteric ischemia than

norepinephrine

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Vasopressors:

Epinephrine: 1st choice in anaphylactic shock Watch for:

Tachycardia and arrhythmia Mesenteric ischemia

Phenylephrine: Pure α-agonist

Good for patients with underlying tachycardia

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Vasopressors:

Vasopressin: In refractory cases not responding to previous

vasopressors ↓ heart rate and cardiac output ↑ blood pressure and pulmonary artery pressure May lead to myocardial ischemia due a

decrease in coronary artery blood flow

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Inotropes:

Dobutamine: β1 and β2 agonists

CO SVR

Milrinone: phosphodiesterase inhibitor It is a potent vasodilator

Decreases both pulmonary vascular resistance and SVR.

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Therapy

Hypovolemic Shock: Rapid reversal with blood, colloid, or

crystalloid

Cardiogenic: Left ventricular MI:

Intra-aortic balloon pump, cardiac angiography, and revascularization

Right ventricular MI: Fluids and inotrops

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Therapy

Extra-cardiac obstructive shock: Cardiac tamponade:

Pericardiocentesis or surgical drainage Pulmonary embolism:

Thrombolytics, Heparin and embolectomy

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Therapy

Distributive shock: Septic:

Antibiotics + fluid resuscitation+ vasopressors or inotropes

Anaphylactic: Steroids, diphenhydramine, H1 and H2 blockers,

and epinephrine

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Questions