Hemodynamic Monitoring By Nancy Jenkins RN,MSN

What is Hemodynamic Monitoring and why do it? It is measuring the pressures in the heart It allows us to see inside the heart and adjust volume as needed

Comparing Hemodynamics to IV pump Fluid =preload Pump= CO or contractility (needs electricity) Tubing =afterload

Nursing Management Hemodynamic Monitoring- You are already doing General appearance Level of consciousness Skin color/temperature Vital signs Peripheral pulses Urine output Lung sounds

Nursing Management Hemodynamic Monitoring **Single hemodynamic values are rarely significant. Monitor trends and evaluate whole clinical picture Goals Recognize early clues Intervene before problems develop or escalate

Hemodynamic Monitoring Components We Will Look at Today Heart Rate Blood Pressure and MAP CVP Pulmonary Artery Pressures Systemic Vascular Pressure (SVR) Pulmonary Vascular Pressure (PVR) Cardiac Output/ Cardiac Index Stroke Volume

Important Equation

Hemodynamic Monitoring General Principles CO: Volume of blood pumped by heart in 1 minute CI: CO adjusted for body size SV: Volume ejected with each heartbeat SVI: SV adjusted for body size Easier to adjust HR than SV **Preload, afterload, and contractility determine SV

Hemodynamics: Normal value Mean Arterial Pressure (MAP) 70 -90 mm Hg Cardiac Index (CI)- 2.2-4.0 L/min/m2 Cardiac Output (CO)- 4-8 L/min Central Venous Pressure (CVP) (also known as Right Atrial Pressure (RA)) 2-8 mmHg Pulmonary Artery Pressure (PA) Systolic 20-30 mmHg (PAS) Diastolic 4-12 mmHg (PAD) Mean 15-25 mmHg Pulmonary Capillary Wedge Pressure (PWCP) 4-12 mmHg Systemic Vascular Resistance(SVR) 800-1200  

Volume of blood within ventricle at end of diastole **Measured by CVP and wedge pressure in ICU

Preload Def- the volume that stretches the LV just before contraction Measured by CVP for RV and PAWP for LV Measures the preload of the LV or LVEDP= wedge or PAW **The greater the preload the greater the stroke volume and the greater the cardiac output

Decreased Preload- leads to Dec. SV and venous return Hypovolemia Tachycardia- why? Vasodilation/ dec. venous return Treatment- fluid **A goal for heart failure

Increased Preload Valvular disease Hypervolemia Heart failure Treatment- diuretics, vasodilators **Vascular system holding tank- vasodilation, vasoconstriction depending on need

Measured by SVR and PVR in the ICU

Afterload Resistance to ejection- arterial B/P Measured by PVR and SVR in the ER Decreased afterload Vasodilation (sepsis, hyperthermia) Hypotention Nitrates

Afterload Increased afterload Vasoconstriction (hypovolemia, hypothermia) Aortic stenosis Hypertension Fight or flight Pulmonary hypertension **The greater the afterload, the lower the cardiac output

Cardiac Output CO=SVxHR; CI= CO/BSA Normal CO 4-8 L/min; CI 2.2-4 Urine output- indirect measurement To compensate for dec. CO get tachycardia Decreased CO Poor ventricular filling- hypovolemia or SVT Poor emptying, dec. contractility (infarct, ischemia, arrhythmias) Vasodilation- sepsis and drugs Increased afterload- hypertension, vasoconstriction

Cardiac Output Increased Increased O2 demand- exercise SNS Drugs- positive inotropics (Continuous infusions: Dobutamine, Dopamine, Primacor Digoxin- IVP

Stroke Volume Def- amount of blood ejected with each heart beat Normal SV= 60-130 Exercise can increase SV Factors that determine SV Preload Afterload Contractility

Contractility Starling’s law Increased contractility SNS Drugs- positive inotropics, epinephrine, calcium Decreased contractility Loss of muscle (acute MI, cardiomyopathy) Hypoxemia Electrolyte imbalance Drugs- (lidocaine, calcium channel blockers, beta blockers

Contractility Determined by the SV and the EF% **Important to know the EF% of all heart failure patients Measured by echo EF- how much blood is ejected during systole compared to how much preload there is. **Normal EF%- 55-65% Ex 90/140= 64%EF

How and when do we measure afterload? Arterial B/P and SVR Continuous arterial pressure monitoring Acute hypertension/hypotension Respiratory failure- frequent ABG sampling Shock Coronary interventional procedures Continuous infusion of vasoactive drugs

Best indicator of tissue perfusion. Needs to be at Best indicator of tissue perfusion. Needs to be at least 60-70 to perfuse organs

Arterial Line

Arterial Pressure Monitoring High- and low-pressure alarms based on patient’s status Risks Hemorrhage, infection, thrombus formation, neurovascular impairment, loss of limb Nursing- Check 5 P’s

Arterial Pressure Waveform Dicrotic notch signifies the closure of the aortic valve.

