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7/27/2019 Lecture in Cardiovascular System Part Two (2)
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CARDIOVASCULAR PHYSIOLOGY
2ND PART
Dr. O. Ogunlade, MBChB, M.Sc., FWACPLecturer/Consultant Cardiologist,
Department of Physiological Sciences,
Obafemi Awolowo University, Ile-Ife.
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Jugular Venous Pulsations
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Denotations of Jugular venous
awave: represents a rise in right atrial pressureaccompanying atrial contraction(systole).
c wave : represents a slight rise in right atrial pressure
associated with closure of tricuspid valve. x descent: represents a fall in right atrial pressure
accompanying atrial relaxation.
v wave : represents a rise in right atrial pressure
accompanying atrial filling during ventricular systole y descent: represents a fall in right atrial pressure
accompanying emptying of blood from the right atrium.
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Clinical Utility of Jugular Venous Pulsations and
Pressure
Jugular venous pulsations can be observed on theright side of the neck
The level of jugular venous pressure can also be
measured non-invasively at bed-side Examination of the jugular venous pulsations and
pressure forms an important integral part ofcardiovascular system examination.
Jugular venous pulsations and pressure are importantdiagnostic parameters in the assessment ofcardiovascular diseases such as heart failure
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CARDIAC OUTPUT
Cardiac output is the volume of blood pumped out by eachventricle per minute.
Cardiac output is the product of the stroke volume and theheart rate
CO = SV x HR, SV = Stroke volume, HR = heart rateStroke volume is the volume of blood pumped out by each
ventricle per beat
Stroke volume 70ml Normal cardiac output in an adult of about 70kg 5L/min
It is an important parameter in the assessment ofcardiovascular status both in the cardiovascular physiologylaboratory and in clinical practice
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Cardiac Index
Cardiac index is the volume of blood
pumped out by each ventricle per minute
per body surface area. Cardiac index = CO/ BSA
BSA body surface area
Normal cardiac index : 2.6-4.2L/min/m2
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Determinants of Cardiac Output
The major determinants of cardiac output
include;
1. Heart rate
2. Preload
3. Afterload
4. Myocardial contractility
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Heart Rate
Heart rate refers to the frequency of cardiac
cycle per minute
Normal heart rate: 60-100beats per minute
There is slight variation in heart rate with state
of activity of individual, however, this may not
alter cardiac out significantly.
A marked increase or decrease in heart rate
may significantly alter the cardiac output.
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Increase in heart rate
Factors that increase heart rate include;
1. Exercise
2. Anxiety
3. Drugs e.g. sympathomimetic drugs
4. Hypovolaemia
5. Hyperthyroidism
6. Heart failure
In all the factors above, there is increase
sympathetic system stimulation
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Decrease Heart Rate
Factors that decrease heart rate include;
1. Hypothermia
2. Hypothyroidism3. Beta blocker e.g atenolol, propranolol
4. Well trained athletes
5. Heart blocks
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Preload
Preload refers to the stretch on myocardial fibres at
the end of diastole.
The degree of stretch of the fibres increases the fibre
length. The fibre length determines the force of myocardial
contractility and volume of cardiac output.
The force of contraction and cardiac output of theventricles are directly proportional to the preload.
This relationship is illustrated by Frank-Starling Law
of heart.
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Frank-Starling Law
Frank-Starling Law states that the force of
contraction of the heart is directly is
proportional to the initial length of myocardial
fibres.
The law was named after the two
physiologists, Otto Frank and Ernest Starling
who first recorded the observation.
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Factors Affecting Preload
Venous return: volume of blood which enters
the heart from different parts of the body.
Venous return is the most important determining factor of
preload. It determines the ventricular filling.
Venous return is aided by muscle pump, respiratory pump,
gravity, sympathetic tone and venous pressure.
