MODULE 2

Haemodynamic Monitoring in Cardiac Critical Care

Haemodynamic Monitoring in Cardiac Critical Care

GOAL

To maintain adequate tissue perfusionTo maintain adequate tissue perfusion

Haemodynamic Monitoring

Classically based on Invasive measurement of:

• Systemic arterial and venous pressures

• Pulmonary arterial and venous pressures

• Cardiac output

Critical Care 2002, 6: 52-59

As organ perfusion cannot be directly measured –

• Arterial blood pressure used - to estimate adequacy of tissue perfusion

Critical Care 2002, 6: 52-59

Haemodynamic Monitoring

Monitoring Circulation

• ECG• Blood Pressure• Pulse Oximetry• Central Venous Pressure • Pulmonary artery catheter• Transesophageal Echocardiography• Arterial Blood Gases

ECG

ECG

* Documents electrical activity -may not reflect output

* Monitor HR & Rhythm* Wave form varies with lead placement -know standard lead placement* ST segment analysis and Type of arrhythmia* May detect Electrolyte abnormalities

(hyper/hypokalaemia)

Blood Pressure

Provides information related to overall circulatory condition

(cardiac function & peripheral circulation)

Measuring Blood Pressure

• Non-Invasive

• Invasive

Non-invasive measurement of BP

• Auscultation- Korotkoff sounds• Oscillometry• Plethysmography• Doppler

Accuracy Depends Upon

• Size of cuff– cuff too small: high BP– cuff too big: low BP

• Site of cuff placement– increased SBP & decreased DBP as BP

is measured more peripheral

• Intraarterial BP- Arterial line

• Beat to beat BP• Provides waveform• Provides sampling port

Invasive measurement of BP

Arterial Line Information

• Systolic Blood Pressure

• Diastolic Blood Pressure

• Mean Blood Pressure

• Wave form

Arterial Line Wave Form

• Upstroke – contractility

• Downstroke - peripheral resistance

• Area under the curve - cardiac output

• Size varies with ventilation - hypovolemia

Sites for Arterial Line

• Radial

• Femoral

• Dorsalis Pedis

• Ulnar

• Brachial

• Axillary

Pulse oximeters

• Non-invasive procedure

• To monitor oxygenation and pulse rates

• Consists of a peripheral probe, a microprocessor unit

• Most oximeters also have an audible pulse tone- pitch proportional to O2 saturation - useful when one cannot see the oximeter display.

Pulse oximeters

The various wave forms seen in a Pulse oximeter

Pulse Oximeter

SpO2 90% = PaO2 60mm HgReduces the need of ABG for oxygenationDoes not indicate the adequacy of VentilationNot reliable in Hypotension Poor Perfusion Carboxy/Methemoglobinaemia

Central venous Pressure

Purpose of CVP line

Monitoring central venous pressure

Vascular access

Access for pulmonary art cath

Therapeutic uses

Sites for Insertion of CVP

Right internal jugular

Subclavian

Left internal jugular

External jugular

Antecubital

Femoral

CVP

Water density – 1: Mercury density – 13.6To convert cms H2O to mm Hg multiply by 1.36To convert mm Hg to cms H2O divide by 1.36

CVP

Calibration – known pressure is applied & change is measured

Leveling – 5 cm below sternal angle vertically (midthoracic position at the level of 4th rib)

Zeroing – substracting the atmospheric pressure (opening the fluid column to atmosphere & starting value at zero

CVP Waveforms

A-wave - atrial contraction

C-wave - RV contraction

X Descent - relaxed R atrium

V wave - venous filling of atria

y descent - opening of tricuspid

CVP Waveforms

CVP: Things to Note

Large V wave papillary muscle ischemia tricuspid regurgitation

Elevated pressure with prominent A and V wave diminished RV compliance

Contd..

Things to Note

Monophasic with lost y descent

Equalization of CVP, RV and PAOP cardiac tamponade

Indications for CVP

Hypovolemia

Large fluid shifts

Trauma

Shock

Important Concept

The CVP is only accurate with normal LV function. In the presence of LV dysfunction a pulmonary artery catheter is required.

