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MODULE 2. Haemodynamic Monitoring in Cardiac Critical Care. GOAL. To maintain adequate tissue perfusion. Haemodynamic Monitoring. Classically based on Invasive measurement of: Systemic arterial and venous pressures Pulmonary arterial and venous pressures Cardiac output.
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MODULE 2 Haemodynamic Monitoring in Cardiac Critical Care
GOAL To 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
Haemodynamic Monitoring • As organ perfusion cannot be directly measured – • Arterial blood pressure used - to estimate adequacy of tissue perfusion Critical Care 2002, 6: 52-59
Monitoring Circulation • ECG • Blood Pressure • Pulse Oximetry • Central Venous Pressure • Pulmonary artery catheter • Transesophageal Echocardiography • Arterial Blood Gases
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
Invasive measurement of BP • Intraarterial BP- Arterial line • Beat to beat BP • Provides waveform • Provides sampling port
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.
The various wave forms seen in a Pulse oximeter
Pulse Oximeter • SpO2 90% = PaO2 60mm Hg • Reduces the need of ABG for oxygenation • Does not indicate the adequacy of Ventilation • Not reliable in Hypotension Poor Perfusion Carboxy/Methemoglobinaemia
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 – 13.6 To convert cms H2O to mm Hg multiply by 1.36 To 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: 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 PEEP Active expiration Measure 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
Interpretation of arterial blood gases • Oxygenation • Ventilation • Acid base status
Oxygenation • 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.
Ventilation & Acid-base status • 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.
ABG N RA MA • pH - 7.35 - 7.45 <7.35 <7.35 • pCO2 - 35 - 45 >45 <45 • pO2 - > 80 • HCO3 - 20 - 28 N <20
Base Excess May indicate tissue acidosis Crude indicator of tissue dysoxia Tissue hpoperfusion can occur without BE Long lag phase between correction of intravascular volume deficit & normalization of BE Should 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 ventilated ABG: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 method Echocardiography Oesophageal Doppler NiCCO – CO2 parialrebreathing technique Pulse Contour Analysis - PiCCO
Lactate Increased in Oxygen deficit, exercise, GTCS Used as a marker of tissue perfusion & adequacy of resuscitation In Sepsis – marker of illness severity Lactate removal may be impaired in critically ill patients Blood Lactate > 4mEq/l – high risk of death Lactate clearance lags many hours following therapeutic interventions Lactate 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