HEMODYNAMIC MONITORING

OBJECTIVES

The student will review

cardiac and pulmonary considerations for invasive monitoring Procedural considerations for invasive monitoring Waveform identification related to invasive monitors

EVALUATING THE PATIENT A REVIEW

PULMONARY

Breath sounds Level of mentation Oxygenation

cyanosis

Edema Chest circumference

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EVALUATING THE PATIENT CARDIOVASCULAR

Pain issues Skin color/temp Weakness/fatigue Urinary output HR, rhythm, JVP
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EVALUATING THE PATIENT

JVP

supine

Sl distention No distention

Head up

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NONINVASIVE MONITORS

Routine

NIBP EKG Pulse ox Temperature Urine

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CARDIAC FUNCTIONAL ANATOMY

Low pressure system

Right heart Pulmonary Left heart Systemic

High pressure system

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CARDIAC CONDUCTION

Atrial depolarization

SA nodethru atria

Ventricular depolarization

AV nodebundlespurkinjes

Atrial repolarization Ventricular repolarization

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MECHANICS OF CARDIAC CYCLE

Isovolumetric phase

Active-requires energy

Ventricular ejection (rapid) Ventricular ejection (reduced) Isovolumetric relaxation Rapid ventricular filling

Beg when ventric pressure <atrial pressure

End diastole = atrial kick

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WHAT ABOUT CARDIAC OUTPUT?

CO=HR X SV

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CARDIAC OUTPUT

Determined by

Preload Afterload Contractility EF=SV/EDV X 100

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FRANK-STARLING

Described in early 1900s Relationship between myocardial muscle LENGTH and force of contraction More diastolic stretch = more ventricular vol = stronger contraction True to a limit (physiological)
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FRANK-STARLING

Resting length affected by degree of preload CO begins to fall in CHF b/o inc preload

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CARDIAC COMPENSATION

Contractility HR Arteriolar responses Venuole responses

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INOTROPES

Sympathomimetic amines Phosphodiesterase inhibitors Calcium chloride Digitalis glycosides glucagon

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SYMPATHOMIMETIC AMINES

Catecholamines

Epinephrine Norpinephrine Dopamine dobutamine

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NONCATECHOLAMINES

Ephedrine Metaraminol Phenylephrine Methoxamine

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PHOSPHODIESTERASE INHIBITORS

Amrinone Milrinone

20X more potent than amrinone

aminophylline

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INOTROPES

Calcium Chloride Glucagon Digitalis

Slows HR, conduction Inc contractility

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VASODILATORS

Nitroprusside NTG Phentolamine Hydralazine captopril

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WHAT IS PRELOAD?

End diastolic length of myocardial fiber(wall stress) Amount of volume in ventricle at end diastole Muscle wall compliance important factor Normal ventricle:lge inc volume = small inc pressure Stiff ventricle: small inc in volume = large inc pressure
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WHAT IS AFTERLOAD?

Pressure that has to be overcome by LV for ejection of ventricular volume Resistance, impedance, pressure SVR PVR Inc resistancedec contractility/SV

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AFTERLOAD

Volume of blood ejected Size & thickness ventricular wall Impedance of vessels

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DYNAMICS OF VENTRICULAR FUNCTION

Rate Rhythm Preload Afterload Contractility

Expressed as EF SV/EDV LVEF 60-70% RVEF 45-50%

Heerdt, 2000

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WHAT ABOUT CONTRACTILITY?

Inotropism Shortening of muscle fibers without altering fiber length or preload Effected by

ANS Positive Inotropes Acidosis (dec) Negative inotropes (dec)

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ISSUES OF MYOCARDIAL O2

Uses 65-80% No direct method of measurement Supply and demand Disease states

May not be able to inc supply May have greater demand Poor reserve = ischemia/infarct risk
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CORONARY PERFUSION

Occurs during diastole LV thick wall

Endocardium flow influence during systole RCA and RV flow during systole

RV wall less thick

Diastolic pressure provides flow thru aortic root into coronaries

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WHAT ABOUT SVO2?

Mixed venous oxygen saturation Reflect O2 reserve Samples from PA catheter <60% (nl 60-80%)

Dec O2 delivery

Anemia Low CO states Hypovolemia Hypoxia

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DECREASING SVO2

Also b/o O2 demand increase

Hyperthermia Seizures Pain Shivering/agitation Exercise Burns hyperthyroidism

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HOW DO WE INCREASE SVO2?

