Hemodynamic monitoring Flashcards
Describe the set-up for invasive arterial blood pressure monitoring
(summarized)
- arterial catheter
- non-compliant tubing with 3-way stopcock
- transducer (at the level of right atrium) connected to monitor
- bag of 0.9%NaCl with heparin 1 unit/mL kept pressurized at 300 mHg and running at 3 mL/h connected to circuit to prevent backflow and maintain patency
- all lines primed / flushed with the heparinized saline before connection
Need to level and zero the circuit
Name complications of invasive blood pressure monitoring
- Hemorrhage
- Infection
- Distal limb necrosis
- Thrombosis
- Excessive heparinization
How to assess damping with invasive arterial pressure monitoring
Dynamic response / square wave test: open fast flush and count oscillations after square wave before return to baseline.
Optimal damping = 1-2 oscillations after square wave, amplitude of each oscillation no greater than 1/3 of previous one and interval between oscillations < 30 msec
Overdamping = no oscillations after square wave
Underdamping = multiple oscillations
How does overdamping influence the arterial waveform? Underdamping?
Overdamping -> lower SBP, higher DBP, loss of dicrotic notch
Underdamping -> higher SBP, lower DBP, artifacts on waveform
What are causes of overdamping / underdamping in invasive blood pressure monitoring
Overdamping: clot in catheter, catheter agains vessel wall, kinked catheter / tubing, air bubbles in system, compliant tubing
Underdamping: excessively long tubing, multiple 3-way stopcocks
How to calculate pulse pressure variation? What value is associated with fluid responsiveness?
PPV (%) = 100*(PPmax-PPmin)/[(PPmax + PPmin)/2]
Values >10% associated with fluid responsiveness, values >13% correlate with hypotension and fluid responsiveness
Explain why peripheral PPV overestimates central PPV
- Forward (or incident) wave travels from the left ventricle to the periphery – its amplitude is based on ventricular contraction and pulse wave velocity
- Backward (or reflected) wave travels in the opposite direction – generated by reflexion of forward wave
- Both waves superimpose in order to create the pressure waveform
- In the aorta, rise of systolic pressure is determined by aortic compliance and SV
- As the arterial pressure waveform moves into the periphery (more compliant, smaller conduit), the pulse pressure is amplified
- MAP remains unchanged to mildly decreased
Where should the transducer or the bottom of the manometer be placed for CVP monitoring
At the level of the right atrium ->manubrium in lateral recumbency / point of shoulder in sternal recumbency
Draw and explain a CVP waveform
a wave = right atrial contraction
c wave = bulging of tricuspid valve
v wave = blood flowing into right atrium
x descent = ventricular contraction / ejection
y descent = emptying of right atrium after opening of tricuspid valve
What is a normal CVP
0-5 cmH2O
(/!\ measured in cmH2O)
What do changes in CVP indicate
High > 10 cmH2O: volume overload, right sided heart failure, pericardial disease, pulmonic stenosis, marked pleural effusion / pneumothorax
Low < 10 cmH2O: hypovolemia or vasodilation
How will CVP change following a fluid challenge in a hypovolemic patient? Euvolemic? Hypervolemic?
Hypovolemic: no change in CVP or mild transient increase
Euvolemic: increase of 2-4 cmH2O and return to baseline within 15 min
Hypervolemic: increase > 4 cmH2O and return to baseline > 30 min
What is the normal CO for dogs and cats
Dogs: 125-200 ml/kg/min
Cats: 120 ml/kg/min
What values can be measured or calculated with a Swan-Ganz catheter
- Pulmonary artery pressure
- Pulmonary artery occlusion pressure (= pulmonary wedge pressure) -> indicates preload to left heart
- Right atrial pressure (= central venous pressure)
- CO with thermodilution
- SvO2 (central venous and mixed venous)
Calculated:
- Cardiac index (= CO/body surface area)
- Stroke volume (= CO/HR)
- Stroke volume index (= SV/body surface area)
- Systemic vascular resistance (= (MAP-RAP)/cardiac index)
- DO2, O2 consumption, O2 extraction
Label this waveform from a Swan-Ganz catheter being inserted and indicate what are the pressures
See picture
What is the difference between mixed venous oxygen saturation (SvO2) and central venous oxygen saturation (ScvO2)
- Mixed venous = measured from pulmonary artery
Normal = 70-75% - Central venous = measured from jugular vein / cranial vena cava -> only reflects cranial half of the body (can be a little lower because brain consumes a lot of O2)
Normal = 65-70%
Usually correlate quite well but in severe shock can vary up to 18% (ScvO2 will be higher than SvO2 because cerebral perfusion is prioritized over splanchnic)
What does SvO2 indicate and how can it be used
It indicates oxygen extraction by tissues => reflects systemic oxygen balance and cumulative oxygen debt
SvO2 > 70% can be an endpoint of hemodynamic resuscitation.
Low ScvO2 is associated with increased mortality
What can lead to erroneous interpretation of SvO2
- Abnormal hemoglobin concentration
- Hypoxemia (low SaO2)
- Large difference between SvO2 and ScvO2 in severe shock
- Impaired O2 extraction by tissues (sepsis) -> falsely elevated
For each type of shock (hypovolemic, obstructive, cardiogenic, maldistributive) indicate if CO, contractility, and SVR are increased or decreased
Hypovolemic: decreased CO / increased contractility / increased SVR
Obstructive: decreased / normal to increased / increased
Cardiogenic: decreased / decreased / increased
Maldistributive: increased or decreased / increased or decreased / decreased
What are limitations of the Fick’s methods of CO monitoring
- Requires intubation (+ ventilation for NICO)
- Requires pulmonary artery catheter for O2 consumption method
- Requires rebreathing for CO2 production method (size limitation + issue with pulmonary disease)
- Not real time
- Affected by shunting (intracardiac / intrapulmonary)
CO = [Oxygen consumption (VO2) / arteriovenous oxygen difference (Ca-Cv)] x 100
List possible complications of Swan-Ganz catheter
- Gas pulmonary embolism
- Cardiac perforation
- Pulmonary hemorrhage
- Arrhythmias
- Pneumothorax
- Thrombosis / PTE
Name methods of CO monitoring
- Fick’s method (O2 consumption or NICO for CO2 production)
- Indicator dilution method (thermodilution and lithium dilution)
- Arterial waveform analysis (pulse contour analysis, pulse pressure analysis = PiCCO, PulseCO)
- Echocardiography (doppler and non-doppler)
- Transthoracic ultrasound
List methods to assess intravascular volume
Static markers:
- Physical exam findings (mentation, HR, pulse quality, MM colour, CRT, temperature, jugular vein distension, urine output)
- MAP
- Shock index
- Lactate
- CVP
- Pulmonary artery occlusion pressure
- Cardiac POCUS (left atrial size, left ventricular size, wall thickness)
- Caudal vena cava diameter
Dynamic markers:
- Any change in static markers following fluid challenge
- Caudal vena cava collapsibility
- Pulse pressure variation, systolic pressure variation, stroke volume variation
- Plethysmographic variability index
CVC collapsibility index meaning
> 50% suggestive of hypovolemia
<50% suggestive of fluid overload