Circulating blood volume:
Venous capacitance:which can be altered by
vasocontrictor or vasodilator
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Myocardial Contractility
Myocardial contractility refers to the force and
velocity with which the myocardial fibres
contract.
Its also refers to as inotropy or inotropic state
of myocardium.
It can be assessed in isolated muscle
preparation.
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Afterload
Afterload refers to the force opposing the flow of blood out of
the ventricles during systole.
Its clinically referred to as the systemic vascular resistance.
During the ejection phase of ventricular systole, blood is
ejected into the great vessels(aorta and pulmonary artery)
with resultant rise in the intravascular pressure. For further
ejection , the ventricles have to work against this pressure.
Thus the afterload on the left is determined by the aortic
pressure while on the right by the pulmonary artery pressure.
The force of contraction and the cardiac output of the
ventricles are inversely proportional to the afterload.
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Methods of Measurement of Cardiac Output
Methods of measurement of Cardiac Output could
be invasive and non-invasive.
A. Invasive methods: Methods which involves
penetration of body.1. Direct Fick Method
2. Indicator Dilution Method
B. Non-invasive method: no penetration of the body Echocardiography
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Direct Fick Method
Based on Fick Principle
First described by Adolf E. Fick in 1870 .
This is based on the assumption that the rate of
oxygen consumption is a function of blood flowand rate at which the oxygen is picked up by thered blood cells.
Cardiac output is determined by measurement ofthe amount of O2 consumed by the body in agiven period and dividing this value by thearteriovenous differences across the lung.
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Formula for CO Estimation
CO = O2 Consumption (ml/min)
AO2 - VO2
AO2- oxygen content of arterial bloodVO2-oxygen content of mixed venous blood
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The Procedure
1. O2 consumption per min is measured using a
spirometer and a CO2 absorber
2. Oxygen content of mixed venous blood is
obtained from the pulmonary artery by means
of a cardiac catheter guided into the heart by
fluoroscope.
3. Oxygen content of arterial blood obtained
from a peripheral artery.
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Calculation of CO
If O2 consumption is 250ml/min
AO2 = 190ml/L
VO2 = 140ml/LCO = 250 = 5L/min
190-140
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Indicator Dilution Method
This method utilizes an indicator dye and assumes that the
rate at which the indicator is diluted reflects the cardiac
output.
A known amount of indicator is injected into an arm vein and
its concentration assessed in serial samples of arterial blood.
The cardiac output is equal to the amount of the indicator
injected divided by its average concentration in arterial blood
after a single circulation through the heart.
An example of an indicator dilution method utilizing cold
saline as an indicator is called thermodilution
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Echocardiography
Echocardiography refers to cardiac
ultrasonography
It utilizes ultrasound for cardiac imaging
It is very useful in the study of cardiac
structure and function
Cardiac output can be estimated
non-invasively by through echocardiography
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ECHO Machine
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Estimation of CO using Echo.
SV= EDV- ESV
EDV- end diastolic volume
ESV- end systolic volume
CO = SV x HR
EDV: 120ml , ESV: 50ml, SV: 70ml
at the heart rate of 72bpm,CO = 70 X 72 = 5040ml 5L/min
Ejection Fraction = SV X 100
EDV
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Ejection Fraction
Ejection fraction is an index of systolic
function
It can be estimated from the formula;
Ejection Fraction = SV X 100
EDVNormal Left ventricular ejection fraction: 50-75%
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ARTERIAL PULSE
Arterial pulse refers to the expansive force
palpated at the wall of arteries due to
pressure waves of ventricular systole
propagated within the vessel
The frequency of the pulse is called pulse rate
Normal pulse rate : 60-100beats per minute
Pulse deficit: Heart rate pulse rate
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Aotic Pulse Wave
Concerning the dicrotic notch;
A small oscillation on the falling phase of the pulse wave
Due to vibrations set up by the closure of aortic valve
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BLOOD PRESSURE
Blood Pressure is the force of circulating blood on
the wall of the blood vessels
Systemic arterial blood pressure is the force of
circulating blood on the wall of the systemic arteries In human blood pressure refers to the pressure
measured at the persons upper arm (brachial
artery).