Increase O2 delivery Decrease O2 demand

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INCREASE O2 DELIVERY

Increase FIO2 Increase CO

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HOW DO WE DECREASE O2 DEMAND?

Hypothermia Anesthesia Neuromuscular blockade Early stages of sepsis Hypothyroidism Shock states
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INVASIVE CARDIAC MONITORING

Swan-Ganz catheter

Developed 1960s Assess cardiopulmonary function

Cardiac disease

LV function Valves Issues of CHF, tamponade, cor pulmonale

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SWAN GANZ MONITORING

Pulmonary issues

ARDS/respiratory failure Severe COPD Shock Sepsis ARF Burns

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Complex fluid management

SWAN-GANZ ADDITIONAL INDICATIONS

CABG/RECENT MI AAA Sitting cranis Unstable sepsis Liver tx/shunts High risk OB PE Pts on IABP
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SWAN-GANZ RELATIVE CONTRAINDICATIONS

LBBB WPW syndrome Ebsteins malformation

Tachyarrythmias

Hypercoagulation Sepsis

Site of infection
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SWAN-GANZ CATHETER

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PLACEMENT GUIDELINES

Whats the distance to SVC/RA junction?

IJ SVC Femoral RAC LAC

15-20 cm 10-15 cm 30 cm 40 cm 50 cm
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PLACEMENT

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BALLOON PEARLS

1-1.5 cc used to wedge <1 cc=too far::pull back Wedge time <10-15 sec Never flush with inflated balloon PCWP = LVEDP (normal heart)

PCWP = LV function RA = RV function

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PLACEMENT

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PLACEMENT

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PLACEMENT

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WEDGE

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PCWP WAVEFORM

A=contraction

After QRS

C=closure mitral valve

May not see easily

Late T-P interval

V=atrial filling (MV closed)

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PCWP>LVEDP

Mitral stenosis LA myxoma PE Mitral regurgitation

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PCWP<LVEDP

Decreased LV compliance

Stiff ventricle LVEDP >25 mmHg Aortic regurg

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PAD AND PCWP

If not = (1-4 mmHg)

Inc PVR Cor pulmonale PE CHD Causing Pul HTN

Eisenmengers

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RA READING

High

RV failure Tamponade Pulmonary HTN COPD Chronic LV failure Volume overload

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RA READING

Low readings

Hypovolemia Sepsis Cirrhosis anemia

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RV

ESSENTIALLY SAME AS RA Additional high

VSD

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PA SYSTOLIC

High

Shunts Constrictive pericarditis Hypoxemia ARDS LV failure overload

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PA SYSTOLIC

Low

Hypovolemia Sepsis Cirrhosis anemia

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PAD

High

Inc PVR PE COPD ARDS LV failure overload

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PAD

Low

Hypovolemia Sepsis Cirrhosis anemia

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PCWP

High

LV failure Overload Mitral v. issues Tamponade Pericardial effusion Stiff LV PPV

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PCWP

Low

Hypovolemia Sepsis Cirrhosis anemia

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PA COMPLICATIONS

Dysrhythmias RBBB/CHB in pt with LBBB PA/RA/RV rupture Knot/kink/coil catheter Infection Balloon rupture Thrombus Air embolus Pneumo Phrenic n. block Horners

R/T stellate ganglion damage Eyelid ptosis

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MORE PA COMPLICATIONS

Pulmonary infarct

Balloon overinflation Prolonged wedge Vigorous flushing Thrombus formation Catheter migration Pulmonary HTN Death
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CENTRAL VENOUS PRESSURE MONITORING

Indirect measure of volume RAP reflects RVEDP CVP INDICATIONS

Cardiac disease Expected volume shifts Hypovolemia Shock states Massive trauma
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CVP ACCESS

