BASIC HEMODYNAMIC MONITORING Flashcards
What is hemodynamics?
- Includes techniques and equipment that improve diagnosis
- Allow evaluation of a patient’s condition by providing us with the ability to measure pressures that reflect systemic and pulmonary circulation
- blood returning to the heart is still oxygenated 60-80%
— in sepsis or pulmonary disease its lower - non-invasive hemodynamic monitoring: HR, BP, SaO2, etc.
- invasive hemodynamic monitoring: looks inside the heart: filling pressures, preload, after load (LV pressure)
- CVP: sits at SVC junction
- arterial pressure monitoring: radial or femoral
- PAC: tip sits in pulmonary artery: measures pressure (ex: pulmonary HTN/ low fluid)
— can inflate balloon on end of catheter and cause wedge into pulmonary artery bed: looks at left side of heart and gives us an occlusive/ wedge pressure
— normal wedge pressure 8 - 12
— normal PAP: 25/10
— normal CVP: 2-6
*Not tested on numbers
Hemodynamic Monitoring
How & Why?
- Measures factors that influence the force and flow of blood
- Aids in diagnosing, monitoring and managing critically ill patients.
- Invasive hemodynamic monitoring is done using a special catheter developed by Dr. H. Swan and an engineer named Ganz in 1970. (Pulmonary Artery Catheter [PAC])
- The information obtained can be used to calculate systemic and pulmonary resistance and oxygen delivery, as well as oxygen consumption.
- we do this to bc we need more info or to DX a pt
- we use it to determine
— CO
— determine fluid volume status
— different shock states
— monitor and manage unstable pts response to treatments
— measure SVR, PVR, PAP, Wedge pressure, CVP, CO, CI, - SWAN-Ganz catheter= PAC
— increased PAP could be lung disease
— increased wedge pressure could be fluid over load/ LHF
— low CVP pt could be low in fluids
Low SVR + norepi (vasoconstrictor) = increased SVR
— Milronone: positive inotrope/ decreases preload and afterload (vasodialates)/ increases CO/CI
Why do we use Invasive Hemodynamic monitoring?
Scenarios for use of PAC
- Management of volume status in the critically ill patient
— Sepsis( increased vasodilation), Trauma (blood loss) , GI Bleed - Management post MI
— Severe cardiogenic shock
— helps measure CO/CI - Management of Pulmonary Hypertension
- Management of high-risk surgical patients
— CABG, Valve, Vascular, debulkings
Cardiac Output
Amount of blood pumped in liters per minute
Preload
The amount of ventricular stretch at the end of diastole. (LVEDP)
Afterload
the resistance the ventricles must push against with systolic ejection (SVR)
Contractility
The ability of the heart to contract and generate force
Starling’s Law
the more the heart muscle stretches during diastole the more forcefully the contraction during systole
— greater volume= greater stretch = increased pump
—- decreased volume= decreased stretch= decreased pump
— dialated cardiomyopathy= decreased contractability
BP
Arterial Line or Non invasive BP
CO/CI
Cardiac Output/Cardiac Index
SV/SVI
Stroke volume/Stroke volume index
SVO2
Mixed Venous Saturation
- amount of O2 in blood returning to the Right side of heart in the pulmonary artery bed
— 60-80%
SVR
PVR
Pulmonary Vascular Resistance
- the resistance that the right ventricle needs to overcome in order to open the pulmonary artery valve
PAOP
Pulmonary Artery Occlusive Pressure
- wedge pressure
— PAC balloon inflates and occludes into the pulmonary artery bed and gives a pressure
CVP
Central Venous Pressure
PAP
Pulmonary Artery Pressure
Stroke Volume
Factors that influence SV;
- Preload
- afterload & contractility
- Frank Starling’s law
Contractility
- Ability of the myocardial muscle fibers to shorten independent of preload and afterload
- inotropes= help heart pump
- cronotropic= effect heart rate
- Inotropy=Pump
- Ejection fraction used to evaluate the ability of the heart to contract
— Normal EF for healthy person 55-65%
Cardiac Output vs Cardiac Index
CO = SV X HR
CI = CO/BSA
Normal CI= 2.5-4L
Body builder
- CO =4L/min
- BSA = 2.0 m2
- CI = 2.0L/min/m2
*
Stick person
CO =4L/min
BSA = 1.4 m2
CI =2.86L/min/m2
Normal Hemodynamic Values
SVO2
60-75 %
Normal Hemodynamic Values
Stroke Volume
50-100 ml
Normal Hemodynamic Values
Cardiac output
4-8 L/min
Normal Hemodynamic Values
Cardiac index
2.5-4.0 L/min/M2
Normal Hemodynamic Values
MAP
60-100 mm Hg
Normal Hemodynamic Values
CVP
2-6 mm Hg
Normal Hemodynamic Values
PAP systolic:
20-30 mm Hg
Normal Hemodynamic Values
PAP diastolic
5-15 mm Hg
Normal Hemodynamic Values
PAOP (wedge)
8-12 mm Hg
Normal Hemodynamic Values
SVR
900-1300 dynes sec cm-5
Arterial Waveform
Arterial Waveform=Arterial line
- dicrotic notch: closing of valves
- peak of wave (systolic pressure)
- trough of wave: (diastolic pressure)
- each wave is 1 cardiac cycle
— s1: closure of AV valves (mitral/tricuspid)
— s2: aortic & pulmonic valve (dicrotic notch)
Direct Arterial Blood Measurement
Nurse job:
- set up flush bag / prime tubing
- zero:
— To zero an arterial line, you need to ensure that the transducer is at the level of the phlebostatic axis, which is roughly at the level of the right atrium. Here’s a general process:
- Position the patient appropriately: Ensure the patient is supine with the transducer at the level of the right atrium.