Haemodynamically, Blood Pressure = CO X PVRCO= Cardiac output, PVR = Peripheral Vascular Resistance
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Systolic & Diastolic Blood Pressure
Blood pressure is recorded as X/Y mmHg,
whereX = Systolic Blood Pressure, Y = Diastolic blood pressure
Systolic blood pressure: maximum arterialpressure during ventricular systole
Diastolic blood pressure: minimum arterial
pressure during ventricular diastole
Normal BP: 120/80mmHg
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Pulse Pressure
Pulse Pressure refers to the difference
between the systolic and diastolic blood
pressures
Pulse Pressure = SBP- DBP
If blood pressure = 120/80mmHg,
Pulse pressure ; 120-80mmHg = 40mmHg
Normal range of Pulse Pressure: 40-60mmHg
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Mean Arterial Pressure (MAP)
Mean arterial Pressure (MAP) refers to the
average blood pressure level during the
cardiac cycle
MAP = (CO x PVR ) + CVP
where CO = cardiac output, PVR=peripheral vascular
resistance, CVP= central venous pressure
MAP : 70-110mmHg
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Estimation of MAP
Method 1
MAP = DBP + 1/3 (PP)
If the BP = 120/80mmHg, therefore,
MAP = 80 + 1/3 ( 40) = 93mmHg
Method 2
MAP = (2/3 DBP) + (1/3 SBP)
Method 3
MAP = 2DBP + SBP
3
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Methods of Measurement of
Blood Pressure
Non-invasive method: indirect methods
of BP measurement
1. Palpation method2. Auscultatory method
3. Oscillometric method
Invasive method: direct measurement of
BP through intra-arterial line thats
connected to pressure sensor
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BP Measurement
Palpation Method: by palpation and use of
sphygmomanometer
Auscultatory method: by use of stethoscope
and sphygmomanometer
Oscillometric method: utilizes
sphygmomanometer with special pressure
sensor that detects cuff pressure oscillations.
The result is recorded digitally.
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Types of Sphygmomanometer
1. Mercury sphygmomanometer
2. Aneroid sphygmomanometer
3. Digital sphygmomanometer
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Mercury Sphygmomanometer
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Aneroid Sphygmomanometer
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Digital Sphygmomanometer
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Auscultatory Method Auscultatory method make use of either mercury or
aneroid sphygmomanometer with stethoscope.
An appropriate size inflatable sphygmomanometer
cuff is placed around the arm and then inflated until
the brachial artery is completely occluded While listening with the stethoscope at the elbow,
the examiner slowly releases the pressure in the cuff
When blood just starts to flow in the artery, theturbulent flow creates a tapping sound (first
Korotkoff sound).
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Korotkoff Sounds
Korotkoff Sounds are the sounds that are
heard over the brachial artery when taking
blood pressure using a non-invasive procedure
They are named after Dr. Nikolai Korotkoff, a
Russian physician who described them in 1905
Korotkoff sounds occurs in five phases
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Phases of Korotkoff Sound
Phase I: tapping sound
Phase II: murmur
Phase III: tapping sound
Phase IV: muffling sound
Phase V: silence
Systolic blood pressure is taken to be the pressure at which
the first Korotkoff sound is heard (beginning of phase I) Diastolic blood pressure is the pressure at which the fourth
Korotkoff sound becomes inaudible( phase V)
C i hi h DBP i k
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Cases in which DBP is taken at
Phase IV
Cases in which DBP is taken at phase IV include;
1. Children
2. Pregnancy
3. Hyperthyroidism
4. Aortic Regurgitation
Phase IV should used because there is no phase V
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Classification of Blood Pressure
Class SBP(mmHg)
DBP
(mmHg)
Hypotension
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Factors Affecting Blood
Pressure(BP) Age: BP increases with age
Gender: BP is higher in male than female before the age of
menopause( a female attribute) . After menopause BP of both
gender of same age should be equal.
