Hemodynamics part 1 Flashcards

1
Q

Cardiac Output

A

heart rate x stroke volume

normal: 4-8L/min

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2
Q

stroke volume

A

preload + contractility + after load

preload includes:
CVP (right ventricular)
PAOP (left ventricular)

afterload includes:
PVR (right ventricular)
SVR (left ventricular)

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3
Q

Cardiac index

A

takes into account the body surface area and is a more meaningful value than CO.

normal CI is 2.5-4.0 L/min/m^2

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4
Q

Heart rate

A

as HR increases, CO increases up to a point. Generally 130-170 bpm is the max heart rate that is attainable for most people.

Extreme bradycardia results in low CO and hypotension. An increase in HR is the first sign of compensation for a low CO. Occurs before the BP drops. Patients on beta-blockers, or any drug that decreases HR, may not be able to compensate well.

Extreme tachycardia will also decrease the CO no matter the patient’s age or the condition of the ventricles. Why? A loss of diastolic filling time occurs. If diastolic filling time is decreased, the ventricles do not have time to fill, ventricular preload drops, and ultimately the ventricle cannot put out what is not delivered.

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5
Q

Stroke Volume

A

as SV increases, CO increases.

How many mL per beat the left ventricle ejects. It is determined by the preload, afterload, and contractility.

Normal SV is 50-100mL/beat

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6
Q

Preload

A

the volume/pressure in the ventricle at the end of diastole after the AV valves close, just prior to ejection.

The right atrial (RA) pressure or central venous pressure (CVP) reflects the right ventricular preload.

The PAOP reflects the left ventricular preload.

As preload increases, the SV and CO increases up to a point. Too high preload can lead to heart failure. Preload will seldom be elevated is the heart is disease free and no metabolic abnormalities.

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7
Q

Afterload

A

the pressure (resistance) against which the ventricle must pump to open the valve (pulmonic and aortic).

Clinically measured by the pulmonary vascular resistance (PVR) for the right ventricle or the systemic vascular resistance (SVR) for the left ventricle.

As afterload increases, the SV and CO decrease.

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8
Q

Contractility

A

the contractile force of the myofibrils, independent of preload and afterload.

As contractility increases, the SV and CO increase.

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9
Q

Preload therapies

A

Increases: volume expanders (colloids, crystalloids), pressors

Decreases: diuretics, dilators (nitrates, nitroprusside, nesiritide), morphine

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10
Q

Afterload therapies

A

Increases: norepinephrine, phenylephrine, high-dose dopamine (11-20 mcg/kg/min), epinephrine drip

decreases: nitroprusside, ACE inhibitors, hydralazine, Calcium Channel Blockers, IABP, Nitroglycerin (high dose)

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11
Q

Contractility Therapies

A

Increases: positive inotropes (dobutamine, dopamine 5-10 mcg/kg/min, primacy, epinephrine drip)

Decreases: negative inotropes (beta blockers, CCB), metabolic problems ( ie metabolic acidosis, endotoxins of sepsis)

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12
Q

SvO2 (mixed venous oxygen saturation)

A

normal is 60-75%; the most sensitive indicator of cellular oxygenation

Increased with septic shock, hypothermia, and paralysis
If increased: assess for sepsis, septic shock, assess for hypothermia

Decreased with low cardiac output, decreased PaO2 (d/t the increased demand for O2 with shivering, fever, seizures, and WOB)
If decreased: assess for hypoxemia (increased WOB), assess for hypotension, assess for hypovolemia, assess hemoglobin (drop), assess temperature (fever), assess for arrhythmias

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13
Q

Giant V-waves on the PAOP tracing indicate:

A

acute mitral valve insufficiency

This is often associated with acute inferior wall myocardial infarction/papillary muscle dysfunction/rupture

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14
Q

Square Wave Test (Dynamic Response Test)

A

performed to assess the accuracy of the hemodynamic monitoring system. This is done immediately after insertion, at the beginning of each shift, after zeroing, and whenever values are questionable. Know what it is and the implications of being over- or underdamped.

OVERDAMPED response:
Results in falsely LOW SYSTOLIC pressure and a falsely high diastolic pressure as well as poorly defined components of the tracing such as a diminished or absent dicrotic notch.
May be d/t air or a blood clot in the system, loose connections, loss of air in the pressure bag, or kinking of the catheter/tubing system

UNDERDAMPED response:
Results in a falsely HIGH SYSTOLIC pressure (overshoot), a possible falsely low diastolic pressure, and “ringing” artifacts on the waveform
May be d/t pinpoint air bubbles in the system, add-on tubing, or a defective transducer

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