*You can estimate this by placing the transducer at the fourth intercostal space midaxillary line on the left side of chest (phlebostatic axis). - Stop the transducer: Stop any pressure infusions and ensure the transducer is open to air.
- Zero the transducer: Use the monitor’s zero function or adjust the transducer’s zero knob until the pressure reading is zeroed.
- Confirm zero reading: Check that the monitor reads zero when the transducer is at the phlebostatic axis level.
- Secure the transducer: Once zeroed, secure the transducer to prevent movement.
Always follow your facility’s specific protocol for zeroing arterial lines, as the process may vary slightly depending on the equipment and guidelines in place.
Pressure bags
- Every invasive line will need a pressure bag *Pressurized to 300 mmHg.
- This pressure allows the infusion of about 3ml of fluid each hour, keeping the line patent and the transducer free of contaminants.
- *Gradients: pressure should be higher in bag than what is being exerted from invasive distal end.
- Always use Normal Saline
- Never use Heparinized solutions bc of HIT (heparin induced thrombocytopenia)
- *Zeroing lines: Negating the influence of atmospheric pressure should be done at least once a shift.
A transducer converts the pressure via a monitor to a diagnostic waveform
Leveling the Transducer to the phlebostatic axis
- Located at the 4th intercostal space at the mid-anterior-posterior diameter of the chest wall
- Where the tip of the CVP catheter would lay
Central Venous Pressure Waveform
CVP catheter in SVC junction
- sits right at the top of the RA
- dont need to remember the wave form (will in ICU)
Pulmonary Artery Catheter
PAC
Pulmonary Artery Catheter Placement
Complications of PAC
- General central line complications
- Pneumothorax
- Arterial injury
- Infection
- Embolization
- Inability to place PAC into PA
- Arrhythmias (heart block)
- Pulmonary artery rupture
Pulmonary artery catheter (pac) IN RA
CVP= 2-8 mmHG
Pac IN RV
- RV Systolic = 10-25
- Diastolic = 0-8
PAC IN PA
PA
- Systolic=15-25
- Diastolic=8-12
(25/10)
PAC IN WEDGE POSITION
PCWP “Wedge” 8-12
- dont keep balloon inflated
— could cause : necrosis, PE, rupture (1.5ml pre measured syringe)
- increased wedge pressure= fluid over load/ aortic stenosis or regurge/ mitral stenosis/ LV failure/ cardiac tamponade/ or restrictive pericarditis
- low wedge pressure= pt is dry: Hypovolemic/ vasodilated
— norepi increases SVR via vasoconstriction= increased wedge pressure
AFTER PCW (wedge) , BACK IN PA
PA waveform should return to normal once balloon is deflated
- Systolic=15-25
- Diastolic=8-12
Cardiac Output & SVO2
- Cardiac Output – Continuous or Intermittent
- SVO2 – at the end of the catheter
- Needs to be correlated
- CO= 4-8 L
- CI= 2.5-4 L
Case Study # 1
- A 50 year old male presents with syncope and shock. Room air ABG and Hemodynamic measurements shown below.
- CVP 15
- PA 45/20
- PCWP 7
- BP 80/50
- MAP 60
- PH 7.32
- PO2 59
- O2Sat .89
- CO2 32
- Mixed venous (SVO2) .49
- What values are abnormal? What is the likely diagnosis?
In this case, the abnormal values are:
- Low blood pressure (BP 80/50)
- Low mean arterial pressure (MAP 60)
- Low partial pressure of oxygen (PO2 59)
- Low oxygen saturation (O2Sat 0.89)
- Low mixed venous oxygen saturation (SVO2 0.49)
- Elevated central venous pressure (CVP 15)
- Elevated pulmonary artery pressure (PA 45/20)
- Low pulmonary capillary wedge pressure (PCWP 7)
The likely diagnosis based on these findings is cardiogenic shock, specifically right heart failure leading to cardiogenic shock. The elevated CVP and PA pressures along with low CO2 suggest poor cardiac output and impaired oxygen delivery to tissues, leading to syncope and shock. The low PO2 and O2Sat indicate hypoxemia, likely due to poor cardiac output and inadequate oxygen delivery to tissues. The low SVO2 suggests increased oxygen extraction by tissues due to inadequate oxygen delivery.
- Case study # 2
- A 90 year old male with tachypnea, confusion and hypotension.
- CVP 2
- PA 45/15
- PCWP 8
- BP 70/40
- MAP 50
- O2sat .85 on RA
- SVO2 .70
- What values are abnormal?
- What is the likely diagnosis?
In this case, the abnormal values are:
- Low central venous pressure (CVP) of 2 mmHg
- Low blood pressure (BP) of 70/40 mmHg
- Low mean arterial pressure (MAP) of 50 mmHg
- Low oxygen saturation (O2Sat) of 0.85 on room air
- Low mixed venous oxygen saturation (SVO2) of 0.70
The likely diagnosis based on these findings is distributive shock, most likely septic shock. The low CVP, low BP, and low MAP are indicative of hypotension, a key feature of shock. The tachypnea, confusion, and hypotension are consistent with the clinical presentation of shock. The low O2Sat and SVO2 suggest inadequate tissue perfusion and oxygen delivery, which are characteristic of distributive shock, such as septic shock, where there is widespread vasodilation and impaired microcirculatory perfusion.
