MODULE 2 Haemodynamic Monitoring in Cardiac Critical Care.
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Transcript of MODULE 2 Haemodynamic Monitoring in Cardiac Critical Care.
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MODULE 2
Haemodynamic Monitoring in Cardiac Critical Care
Haemodynamic Monitoring in Cardiac Critical Care
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GOAL
To maintain adequate tissue perfusionTo maintain adequate tissue perfusion
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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
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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
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Monitoring Circulation
• ECG• Blood Pressure• Pulse Oximetry• Central Venous Pressure • Pulmonary artery catheter• Transesophageal Echocardiography• Arterial Blood Gases
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ECG
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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)
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Blood Pressure
Provides information related to overall circulatory condition
(cardiac function & peripheral circulation)
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Measuring Blood Pressure
• Non-Invasive
• Invasive
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Non-invasive measurement of BP
• Auscultation- Korotkoff sounds• Oscillometry• Plethysmography• Doppler
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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
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• Intraarterial BP- Arterial line
• Beat to beat BP• Provides waveform• Provides sampling port
Invasive measurement of BP
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Arterial Line Information
• Systolic Blood Pressure
• Diastolic Blood Pressure
• Mean Blood Pressure
• Wave form
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Arterial Line Wave Form
• Upstroke – contractility
• Downstroke - peripheral resistance
• Area under the curve - cardiac output
• Size varies with ventilation - hypovolemia
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Sites for Arterial Line
• Radial
• Femoral
• Dorsalis Pedis
• Ulnar
• Brachial
• Axillary
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Pulse oximeters
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• 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
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The various wave forms seen in a Pulse oximeter
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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
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Central venous Pressure
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Purpose of CVP line
Monitoring central venous pressure
Vascular access
Access for pulmonary art cath
Therapeutic uses
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Sites for Insertion of CVP
Right internal jugular
Subclavian
Left internal jugular
External jugular
Antecubital
Femoral
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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
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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
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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
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CVP Waveforms
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CVP: Things to Note
Large V wave papillary muscle ischemia tricuspid regurgitation
Elevated pressure with prominent A and V wave diminished RV compliance
Contd..
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Things to Note
Monophasic with lost y descent
Equalization of CVP, RV and PAOP cardiac tamponade
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Indications for CVP
Hypovolemia
Large fluid shifts
Trauma
Shock
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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
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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
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Complications of CVP
Carotid puncture
Dysrhythmias
Pneumothorax / haemothorax
Brachial plexus injury
Infection
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Arterial Blood Gases
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Interpretation of arterial blood gases
• Oxygenation
• Ventilation
• Acid base status
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• 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
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• 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
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ABG
N RA MApH - 7.35 - 7.45 <7.35 <7.35pCO2 - 35 - 45 >45 <45pO2 - > 80HCO3 - 20 - 28 N <20
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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
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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)
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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
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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,
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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
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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
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Cardiac Output
PAC using bolus thermodilution methodEchocardiographyOesophageal DopplerNiCCO – CO2 parial rebreathing techniquePulse Contour Analysis - PiCCO
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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
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ScVO2
Low ScVO2 in absence of arterial hypoxemia is usually an indicator of inadequate cardiac output
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Sublingual Capnometry
Tecnically simple, noninvasive, inexpensive, that provides near instantaneous information as to the adequacy of tissue perfusion in critically ill & injured patients
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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