Hemodynamic Monitoring

Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

Stroke Volume = amnt of blood pumped out with each heartbeat
Decr. In SV compensatory tachycardia (HR will increase to maintain CO)
HR > 150, diastolic filling time is too short drop in SV, CO is not maintained

SV = Preload, Afterload and Contractility

Preload (LVEDV left ventricular end diastolic volume)
Amount of stretch on the heart at the end of diastole (when the ventricle is at its fullest)
Directly affected by the amount of fluid volume in the ventricle
Influenced by HR and rhythm, contractility, ventricular performance, venous
return, vascular compliance

Starlings Curve
Slingshot: the farther the slingshot is stretched, the
further the stone goes. If the slingshot is only
stretched a little, the stone doesnt go very far. If
the slingshot is repeatedly stretched, it gets weak
and can barely launch the stone far at all.

Too little preload and the CO cant propel enough
blood forward. Too much, the heart is
overwhelmed and this leads to failure. Just enough
of preload gives the best CO preload optimization.

Pressure is not equal to volume. Preload is also affected by intrathoracic pressure, intra-
abdominal pressure and myocardial compliance. Pressure is trended as an indicator of
volume status but must be correlated to physical assessment findings and the patients
history.

Signs of inadequate preload:
Poor skin turgor
Dry mucus membranes
Low urine output
Tachycardia
Thirst
Weak pulses
Flat neck veins

Signs of excess preload (with adequate cardiac fx):
Distended neck veins
Crackles in the lungs
Bounding pulses
Signs of excess preload (poor cardiac fx)
Crackles in the lungs
S3 heart sound
Low urine output
Tachycardia
Cold clammy skin with weak pulses
Edema

Insufficient preload = hypovolemia/dehydration. This causes the SNS to be stimulated to
release epinephrine and norepinephrine (vasoconstriction and incr. HR). If pt is treated with
these drugs instead of volume, tachycardia and vasoconstriction worsens, organs fail and distal
extremities become ischemic.

Afterload: the resistance that the ventricle must overcome to eject its volume of blood
Most important determinant is vascular resistance
Factors that affect afterload
o Blood viscosity
o Aortic compliance
o Valvular disease

Incr. afterload incr. myocardial work decr. SV

Symptoms of high afterload: (arterial vasoconstriction)
Cool clammy skin
> 5 sec. capillary refill
Narrow pulse pressure (SBP DBP)
o Normal = 40 mmHg
Symptoms of low afterload (incr. SV)
Warm flushed skin
Bounding pulses
Wide pulse pressure
Hypotension may result

Contractility: inherent ability of the cardiac muscle to contract
Enhanced by exercise, catecholamines and positive inotropic drugs
Decreased by hypothermia, hypoxemia, acidosis and neg. inotropic drugs
Compliance: ventricles ability to stretch to receive a given volume of blood

Sv02 - mixed venous oxygen saturation
Assesses the adequacy of tissue perfusion and oxygenation Sv02 > 60%
Low Sv02 = decreased oxygen delivery or increased oxygen extraction by tissues
(suggestive of a reduction in CO)
High Sv02 = oxygen delivery or utilization may be impaired and an otherwise normal
CO may be insufficient to provide adequate tissue oxygenation
Affected by
o Shivering, pain, agitation, temperature, anemia, alteration in FiO2, and efficiency
of alveolar gas exchange

Arterial Blood Pressure Monitoring
MAP (mean arterial pressure) avg driving force in the arterial system essentially the same in all
parts of the body.

Minimal MAP of 60-65 is required to perfuse the heart, brain and kidneys
MAP 70 90 desirable to reduce left ventricular workload
MAP 90-110 may be required to maintain cerebral perfusion

Arterial Waveforms





Anacrotic limb: begins at the opening of the aortic valve in early systole
Systolic peak: highest pressure generatored by the left ventricle during myocardial contraction
(actual systolic blood pressure)
Dicrotic limb: late systole as the flow of blood out of the left ventricle starts to decr.
Dicrotic notch: closure of the aortic valve, beginning of diastole
End diastole: location at which the patients actual diastolic pressure is measured