Fluid Challenge Normal 5-8mm Hg

Sources of Error in CVP

PEEPActive expirationMeasure at the base of c wave (base of a wave)Dampening – Under damping is sometimes due to

microbubbles; flushing the system resolves problem

Complications of CVP

Carotid puncture

Dysrhythmias

Pneumothorax / haemothorax

Brachial plexus injury

Infection

Arterial Blood Gases

Interpretation of arterial blood gases

• Oxygenation

• Ventilation

• Acid base status

• Derived from PaO2 (partial pressure of oxygen in blood) and Saturation

• PaO2- measured directly by the blood gas machine

• Saturation- calculated value

• Some ABG machines- in-built oximeter can give a directly measured value for saturation.

Oxygenation

• Assessment of ventilation and acid base status go hand in hand

• pH and PCO2- directly measured by the ABG machine

• Bicarbonate and base excess- calculated values.

Ventilation & Acid-base status

ABG

N RA MApH - 7.35 - 7.45 <7.35 <7.35pCO2 - 35 - 45 >45 <45pO2 - > 80HCO3 - 20 - 28 N <20

Base Excess

May indicate tissue acidosisCrude indicator of tissue dysoxiaTissue hpoperfusion can occur without BELong lag phase between correction of intravascular

volume deficit & normalization of BEShould not be used as end point of goal directed

therapy

Case 1

A 28year female presented to the hospital with fever for 2days & Status Epilepticus. She had an cardiac arrest during a prolonged seizure & was immediately intubated, CPR was started, cardiac rhythm was restored & she was connected to a ventilator. Her ABG done was :

pH-6.788, pCO2-65,pO2-392(1)One hour later pH-7.175,pCO2-23,pO2-254(.8)7hours later pH-7.456,pCO2-24, pO2-300(.8)

Case 2

A 48year male CRF patient presented with bradycardia, hypotension & gasping respiration. ABG: pH-7.175,pCO2-31,pO2-122(NC) HCO3-11, Na-132,K-8.6

Temporary cardiac pacing was done & patient sent for haemodialysis.

2hours later ABG: pH-7.262,pCO2-29.3, HCO3-12.4,Na-139,K-6.2

Case 3

A 82year male DM,HTN had 3 bouts of vomiting, no urination for 12hours, gasping respiration, bradycardia(CHB), hypotension(BP-80), & impending cardio-respiratory arrest.

ABG:pH-6.9, pCO2-19,pO2-105(NC), HCO3-3.7,Na-147, K-6.1

9hours later ABG:pH-7.4,pCO2-14.5, pO2-132(NC),HCO3-17.2,

Case 4

A 30year female with quadriparesis 15days developed respiratory distress.

ABG:pH-7.275,pCO2-116,pO2-71, HCO3-88.She was ventilatedABG:pH-7.43,pCO2-45,pO2-80,HCO3-28

Shock

Body can develop oxygen debt in setting of normal BP

Cryptic Shock – normal vital signs despite inadequate organ perfusion

Upstream markers – BP, HR, CVP, PCWP, Cardiac Output

Downstream markers – urine output, blood lactate, base excess, tissue CO2, mixed venous O2 & CO2

Cardiac Output

PAC using bolus thermodilution methodEchocardiographyOesophageal DopplerNiCCO – CO2 parial rebreathing techniquePulse Contour Analysis - PiCCO

LactateIncreased in Oxygen deficit, exercise, GTCSUsed as a marker of tissue perfusion & adequacy

of resuscitationIn Sepsis – marker of illness severityLactate removal may be impaired in critically ill

patientsBlood Lactate > 4mEq/l – high risk of deathLactate clearance lags many hours following

therapeutic interventionsLactate should be used as marker of index

severity & trigger to initiate aggressive care but that care should not be titrated to the lactate level

ScVO2

Low ScVO2 in absence of arterial hypoxemia is usually an indicator of inadequate cardiac output

Sublingual Capnometry

Tecnically simple, noninvasive, inexpensive, that provides near instantaneous information as to the adequacy of tissue perfusion in critically ill & injured patients

Summary

CO should be interpreted in conjunction with dynamic indices of volume responsiveness & downstream markers of tissue oxygenation

Patients cannot be managed by simplistic algorithms or bundles but rather a thoughtful intensivists, who at the bedside can integrate a body of complex & interrelated information & chart a course based on the best available scientific evidence