Posture: In normal individual, rising from supine to erect
position, systolic blood pressure falls while diastolic blood
pressure slightly rises.
Sleep: BP decreases during sleep but may rise during dream
Anxiety: BP rises due to release of sympathomimetic
hormone,adrenaline
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Hypertension
Hypertension : sustained elevation of systemic
arterial blood pressure
The diagnosis of hypertension is made when the
blood pressure 140/90mmHg on two or moreoccasions
Hypertension is one of the major cardiovascular
diseases.
It may results in target organ damage.
Its a major cause of morbidity and mortality in
Nigeria
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Cardiac Innervations
Heart is innervated by vagal and sympathetic fibres.
The right vagus nerve primarily innervates the SA
node, whereas the left vagus innervates the AV node;
however, there can be significant overlap in theanatomical distribution.
Atrial muscle is innervated by vagal efferents,
whereas the ventricular myocardium is only sparsely
innervated by vagal efferents.
Sympathetic efferent nerves are present throughout
the atria and ventricles including the conduction
system of the heart.
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Effects of Cardiac Innervations
Sympathetic stimulation increases heart rate
(positive chronotropy),myocardial
contractility(positiveinotropy and conduction
velocity (positive dromotropy), whereasparasympathetic stimulation of the heart has
opposite effects.
The sympathetic and parasympathetic effectson heart function are mediated by beta-
adrenoceptors and muscarinic receptors,
respectively.
Eff t f Bl k d f C di
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Effects of Blockade of Cardiac
Innervation
Blockade of parasympathetic discharge to the
heart, heart rate increases from approximately
72bpm to about 150-180bpm because of
unopposed action of sympathetic tone.
This implies that the resting heart rate is
maintained by the parasympathetic system.
Blockade of both sympathetic andparasympathetic discharge in human, the
heart rate becomes 100bpm
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BLOOD PRESSURE REGULATION
The blood pressure is regulated in such a way
to maintain the value within the normal range.
Failure of the regulatory mechanism may
results in alteration in blood pressure
Blood pressure above or below normal range
is counterproductive to the cardiovascular
systems and other vital systems in the body
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Mechanisms of BP Regulation
The mechanisms for regulation of blood
pressure include;
1. Neural Mechanism
2. Renal mechanism
3. Humoral Mechanism
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Neural Mechanism
Neural mechanism refers to regulation of the
blood pressure by the nervous system
The neural mechanism is for short term blood
pressure control
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Components of the Neural Mechanisms
Brain
Cortex & Hypothalamus
Brain stem: Medulla
Receptors Baroreceptors-carotid sinus & aortic arch
Chemoreceptors-carotid body & aortic body
Autonomic nerves Sympathetic fibres
Parasympathetic fibres
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Organization of Neural Mechanism
Cortex & Hypothalamus
Baroreceptors Medulla Chemoreceptors(Brainstem)
Sympathetic & parasympathetic fibres
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Neural Mechanism
The medulla in the brainstem is the primary site in the brain
for regulating sympathetic and parasympathetic (vagal)
outflow to the heart and blood vessels.
The medulla contains nucleus of tractus solitarius (NTS)
which receives sensory input from baroreceptors andchemoreceptors
The medulla also receives information from other brain
regions e.g cortex and hypothalamus to modulate blood
pressure Autonomic outflow from the medulla is divided principally
into sympathetic and parasympathetic (vagal) branches which
innervates the heart and blood vessels
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Medulla-Vasomotor Centre
The vasomotor centre is located in the medulla
It consists of three areas; sensory, vasoconstrictor and
vasodilator areas.
1. Sensory area : nucleus of tractus solitarius/solitary tract which
inhibits/stimulates the vasocontrictor or vasodilator area
depending on blood pressure signal received from the
baroreceptors or chemoreceptors.
