module 2 haemodynamic monitoring in cardiac critical care
TRANSCRIPT
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