CARDIOVASCULAR PHYSIOLOGY 2ND PART

Dr. O. Ogunlade, MBChB, M.Sc., FWACP

Lecturer/Consultant Cardiologist, Department of Physiological Sciences, Obafemi Awolowo University, Ile-Ife.

JUGULAR VENOUS PULSATIONS AND PRESSURE

Jugular venous pulsations reflect the phasic pressure changes in the right atrium during the cardiac cycle It has three peaks and two troughs The three peaks include; a, c and v waves The two troughs include ; x and y descents

Jugular Venous Pulsations

Denotations of Jugular venous

a wave: represents a rise in right atrial pressure accompanying 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.

Clinical Utility of Jugular Venous Pulsations and Pressure

Jugular venous pulsations can be observed on the right 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 of cardiovascular system examination. Jugular venous pulsations and pressure are important diagnostic parameters in the assessment of cardiovascular diseases such as heart failure

CARDIAC OUTPUT
Cardiac output is the volume of blood pumped out by each ventricle per minute. Cardiac output is the product of the stroke volume and the heart rate CO = SV x HR, SV = Stroke volume, HR = heart rate Stroke 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 of cardiovascular status both in the cardiovascular physiology laboratory and in clinical practice

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

Determinants of Cardiac Output

The major determinants of cardiac output include; 1. Heart rate 2. Preload 3. Afterload 4. Myocardial contractility

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.

Increase in heart rate

Factors that increase heart rate include;
1. 2. 3. 4. 5. 6. Exercise Anxiety Drugs e.g. sympathomimetic drugs Hypovolaemia Hyperthyroidism Heart failure

In all the factors above, there is increase sympathetic system stimulation

Decrease Heart Rate

Factors that decrease heart rate include; 1. Hypothermia 2. Hypothyroidism 3. Beta blocker e.g atenolol, propranolol 4. Well trained athletes 5. Heart blocks

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 the ventricles are directly proportional to the preload. This relationship is illustrated by Frank-Starling Law of heart.

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.

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

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.

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.

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

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 flow and rate at which the oxygen is picked up by the red blood cells. Cardiac output is determined by measurement of the amount of O2 consumed by the body in a given period and dividing this value by the arteriovenous differences across the lung.

Formula for CO Estimation

CO = O2 Consumption (ml/min) AO2 - VO2

AO2- oxygen content of arterial blood VO2-oxygen content of mixed venous blood

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.

Calculation of CO
If O2 consumption is 250ml/min AO2 = 190ml/L VO2 = 140ml/L CO = 250 = 5L/min 190-140

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

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

ECHO Machine

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

Ejection Fraction
Ejection fraction is an index of systolic function It can be estimated from the formula; Ejection Fraction = SV X 100 EDV
Normal Left ventricular ejection fraction: 50-75%

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

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

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 PVR
CO= Cardiac output, PVR = Peripheral Vascular Resistance

Systolic & Diastolic Blood Pressure

Blood pressure is recorded as X/Y mmHg,
where X = Systolic Blood Pressure, Y = Diastolic blood pressure

Systolic blood pressure: maximum arterial pressure during ventricular systole Diastolic blood pressure: minimum arterial pressure during ventricular diastole Normal BP: 120/80mmHg

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

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

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

Methods of Measurement of Blood Pressure

Non-invasive method: indirect methods of BP measurement 1. Palpation method 2. Auscultatory method 3. Oscillometric method Invasive method: direct measurement of BP through intra-arterial line thats connected to pressure sensor

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.

Types of Sphygmomanometer
1. Mercury sphygmomanometer 2. Aneroid sphygmomanometer 3. Digital sphygmomanometer

Mercury Sphygmomanometer

Aneroid Sphygmomanometer

Digital Sphygmomanometer

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, the turbulent flow creates a tapping sound (first Korotkoff sound).

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

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)

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

Classification of Blood Pressure

Class
Hypotension Normal Blood Pressure Prehypertension Stage 1 Hypertension Stage 2 Hypertension SBP (mmHg) <90 90-120 121-139 140-159 160 DBP (mmHg) <60 60-80 81-89 90-99 100

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

Hypertension
Hypertension : sustained elevation of systemic arterial blood pressure The diagnosis of hypertension is made when the blood pressure 140/90mmHg on two or more occasions 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

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 the anatomical 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.

Effects of Cardiac Innervations

Sympathetic stimulation increases heart rate (positive chronotropy),myocardial contractility(positive inotropy and conduction velocity (positive dromotropy), whereas parasympathetic stimulation of the heart has opposite effects. The sympathetic and parasympathetic effects on heart function are mediated by betaadrenoceptors and muscarinic receptors, respectively.

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 and parasympathetic discharge in human, the heart rate becomes 100bpm

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

Mechanisms of BP Regulation
The mechanisms for regulation of blood pressure include; 1. Neural Mechanism 2. Renal mechanism 3. Humoral Mechanism

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

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

Organization of Neural Mechanism

Cortex & Hypothalamus

Baroreceptors

Medulla (Brainstem)

Chemoreceptors

Sympathetic & parasympathetic fibres

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 and chemoreceptors 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

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. Its stimulation causes vasoconstriction. 3. Vasodilator area: the depressor or cardioinhibitory area and is located in the medial portion of vasomotor centre. Its stimulation causes vasodilatation.

Baroreceptors
Baroreceptors are pressure receptor. Types of Baroreceptors
1. Carotic Sinus Baroreceptor:

-situated in the carotid sinus of the internal carotid artery near

the 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

stimulation of carotid sinus baroreceptor Herings nerve stimulation (a branch of glossopharyngeal nerve) stimulation of aortic arch baroreceptor vagus nerve stimulation

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 Normal

NA=nucleus ambiguus, DN=Dorsal nucleus, PVR=peripheral vascular resistance NEURAL MECHANISM OF BLOOD PRESSURE CONTROL

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.

A decrease in BP, decreases blood flow to the organs decrease O2, increase CO2 and H ion conc.

stimulation of chemoreceptors
excitation of vasoconstrictor area

vasoconstriction increase in BP

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

Renin-Angiotensin-Aldosterone System

Angiotensinogen
renin

Angiotensin I
angiontensin converting enzyme (ACE)

Angiotension II

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 which increases 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.

Humoral Mechanisms
Humoral mechanisms refers to regulation by vasoactive substances; hormones and nonhormones. The substances can be classified as vasoconstrictors or vasodilators Vasodilators increases blood pressure while vasodilators decreases blood pressure. The effects of the substances could be systemic or local

Vasoconstrictors
Systemic vasocontrictors include;
Vasopressin, epinephrine, norepinephrine, angiotensin II,urotensin II

Local vasoconstrictors include; serotonin, thromboxane A2, endothelins

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.