Cardiovascular Physiology

DR.DEEPAK SOLANKI M.D. ANAESTHESIA dr.dsolanki@gmail.com

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Cardiovascular system (CVS)

CVS consists of the heart and a series of blood vessels (arteries, veins and capillaries).

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CVS

Function: Homeostasis through:

Generate blood pressure.

Ensuring one way blood flow.

Regulating blood supply.

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Parts of the circulatory system

The circulatory system forms two circuits in series with each other:-

- Systemic circulation (greater circulation) - Pulmonary circulation (lesser circulation)

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The Normal Heart and Regional Circulation

Lungs

Pulmonary Semilunar Valve Superior Vena Cava

Aorta Left Pulmonary Artery Left Pulmonary Veins

Left Atrium

Right Pulmonary Artery Right Pulmonary Veins Tricuspid Valve

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Aortic Semilunar Valve Bicuspid or Mitral Valve

Inferior Vena Cava

Septum

The Systemic Circulation

Veins (Flexible Compliant Pipes)

Brain

Lungs

Arteries (Stiff Inflexible Pipes) Precapillary Sphincters

Liver Stomach Pancreas Intestines Kidneys Arterioles Skin

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Muscle

Systemic and pulmonary circulations

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Location
Heart is located in thoracic cavity in the mediastinum, between the lungs. The heart lies obliquely in the mediastinum with its base directed posteriorly and slightly superiorly and the apex directed anteriorly and slightly inferiorly. The apex is also directed to the left so that approximately 2/3 of the heart mass lies to the left of midline. The base of the heart is deep to the sternum and extends to the 2nd intercostal space. The apex is approximately 9 cm. to the left of the sternum and is deep to the fifth intercostal space.

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Pericardium
Pericardium: a double layered closed sac that surrounds the heart: 1Fibrous pericardium: outer layer, tough, fibrous connective tissue. Prevents over distension of the heart and anchors it within the mediastinum. Superiorly it is continuous with the connective tissue of the great vessels, and inferiorly attached to the surface of the diaphragm. 2- Serous pericardium: thin transparent inner layer.

Parietal pericardium: part of the serous pericardium that lines the fibrous pericardium. Visceral pericardium: part of the serous pericardium that covers the heart surface.

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Pericardial cavity: between the parietal and visceral pericardium is filled with a thin layer of serous Pericardial fluid: reduces friction of the beating heart.
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Heart Wall Epicardium: thin serous membrane of the outer surface of the heart. Also called the visceral pericardium Myocardium: thick middle layer composed of cardiac muscle. Endocardium: simple squamous epithelium over a layer of connective tissue, continuous with all blood vessels of the body.
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Heart Anatomy
The heart is a strong muscular pump that contracts and relaxes all life. It is the size of the fist of the hand. It is formed of 4 chambers:

Two thin walled low pressure reservoirs, the atria and two thick walled pumping chambers, the

ventricles.

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Functional anatomy of the heart

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Heart beat

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Heart valves Tricuspid valve: 3 cusps, between the right atrium and right ventricle. Bicuspid valve: two cusps, between the left atrium and left ventricle, also known as the mitral valve. Semilunar valves: Consists of three pocket like semilunar cusps, the free inner borders meet in the middle of the artery to block retrograde flow. Aortic valve: between the left ventricle and the aorta. Pulmonary valve: between the right ventricle and the pulmonary artery.

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Heart valves

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A V and Semilunar Valves

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Innervations of heart autonomic nerve supply: 1- Sympathetic: increase activity of whole heart. (increase heart rate and contractility) 2- Parasympathetic: comes through vagus nerve and decrease activity of atria only. (decrease heart rate)

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Autonomic Innervations of the heart

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Mammalian Heart

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THE CARDIAC MUSCLE

Cardiac muscle is formed of myocardial muscle fibers which are elongated branched nucleated cells, the ends of which are joined together by intercalated discs, forming a network. The intercalated discs contain gap junctions which have low electric resistance and allow free diffusion of ions. Thus, excitation in one area spreads throughout the heart.
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 This permits the cardiac muscle to contract as a whole as if it is made of a single muscle cell or as a functional syncytium. The heart is composed of 2 functional syncytia: ATRIA AND VENTRICLES.