2. Vasoconstrictor area: the pressor or cardioaccelerator area
and is located in the lateral portion of vasomotor centre. Itsstimulation causes vasoconstriction.
3. Vasodilator area: the depressor or cardioinhibitory area and is
located in the medial portion of vasomotor centre. Its
stimulation causes vasodilatation.
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Baroreceptors
Baroreceptors are pressure receptor.
Types of Baroreceptors
1. Carotic Sinus Baroreceptor:
-situated in the carotid sinus of the internal carotid artery nearthe bifurcation of the common carotid artery.
-Innervated by Herings nerve, a branch of glossopharyngeal
nerve
2. Aortic Baroreceptor
- situated in the wall of the arch of aorta
- innervated by aortic branch of vagus nerve
Increase in Blood Pressure
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stimulation of carotid sinus stimulation of aortic arch
baroreceptor baroreceptor
Herings nerve stimulation vagus nerve stimulation(a branch of glossopharyngeal nerve)
Nucleus of Tractus Solitarius(NTS)
vasoconstrictor area - + vasodilator area,NA &DN
decreases vasomotor tone increases vagal discharge
vasodilation decreases HR and myocardial contractility
decreases PVR decrease in cardiac output
Blood Pressure Returns to NormalNA=nucleus ambiguus, DN=Dorsal nucleus, PVR=peripheral vascular resistance
NEURAL MECHANISM OF BLOOD PRESSURE CONTROL
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Chemoreceptors
Chemoreceptors are receptors located in the carotid
body and aortic body.
They are sensitive to the changes in the blood
constituents. Chemoreceptors in the carotid body are supplied by
glossopharyngeal nerve
Chemoreceptors in the aortic body are supplied by
vagus nerve
Chemoreceptors are sensitive to hypoxia,
hypercapnia and increase in hydrogen ion conc.
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A decrease in BP, decreases
blood flow to the organs
decrease O2, increase CO2 andH ion conc.
stimulation of chemoreceptors
excitation of vasoconstrictor area
vasoconstriction
increase in BP
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RENAL MECHANISM
Renal mechanism refers to the role of the
kidneys in blood pressure control
Its for a long term blood pressure control The renal mechanism involves the
renin-angiotensin-aldosterone system
(RAAS) and blood volume regulation
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Renin-Angiotensin-Aldosterone System
Angiotensinogen
renin
Angiotensin Iangiontensin
convertingenzyme (ACE)
Angiotension II
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Renal control of Blood Pressure
A decrease in blood pressure, ECC volume or plasma
sodium level stimulates RAAS which mainly produce
angiotensin II.
Angiotensin II causes vasoconstriction whichincreases peripheral vascular resistance.
It stimulates aldosterone release from adrenal cortex
and aldosterone causes salt and water retention,
thereby increasing blood volume.
When Blood Pressure is elevated above normal due
to fluid overload, the kidney excretes more salt and
water to low the blood pressure.
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Humoral Mechanisms
Humoral mechanisms refers to regulation by
vasoactive substances; hormones and non-
hormones.
The substances can be classified asvasoconstrictors or vasodilators
Vasodilators increases blood pressure while
vasodilators decreases blood pressure.
The effects of the substances could be
systemic or local
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Vasoconstrictors
Systemic vasocontrictors include;Vasopressin, epinephrine, norepinephrine,
angiotensin II,urotensin II
Local vasoconstrictors include;
serotonin, thromboxane A2, endothelins
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Vasodilators
Systemic vasodilators include;
kinins, Vasoactive intestinal peptide(VIP),
atrial natriuretic peptide(ANP) ,Brain
natriutretic peptide (BNP)
Local vasodilator include; histamine,
adenosine, lactate, prostacyclin, nitric oxide,
decrease PaO2, decrease PH, increase PaCO2.