3. Objectives
 The participant will be able to discuss hemodynamic
definitions (cvp, pa, pcwp, co, ci, svr and pvr) and how
they relate to the respiratory patient.
 •The participant will use critical thinking skills in
assessing changes in respiratory status/ventilation
with changes in hemodynamic status.

4. INDICATIONS FOR HEMODYNAMIC MONITORING
Shock
 Pulmonary edema of uncertain etiology
 Postcardiac surgery
 Cardiac tamponade
 Acute respiratory failure
 Need to evaluate for fluid status/guideline for fluid
resuscitation
 Need to evaluate hemodynamic response to potent
pharmacologic agents
MI
 especially with an acute right or left ventricular failure
 Refractory pain
 Significant hypotension or hypertension

5. Blood pressure
 Blood pressure=CO X SVR
 Changes in blood pressure are caused by either a change in
cardiac output or by systemic vascular resistance
 MAP
Mean arterial pressure=
 SBP + (DBP x 2)= 70-105 mm Hg
3
 The average blood pressure occurring in the aorta and its
major branches during the cardiac cycle

6. Stroke volume: CO ÷HR
The amount of blood ejected by the left ventricle during systole.
N= 60-120 ml/beat
Stroke Index: SV ÷BSA
The SV indexed for differences in body size by dividing by BSA.
N= 30-65 ml/m2/beat
Ejection Fraction:
% of blood in the ventricle that is ejected
during systole. Normally, greater than 50%.

7. SBP + (DBP x 2)= 70-105 mm Hg
3
CHECK YOURSELF
Calculation of Mean Arterial Pressure (MAP)
Blood Pressure = 100/60
MAP = _________________
Blood Pressure = 180/98
MAP=_________________
Blood Pressure = 150/70
MAP = _________________

9. Stroke volume is the volume of blood pumped out of the heart with each heartbeat. If the
stroke volume drops, the body will compensate by increasing the heart rate to maintain
cardiac output. This is known as compensatory tachycardia.
Tachycardia is an effective compensatory mechanism up to a point.
At heart rates greater than 150 bpm, diastolic filling time becomes
so short that the tachycardia itself produces a drop in stroke
volume, and cardiac output can no longer be maintained. Stroke
volume is affected by three factors, preload, afterload, and
contractility.

10. Preload
 Preload is defined as the amount of stretch on the
cardiac myofibril at the end of diastole (when the
ventricle is at its fullest). The amount of stretch is
directly affected by the amount of fluid volume in the
ventricle thus preload is most directly related to fluid
volume.

11. Preload
 As preload (fluid volume) increases, cardiac output will
also increase until the cardiac output levels off.
 If additional fluid is added after this point, cardiac output
begins to fall. This reaction of the heart muscle to stretch
can be likened to a slingshot.
 The same is true of the heart.
 Too little preload and the cardiac output cannot propel
enough blood forward, too much and the heart will
become overwhelmed leading to failure. Just the right
amount of preload produces the best possible cardiac
output; finding this level of preload is called “preload
optimization.”

12. Preload
 How is preload measured? There is not a practical way
to measure myofibril stretch in living beings, nor is
there a widely available method to measure ventricular
end-diastolic volume.
 Physical assessment of preload includes assessment
parameters one would use to evaluate fluid volume
status.

13. Preload
Signs of inadequate preload include :
 poor skin turgor
 dry mucous membranes
 low urine output
 Tachycardia
 Thirst
 weak pulses
 flat neck veins.
 Signs of excess preload in a patient
with adequate cardiac function
include:
 distended neck veins
 crackles in the lungs
 Bounding pulses
 Increased preload in a patient with
poor cardiac function presents with:
 crackles in the lungs
 an S3 heart sound
 low urine output
 Tachycardia
 cold clammy skin with weak pulses,
 edema.
Insufficient preload is commonly called hypovolemia or dehydration.

15. Afterload
 Afterload is defined as the resistance that the ventricle
must overcome to eject its volume of blood. The focus in
this packet is afterload of the left ventricle.
 The most important determinant of afterload is
vascular resistance.
 Other factors affecting afterload include blood:
 viscosity
 aortic compliance
 valvular disease
As arterial vessels constrict, the afterload increases; as they
dilate, afterload decreases.

16. Afterload
 High afterload increases myocardial
 The pulse pressure is calculated by
subtracting the diastolic blood
pressure (DBP) from the systolic
blood pressure (SBP). The normal
work and decreases stroke volume.
Patients with high afterload present
with signs and symptoms of arterial
vasoconstriction including:
pulse pressure at the brachial artery
is 40 mm Hg.
 cool clammy skin
 capillary refill greater than 5
seconds
 narrow pulse pressure.
Pulse Pressure = SBP - DBP
Patients with low afterload present with
symptoms of arterial dilation such as:
• warm flushed skin
• Bounding pulses
• wide pulse pressure.
If the afterload is too low, hypotension may
result.