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THE CARDIAC MUSCLE

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GAP JUNCTIONS

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PROPRTIES OF CARDIAC MUSCLE

1- EXCITABILITY 2- CONTRACTILITY 3- RHYTHMICITY 4- CONDUCTIVITY
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1- EXCITABILITY
Definition: Excitability is the ability of the cardiac muscle to respond to a stimulus by generating an action potential followed by a contraction. Cardiac muscle resting membrane potential and action potential differ in different parts of the heart.

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Cardiac Action Potentials

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THE A.P. OF THE VENTRICLES

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PHASES OF VENTRICULAR A.P.

- Phase 0: Initial rapid depolarization. - Phase 1: Brief initial repolarization. - Phase 2: Prolonged plateau. - Phase 3: Late rapid repolarization. - Phase 4: Resting membrane potential (-100 mv)

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IONIC BASIS OF VENTRICULAR ACTION POTENTIAL

Phase 0: Initial rapid depolarization: due to Na+ inflow due to opening of fast Na+ channels. Phase 1: Brief initial repolarization: due to opening of transient K+ channels. Phase 2: Prolonged plateau: due to opening of slow Ca++ - Na+ channels.( A balance is created between influx of Na+ and Ca+ and outflux of K+) Phase 3: Late rapid repolarization: due to delayed opening of K+ channels. Phase 4: Resting membrane potential ( -100 mv)
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LONG REFRACTORY PERIOD

Cardiac muscle action potential differs from skeletal muscle action potential. Cardiac action potential is characterized by A LONG REFRACTORY PERIODdue to the plateau phase, during which the heart cannot be restimulated. The action potential results in a mechanical response: contraction (systole) followed by relaxation (diastole).
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Action Potential and Mechanical Response Cardiac Muscle Skeletal Muscle

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NON TETANIZING PROPERTY

The cardiac muscle has a long refractory period (due to plateau phase), which coincides with the whole period of systole. Thus the heart remains non excitable for the entire contraction phase. This ensures that the heart cannot go into a sustained state of contraction (tetanus) which could lead to stopping of circulation.
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2- CONTRACTILITY
Definition: It is the ability of the cardiac muscle to contract to pump blood. The heart is a strong muscular pump that contracts and relaxes all the time day and night, and its cessation means death. There are two types of muscle contraction: a- Isometric contraction: increase muscle tension without shortening (e.g. during early systole) b- Isotonic contraction: Tension is constant but muscle shortens and work is done (e.g. during late systole when blood is ejected)
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CONTRACTILITY (cont)
The cardiac contractility obeys two laws: ALL OR NONE LAW: If other conditions are constant, the cardiac muscle either contracts maximally ( if the stimulus is adequate) or does not contract at all ( if the stimulus is inadequate)
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CONTRACTILITY (cont)
STARLINGs LAW: [LENGTH-TENSION RELATIONSHIP]
The ability of the cardiac muscle to generate force, is dependent on the initial length of the muscle prior to contraction, i.e. end diastolic volume (EDV). The greater the initial length of the muscle fibers, the greater the force of contraction (within limits).

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Application of STARLING LAW

If the amount of blood returning to the heart increases (i.e.venous return) this will stretch the cardiac muscle fibers, i.e. increase its length at end of diastole (EDV: end diastolic volume ) increase the force of contraction at systole increase stroke volume. [ Thus, the heart will pump out whatever volume is delivered to it]
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3- RHYTHMICITY
Definition: It is the ability of the cardiac muscle to initiate its own regular impulses (rhythm), independent of any nerve supply. Cause: The cardiac muscle has a specialized excitatory conductive system, which have the property of auto rhythmicity. Rate of autorhythmicity: SA Node: 70-80 beats/min AV Node: 40-60 beats/min Bundle of His: 30 beats /min Purkinje fibers: 15 beats/min (incompatible with life)
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Excitatory Conductive system

