lecture in cardiovascular system part two (2)

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.

lecture in cardiovascular system part two (2)

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