Inotropic and Vasoactive Drugs

Epinephrine ~ PRESSOR
Dose Range: .01 - .04 mcg/kg/min
Potent B1 inotropic agent
o Incr. CO by an incr in HR and contractility
o 0.02 0.03mcg/kg/min mild peripheral vasodilation
o Greater than 0.03 alpha effects will incr. the SVR and raise BP
Other effects
o Bronchodilation
o Arrhythmias or tachycardia
First line drug for borderline cardiac output
Stimulates sinus node when intrinsic HR is low
Side Effects
Metabolic acidosis
Severe hyperglycemia
Ectopy




Vasopressin (Synthetic ADH) ~ PRESSOR
Dose Range: .02 - .10 units/min
Half Life: 10 20 mins
o Acts on V1 and V2 receptors (smooth muscle - vasoconstriction; renal tubules (incr.
blood volume, inhibits diuresis)
o DIRECT vasoconstrictor
o No inotropic/chronotropic effects
o Can be mixed in an emergency

Phenylephrine (Neo-synephrine) ~PRESSOR
Dose Range: 20 200 mcg/min; max dose: 200mcg/min
Half life: ~ 5mins
o Pure alpha-agent that increases SVR and may cause a reflex decrease in HR.
o No direct cardiac effects
Indications
o Indicated only to incr. the SVR when hypotension coexists with a satisfactory CO

Norepinephrine (Levophed) ~ PRESSOR
Dose Range: 1-20 mcg/min
Half life: 2-3 minutes
o Powerful catecholamine alpha and beta properties (predominantly alpha raises SVR
and blood pressure; beta-1 incr. both contractility and HR)
o NE incr. myocardial O2 demand and can prove detrimental to the ischemic or marginal
myocardium
o Can cause hypoperfusion to kidneys
o Will cause a drop in CO and HR when the drug is weaned
Indications
o NE is used when the pt has a marginally low CO w/ a low BP caused by a low SVR
o Can provide inotropic support if the CI is borderline
o First line pressor for sepsis
**Vesicant central line only**

Milrinone (Primacor) ~ INODILATOR
Dose Range: 0.25 0.75 mcg/kg/min
Half life: 1.5 2hours
(0.25 0.75mcg/kg/min)
Phosphodiesterase III inhibitors (inodilators)
o Incr. cyclic AMP levels, causes a relaxation of myofilaments and this improves
ventricular compliance
Improves CO by
o Decr. SVR and exerts a moderate positive inotropic effect
o Facilitates ventricular relaxation (lusitropy)
o Improves diastolic fx
Causes incr. in HR, lowering of filling pressures, moderate reduction in myocardial O2
demand and may decr. BP

Indications
o Second-line medications for persistent low CO
o Useful in pts with R ventricular dysfunction (elevated PVR pulmonary HTN)
o Heart failure with high SVR

Dopamine

Dobutamine

Flolan

Methylene Blue

Vasodilators

Nitroglycerin
Dose: 5mcg/min; Max: 200mcg/min
Dilates coronary arteries
Improves collateral blood flow to ischemic areas
Decr. Afterload
Incr. CO
o Decr. Myocardial oxygen demand and incr. coronary artery perfusion

Nitroprusside (Nipride)
Dose: 0.1mcg/kg/min; Max: 10mcg/kg/min
Decr. SVR and afterload = incr. CO
Potent arterial dilator (direct action on smooth muscles of blood vessels)
Rapid-acting
Light sensitive

Nicardipine


Antiarrhythmic

Amiodarone



Lidocaine


Beta Blockers
Metroprolol

Esmolol

Carvadelol


Ca Blockers
Diltiazem

Sedation
Versed

Propofol

Dexmedetomidine

Pain
Fentanyl

Morphine

Vicodin

Other
Heparin

Bilvalrudin


Coronary Artery Disease
Patho: CAD results from progressive blockage of coronary arteries by atherothrombotic
disease. Clinical syndromes result from imbalance of oxygen supply and demand resulting in
inadequate myocardial perfusion to meet metabolic demand (ischemia). This can produce a
pattern of chronic stable angina.

Acute coronary syndrome (ACS) unstable angina (UA), non-ST-elevation myocardial
infarction (NSTEMI) and ST-elevation infarction (STEMI)

Risk Factors: HTN, dyslipidemia, DM, Smoking and Obesity