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HEMODYNAMIC MONITORING

Hemodynamic Monitoring

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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

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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 Head up

No distention

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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

High pressure system Left heart Systemic

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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

RV wall less thick RCA and RV flow during systole

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 1960’s 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

Complex fluid management Shock Sepsis ARF Burns

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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 Ebstein’s malformation

Tachyarrythmias Hypercoagulation Sepsis

Site of infection

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SWAN-GANZ CATHETER

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PLACEMENT GUIDELINES

What’s the distance to SVC/RA junction? IJ 15-20 cm SVC 10-15 cm Femoral 30 cm RAC 40 cm LAC 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

V=atrial filling (MV closed) Late T-P interval

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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 Horner’s

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

Risks Carotid Brachial plexus trauma pneumothorax

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CVP PLACEMENT

EJ benefits Superficial Safe

Risks Low success rate Sheath kinking at SC v. Subclavian trauma

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CVP PLACEMENT Subclavian benefits

Accessible Good landmarks

Risks Pneumo Hemothorax Chylothorax Pleural effusion

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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

V=atrial filling/tricuspid v closed Early T-P interval

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COMPLICATIONS Arterial puncture

Hematoma False aneurysm Fistula

Catheter position during placement Wall perf/tamponade Dysrhythmias

Catheter shear Brachial plexus injury Thoracic duct injury

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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

Inc sharp vertical in hyperdynamic states Anemia Hyperthermia Hyperthyroidism SNS Aortic regurg

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ARTERIAL LINE MONITORING SITES Radial

Low complications Allen’s test Poss median n damage b/o dorsiflexion

Ulnar Primary source hand flow Low complications Poss median n. damage

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ARTERIAL LINE MONITORING SITES

Brachial Medial to biceps tendon Potential median n damage

Axillary At junction pectoralis major & deltoid Safer than brachial Low thromboembolic issues

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ARTERIAL LINE MONITORING SITES Femoral

Easy access in shock states Potential hemorrhage (local/retroperitoneal) Requires longer catheter

Doralis Pedis Post tibial collateral circ Estimates systolic higher Contraind in DM & PVD

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ALLEN’S 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 ALLEN’S 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