Pulmonary Artery Catheter Fig. 66-7 PA Catheter Insertion

PPA catheter tells you everything you want to know about the heart: (Snap, Crackle, Pop) -         1) how well the pump is pumping (cardiac output, cardiac index) (snap) -          2)how full the right side of the heart is (CVP), and how full the left side is (wedge pressure) – that’s the volume…(crackle)         3)  and how well your patient’s arteries can squeeze : that’s the SVR – the “systemic vascular resistance”… (pop)

PA Waveforms during Insertion Fig. 66-9

Important Measurements Obtained by PA Catheter Right Atrial Pressure (CVP) PAP Diastolic (PAD) PA Systolic (PAS) PA Wedge (Wedge, PAOP) Cardiac Output Cardiac Index

Pulmonary Artery Pressure Monitoring- CVP Right atrium port- also know as proximal Measurement of CVP Injection of fluid for CO measurement Can you give meds through this port? Blood sampling

Central Venous Pressure Waveforms Fig. 66-11

CVP values Right Heart Presssures Normal 2-8mmHg Dec. Hypovolemia Decreased venous return Inc. Hypervolemia Inc. venous return Right HF, pulmonary hypertension Tricuspid stenosis and regurgitation

PA pressure PAD- should be close to wedge PAS- tells RV pressure PAW- LVEDP or preload of LV

PA Pressures Normal 20-30 mmHg systolic, 4-12mmHg diastolic PAS= RV pressure Inc PAS in pulmonary hypertension Inc. PAD in ventricular failure Dec. in hypovolemia Dec. in shock

PAW Normal 6-12mmHg Equals LVEDP or preload of LV Dec.in hypovolemia or low stroke volume Inc. in LV failure, mitral valve disorders Inc. in hypervolemia *** Fluids for dec. wedge and diuretics for inc. wedge

Measuring Cardiac Output Fig. 66-12

Cardiac Output Cardiac Output Monitoring

Measuring Cardiac Output and SVR SVR can be calculated when CO is measured SVR=(MAP-CVP) x80/ CO ↑ SVR Vasoconstriction from shock Hypertension ↑ Release or administration of epinephrine or other vasoactive inotropes Left ventricular failure Dec. SVR Vasodilation sepsis

Cardiac Output http://www.lidco.com/docs/Brochure.pdf

Complications with PA Catheters Infection and sepsis Asepsis for insertion and maintenance of catheter and tubing mandatory Change flush bag, pressure tubing, transducer, and stopcock every 96 hours Air embolus (e.g., disconnection)

Complications with PA Catheters Ventricular dysrhythmias During PA catheter insertion or removal If tip migrates back from PA to right ventricle PA catheter cannot be wedged May need repositioning

Complications with PA Catheters Pulmonary infarction or PA rupture Balloon rupture (e.g., overinflation) Prolonged inflation Spontaneous wedging Thrombus/embolus formation

Noninvasive Hemodynamic Monitoring Impedance cardiography (ICG) Def-Continuous or intermittent, noninvasive method of obtaining CO and assessing thoracic fluid status Impedance-based hemodynamic parameters (e.g., CO, SV, SVR) are calculated from Zo, dZ/dt, MAP, CVP, and ECG

Noninvasive Hemodynamic Monitoring Major indications Early signs and symptoms of pulmonary or cardiac dysfunction Differentiation of cardiac or pulmonary cause of shortness of breath Evaluation of etiology and management of hypotension

Noninvasive Hemodynamic Monitoring Major indications (cont’d) Monitoring after discontinuing a PA catheter or justification for insertion of a PA catheter Evaluation of pharmacotherapy Diagnosis of rejection following cardiac transplantation

hemodynamic cases (1 and 4) Case Study

Three main types of hypotension (“shock states”) that you’re going to see in the ICU 1. “Pump”- Cardiogenic shock 2. “Volume”- Hypovolemia 3. Squeeze” - Sepsis

- Pump” problems. “Cardiogenic” shock -         Pump” problems? “Cardiogenic” shock? The cardiac output will be low, because the pump isn’t pumping. Blood pressure drops. The body says to itself: “What to do? Got to keep the blood pressure up somehow!”, and starts to tighten up the arterial bed. What number tells how tight the arterial system is? – SVR. So – in cardiogenic shock, the cardiac output goes down, the SVR goes up – the pattern is usually plain as day. “Ooh, look! The output is only 2.2, and the SVR is 2400!” What does the wedge pressure do? (Remember, the LV is pumping poorly, and can’t empty itself…)

- “Volume” problems. “Hypovolemic” shock. Lost a lot of blood -         “Volume” problems? “Hypovolemic” shock? Lost a lot of blood? Running too many marathons? Cardiac output will probably be low, since there isn’t enough volume to pump with. CVP and wedge pressures? Low, right? – again, not enough volume. SVR? Same as cardiogenic: the arteries clamp down, trying to maintain pressure.   Hypovolemic shock: cardiac output low, central pressures low, SVR high.

Septic shock: cardiac output high, central pressures low, SVR low. -         “Squeeze” problem? Any idea what makes this happen? Anybody say, “sepsis”? All that bacteremic endotoxin makes the arteries dilate – blood pressure drops. What to do? Now the body uses the mirror reflex of what it did in the cardiogenic setting: instead of clamping down the arteries, which it can’t do, because that’s where the problem is – now the heart picks up the slack, pumping both faster and harder: heart rate goes up, and cardiac output does too.   Septic shock: cardiac output high, central pressures low, SVR low.