Cardiac Output, Venous Return &

Control Part 2
Original Lecture Written By:
John Chin, MD
Modified 3/29/2017 By:
Rudolph Holguin, MD
Associate Professor Of Emergency Medicine

1
Control of Cardiac Output

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Factors Affecting Cardiac Output

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Factors Affecting Cardiac Output

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Factors Affecting Cardiac Output

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Regulation of stroke Volume: Preload

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Regulation of stroke Volume: Contractility

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 Ejection Fraction (EF)
Normal Values:
50-55% and more
Increase due to
sympathetic
stimulation and other
inotropic action

Measurement:
Most commonly by
Echocardiography
EF= SV/EDV
SV: Systolic Volume
EDV: End diastolic Volume
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 Patient with Hypotension

Hypovolemia Cardiogenic Vasogenic

Low CVP High CVP Low CVP

Low CI Low CI High CI
High SVR High SVRI Low SVRI

Tx: Consider Tx: Consider Tx: Consider

fluid challenge
inotropes/ IABP Vasopressor

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 Pulmonary Artery Catheter (PAC)
PAC Can generate large numbers of hemodynamic variables
Central venous pressure (CVP)
Pulmonary arterial occlusion pressure (PAOP)
= LAP = LVEDP
Cardiac output/ Cardiac index (CO/CI) By Thermodilution

Stroke Volume (SV)

RV ejection fraction/End diastolic volume (RVEF/RVEDV)
Systemic Vascular resistance Index (SVRI)
Pulmonary Vascular resistance Index (PVRI)
Oxygen delivery/ uptake (DO2/VO2)
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Swan Ganz Catheter

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Swan Ganz Catheter

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Swan Ganz Catheter

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Invasive Hemodynamic Monitoring

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Pulmonary Artery Waveforms during Insertion

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Pulmonary Artery Waveforms during Insertion

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 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): 2-8 mm Hg (also known as Right Atrial
Pressure (RA)
Pulmonary Artery Pressure (PA): Mean 15-25 mm Hg
Systolic 20-30 mm Hg (PAS)
Diastolic 4-12 mm Hg (PAD)
Pulmonary Capillary Wedge Pressure (PWCP): 6-12 mm Hg
Systemic Vascular Resistance (SVR): 800-1200 dyn.s/cm5
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 Central Venous Pressure (CVP)
CVP monitors systemic volume filling
Indirectly indicates the efficiency of the hearts pumping action (EDP RV, if no
tricuspid stenosis)
Decrease due to hypovolemia
Increases due to:
Hypervolemia
Right heart failure
Tricuspid stenosis

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 Right Atrial Pressure
Regulated by a balance between the ability of the heart to pump
blood out of the atrium and the rate of blood flowing into the atrium
from peripheral veins
Factors that increase RAP:
Increase blood volume
Increased venous tone
Dilation of the arterioles
Decrease cardiac function

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 Right Atrial Pressure Monitoring
Waveform Analysis
a wave: rise in pressure due to atrial contraction
x decent: fall in pressure due to atrial relaxation
c wave: rise in pressure due to ventricular contraction and closure of the tricuspid
valve
v wave: rise in pressure during atrial filling
y decent: fall in pressure due to opening of the tricuspid valve and onset of
ventricular filling

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 Right Atrial Pressure Monitoring
Waveform Analysis
Elevated RAP
RV failure
Tricuspid regurgitation
Tricuspid stenosis
Pulmonary hypertension
Hypervolemia
Cardiac tamponade
Chronic LV failure
Ventricular Septal Defect
Constrictive pericarditis

Decreased RAP
Hypovolemia
Increased contractility

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 Elevated Pulmonary Artery Pressure
mechanical obstruction of pulmonary circulation
pulmonary arteriolar smooth muscle hypertrophy
inflammatory response to CPB
mechanical obstruction of the airways (for examples)
acidosis and hypoxia
elevated LA pressure
unrestrictive VSD or large PDA
pulmonary hypertension

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 Elevated Left Atrial Pressure
Elevated systemic ventricular end diastolic pressure
mitral valve disease
Large left-to-right shunt
intravascular volume overload
cardiac tamponade
tachyarrhythmia

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 Reduced Left Atrial Pressure

low intravascular fluid status

Inadequate preload

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Summary

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 Mixed Venous Saturation Sv02
(Normal Sv02 70-75%)

Decreased SvO2 Increased SvO2

increased consumption
Increased delivery
high CO
pain, hyperthermia
hyperbaric O2
decreased delivery
Low consumption
low CO
sedation
anemia
paralysis
hypoxia
cyanide toxicity

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 Left Ventricular Cardiac Cycle
1. The LV pressure begins to rise after the QRS
wave of the ECG
2. Pressure rises until the LV pressure exceeds
ECG
the aortic pressure (the blood begins to move
from the ventricle to the aorta)
3. As blood enters the Aorta, the aortic pressure
begins to rise to form the systolic pulse
4. As the LV pressure falls in late systole the
aortic pressure falls until the LV pressure is
below the aortic diastolic pressure
5. Then the aortic valve closes and LV pressure
falls to LA pressure.
A V
The first wave of atrial pressure (the A wave) is due to atrial contraction
The second wave of atrial pressure (the V wave) is due to ventricular
contraction

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Left Ventricular Cardiac Cycle

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 Pressures in Heart Valve Disease
Mitral Stenosis

Simultaneous recording of pressures in the

pulmonary artery wedge position (PAW) and
the left ventricle (LV)
large gradient in diastole across the mitral
valve. The PAW pressure is markedly elevated.
Increased pressure in LA improves diastolic
flow to LV, LA hypertrophies etc.
Increased PAW may lead to pulmonary edema

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 Pressures in Heart Valve Disease
Mitral Regurgitation

increase of pressure in LA
during ventricle
contraction(part of the blood
returns to the atrium)
LA dilation and hypertrophy

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 Pressures in Heart Valve Disease
Aortic Stenosis
AS produces a pressure gradient between the
aorta and LV
For blood to move rapidly through a narrowed
aortic valve orifice, the pressure must be higher in Ventricular
Pressure
the ventricle
The severity of AS is determined by the pressure
drop across the aortic valve or by the aortic valve
area Aortic
Pressure

The high velocity of blood flow through the

narrowed valve causes turbulence and a
characteristic murmur AS can be diagnosed with a Left atrial
stethoscope Pressure

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 Pressures in Heart Valve Disease
Aortic Stenosis

(a) Systolic pressure gradient (left

ventricular-aortic pressure) across
a stenotic aortic valve.

(b) (b) Marked decrease in systolic

pressure gradient with insertion of
an aortic ball valve.

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