17. CLINICAL APPLICATION
Afterload
A key component of treatment for heart failure is
afterload reduction using beta-blockers
and ACE inhibitors. By decreasing the resistance to
ventricular ejection the cardiac output
is increased and myocardial workload is decreased. The
increase in cardiac output
frequently improves the functional status of these
patients.

18. Contractility & Compliance
 Contractility is enhanced
by:
 Exercise
 Catecholamines
 positive inotropic drugs
It is decreased by:
 Hypothermia
 Hypoxemia
 Acidosis
 negative inotropic drugs.
 Myocardial compliance refers
to the ventricle’s ability to
stretch to receive a given
volume of blood.
 If compliance is low, small
changes in volume will result
in large changes in pressure
within the ventricle.
 If the ventricle cannot
stretch, it will be unable to
increase cardiac output with
increased preload as
described by the curve.

19. Right Atrial Pressure-RAP














Normal Value 2-8 mm Hg
Clinical Significance: Equivalent to central venous pressure.
Abnormalities:
Increased
–Right ventricular failure, tricuspid valve abnormalities (stenosis or
regurgitation), cardiac tamponade, right ventricular infarct, VSD with a left to right
shunt.
–Pulmonary stenosis, Positive Pressure ventilation
–Pulmonary Hypertension
Active: hypoxemic pulmonary vasoconstriction
Pa02 < 60 mm Hg.
–Pulmonary Embolus
–COPD
–ARDS
Passive:
–Mitral valve dysfunction either stenosis or regurgitation

20. Right Atrial Pressure-RAP
Decreased:
 Hypovolemia
 Anything that vasodilates the body
 Systemic vasodilation
 Septic Shock
 Neurogenic Shock,
 Anaphylactic Shock
 Venous vasodilation
 Nitroglycerin or Morphine

21. Pulmonary Artery Pressure
PAP
 Systolic:
15-30 mm Hg
 Diastolic: 5-12 mm Hg
 Mean:
10-20 mm Hg
 Clinical Significance: PAP is equal to right ventricular
pressure during systole while the pulmonary valve is open.

22. Pulmonary Artery Pressure
PAP
 Abnormalities:
Increased:
 Hypervolemia, VSD with left to right
shunt, Pulmonary HTN, Positive pressure
ventilation, Mitral valve dysfunction
(both), Tamponade,
 Left ventricular failure
Decreased:
 Hypovolemia
 Excessive vasodilation

23. Pulmonary capillary wedge
pressure PCWP
 Normal value 5-12 mm Hg
 Clinical Significance: pcwp is normally equal to left
atrial presure; sensitive indicator of pulmonary
congestion or left sided CHF.
Abnormalities:
 Increased
 Left ventricular failure with resultant pulmonary
congestions, acute mitral
insufficiency, tamponade, decreased left ventricular
compliance (hypertropy, infarction).

24. Pulmonary capillary wedge
pressure PCWP
 Decreased
 –Hypovolemia
 –Vasodilation

25. PCWP

27. Cardiac Output
CO
 Normal Value 4-8 L/min.
 Clinical Significance: CO=SV x heart rate/1000
Abnormalities:
 Increased
 Sympathetic nervous system innervation(stress/exercise)
 Exogenous catecholamines(ie.
epinephrine, dobutrex, dopamine, isuprel)
 Other positive inotrope: digitalis
 Infection, early sepsis
 Hyperthyroidism
 Anemia

28. Cardiac Output
CO
 Decreased
 –Cardiac dysrhythmias, decreased contracting muscle
mass (myocardial infarction, ischemia)
mitralinsufficiency, VSD.
 –Increased SVR (afterload)-systemic or Pulmonary
HTN, Aortic or Pulmonicstenosisor polycythemia
 –Significantly increased or decreased heart rate.
 Either hyper or hypovolemia

29. Cardiac Index
CI
 Value: 2.5-4 L/min.
 Clinical Significance: CI= CO/BSA
Abnormalities:
 Increased:
 high output failure secondary to fluid overload, hepato
cellular failure, renal disease, septic shock
 Decreased:
 hypovolemia, cardiogenicshock, pulmonary
embolism, hypothyroidism, CHF with failing ventricle.

30. Systemic Vascular resistance
SVR
 Normal Value 900-1300 dyne/sec/cm.
 SVR= (MAP-RAP) x 80 /CO•Clinical Significance:
Resistance against which the left ventricle must work
to eject its stroke volume.
Abnormalities:
 Increased:
 Hypervolemic vaso constrictive states
(hypertension, cardiogenic shock, traumatic shock).
 Decreased:
 septic shock, acute renal failure, pregnancy.

31. Remember!
 There is a inverse relationship with CI and SVR.
 •If the CI is UP, the SVR will be DOWN.
 •If the CI is DOWN, the SVR will be UP.

32. Pulmonary Vascular Resistance
PVR
 Normal Value: 150-250 dyne/sec/cm-5.
 •Clinical Significance: PVR=(mPAP-PCWP) x 80/CO.
Abnormalities:
 Increased:
 corpulmonale, pulmonary embolism, valvular heart
disease, CHF.
 Decreased:
 Hypervolemic states, pregnancy