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

As organ perfusion cannot be directly measured – Arterial blood pressure used - to estimate adequacy of tissue perfusion Critical Care 2002, 6: Haemodynamic Monitoring

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

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 Hg Reduces the need of ABG for oxygenation Does not indicate the adequacy of Ventilation Not 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 – 13.6 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 4 th 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 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

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 MA pH <7.35 <7.35 pCO >45 <45 pO 2 - > 80 HCO 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, pCO 2 -65,pO (1) One hour later pH-7.175,pCO 2 -23,pO (.8) 7hours later pH-7.456,pCO 2 -24, pO (.8)

Case 2 A 48year male CRF patient presented with bradycardia, hypotension & gasping respiration. ABG: pH-7.175,pCO ,pO (NC) HCO 3 -11, Na-132,K-8.6 Temporary cardiac pacing was done & patient sent for haemodialysis. 2hours later ABG: pH-7.262,pCO , HCO ,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, pCO 2 -19,pO (NC), HCO ,Na-147, K hours later ABG:pH-7.4,pCO , pO (NC),HCO ,

Case 4 A 30year female with quadriparesis 15days developed respiratory distress. ABG:pH-7.275,pCO ,pO 2 -71, HCO She was ventilated ABG:pH-7.43,pCO 2 -45,pO 2 -80,HCO 3 -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 parial rebreathing 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