RIJ EJ Subclavian Antecubital Femoral

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CVP PLACEMENT

RIJ benefits

Access Landmarks Carotid Brachial plexus trauma pneumothorax

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Risks

CVP PLACEMENT

EJ benefits

Superficial Safe Low success rate Sheath kinking at SC v. Subclavian trauma

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Risks

CVP PLACEMENT

Subclavian benefits

Accessible Good landmarks Pneumo Hemothorax Chylothorax Pleural effusion

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Risks

CVP PLACEMENT

Antecubital benefits

Low complication rate

Risks

Lowest success Thrombosis/thrombophlebitis Catheter shearing

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CVP PLACEMENT

Femoral advantages

High success

Risks

Sepsis thrombophlebitis

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CVP PLACEMENT

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CVP WAVEFORMS

A=RA contraction

After P wave of EKG

C=closure tricuspid

Near end QRS

Early T-P interval

V=atrial filling/tricuspid v closed

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COMPLICATIONS

Arterial puncture

Catheter position during placement

Hematoma False aneurysm Fistula

Catheter shear Brachial plexus injury Thoracic duct injury

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Wall perf/tamponade Dysrhythmias

READING THE CVP

5 cm below sternum 4 ICS, mid axillary End expiration Supine PPV adds 8-12 cm to reading!

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HIGH READINGS

Ventricular failure (R/L) SVC obstruction Tricuspid regurg Tamponade Pulmonary HTN Overload glomerulonephritis
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LOW READINGS

PERIPHERAL VASODILATION hemorrhage hypovolemia Addisonian crisis Sepsis Regional anesthesia Polyuria Sympathetic dysfunct
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INVASIVE MONITORING READINGS

Normal

CVP/RAP 1-6 mm Hg PCWP 8-12 mm Hg PA 25/10 mm Hg

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ARTERIAL LINE

Beat to beat measurement of B/P Upstroke of wave

Related to velocity of blood ejected Slowed upstroke

AS LV failure Anemia Hyperthermia Hyperthyroidism SNS Aortic regurg

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Inc sharp vertical in hyperdynamic states

ARTERIAL LINE MONITORING SITES

Radial

Low complications Allens test Poss median n damage b/o dorsiflexion Primary source hand flow Low complications Poss median n. damage
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Ulnar

ARTERIAL LINE MONITORING SITES

Brachial

Medial to biceps tendon Potential median n damage At junction pectoralis major & deltoid Safer than brachial Low thromboembolic issues
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Axillary

ARTERIAL LINE MONITORING SITES

Femoral

Easy access in shock states Potential hemorrhage (local/retroperitoneal) Requires longer catheter Post tibial collateral circ Estimates systolic higher Contraind in DM & PVD

Doralis Pedis

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ALLENS TEST

OCCLUDE ulnar and radial arteries Have pt clench fist until hand blanches Release ulnar a with hand open Color return within 5 sec = adequate collateral circ

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MODIFIED ALLENS TEST

Elevate arm above heart Have pt open and close fist several times Tightly clench fist Occlude radial and ulnar a Lower hand, open fist, release ulnar a Color return within 7 sec = OK
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RELATIVE CONTRAINDICATIONS

Inadequate circulation Infection at the site Recent cannulation same artery

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COMPLICATIONS ARTERIAL LINE

Thrombosis/embolus Hematoma Infection Nerve damage/palsy Disconnect=blood loss Fistula Aneurysm Digital ischemia
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ARTERIAL LINE

SV: systolic ejection area under waveform Seen from upsweep to dicrotic notch

End of systole Closure aortic valve

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ARTERIAL LINES

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ARTERIAL LINE ISSUES

READINGS

May be 20-40 mmHg higher and cuffs More peripheral vessel = higher systolic, narrower waveform, delayed/lower dicrotic notch Dorsalis pedis/femoral = 20-40 mmHg higher than brachial/radial

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LOSS OF WAVEFORM

Stopcock Monitor not on correct scale Nonfunctioning monitor Nonfunctioning transducer Kinked/clotted catheter asystole
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DAMPENED WAVEFORM

Air bubble/blood in line Clot Disconnect/loose tubing Underinflated pressure bag Catheter tip against wall Compliant tubing
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UNDERDAMPED WAVEFORM

Too many stopcocks Long tubing Air bubbles Defective transducer

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PULSUS PARDOXUS

Inspiration

Dec systolic >10 mmHg

Expiration

Inc systolic

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PULSUS ALTERNANS

Regular alteration in amplitude radial pulse waveforms Seen in

LVD/cardiomyopathies HTN AS Normal hearts with SVT

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