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PACEMAKER OF THE HEART

The area which determines the pace or rhythm of the heart is called the pacemaker of the heart. The SA Node is the pacemaker of the heart because: 1- it has the highest rhythm 2- and the whole heart obeys it. If the SA Node is destroyed, the AV Node will be pacemaker. VAGAL TONE: It is the continuous impulses in the vagus nerve which decrease the inherent high rhythm of the SA Node from 90-100/min to 7080/min (the normal heart rate)
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PACEMAKER POTENTIAL
Pacemaker cells have unique electric properties:
Prepotential: Unstable membrane potential due to slow continuous leakage of Na+ ions into the myocardium leads to: spontaneous diastolic depolarization. After reaching firing level, the next action potential follows automatically. No plateau is seen. 06/12/11

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HEART RATE is determined by

pacemaker activity of the heart (70-80/min)
Variations in heart rate: 1- Tachycardia (Increase HR) : sympathetic stimulation as in emotions, exercise, hyperthyroidism. 2- Bradycardia (decrease HR) : parasympathetic stimulation as in sleep, hypothyroidism.
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4- CONDUCTIVITY
Definition: It is the ability of the cardiac muscle to conduct or transmit an action potential over the whole heart along specialized conducting system having high conduction velocities. Velocity of conduction: SA Node: 1 m/sec AV Node: 0.05 m/sec Bundle of His: 1 m/sec Purkinje fibers: 4 m/sec
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Conduction Velocity in heart

m/sec 1 1m/sec

m/sec 4 m/sec 0.05

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PROPAGATION OF CARDIAC IMPULSE

Cardiac impulse is initiated by SA Node. It spreads through atria in internodal tissue at a rapid rate to reach AV Node. The conduction velocity slows down in AV Node which is known as AV Nodal delay. This delay is important as it gives time for proper ventricular filling. The wave then travels rapidly down the AV bundle, bundle branches and Purkinje fibers to all parts of the ventricles. The fastest conductivity in Purkinje fibers is important as it excites the whole ventricle as one unit leading to powerful ventricular contraction. Block in transmission of impulse is heart block
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THE CARDIAC CYCLE

Definition: The cyclic events that occur in the heart chambers during each beat. As the normal heart rate is 70 beat/min, the duration of each cardiac cycle is 60/70 = 0.8 sec Each cardiac cycle includes: Atrial systole Ventricular systole Diastole of whole heart. Blood flow in the heart is determined by pressure difference across the orifices of the heart which leads to opening and closure of valves. First and second heart sounds are due to closure of AV and semilunar valves respectively.
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STROKE VOLUME
STROKE VOLUME: is the volume of blood ejected by each ventricle per beat. = End diastolic volume - End systolic volume = 120-50= 70 ml
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CARDIAC OUTPUT
Cardiac output is the volume of blood ejected by each ventricle / min = Stroke volume x Heart rate = 70 x 70 = 5 liter/min

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PHASES OF CARDIAC CYCLE I- SYSTOLE

Atrial systole: [SA Node depolarization] The atria contract propelling the last 30% of its blood into ventricles. Ventricular Systole: [Depolarization of ventricles] 1- Isometric Contraction Phase: - Ventricular pressure>atrial pressureAV valves close. - Now ventricles contract as a closed chamber (all valves are closed) - No change in volume but pressure increase. 2- Ventricular Ejection Phase: - Ventricular pressure> aortic and pulmonary pressure semilunar valves open. - Now blood gushes out of ventricles into aorta and pulmonary vessels

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PHASES OF CARDIAC CYCLE II- DIASTOLE

Ventricular Diastole: [Repolarization of ventricles] 1- Isometric Relaxation Phase: - When ventricular pressure < aortic and pulmonary artery pressure Semilunar valves close. - Now ventricles relax as a closed chamber (with all valves closed) - No change in volume but pressure decrease. 2- Ventricular Filling Phase: - Ventricular pressure<atrial pressure AV valves open. - Now ventricles start to fill with blood from atria. - First 30% (rapid filling), mid 30% ( reduced filling or 06/12/11 61 diastasis), last 30% (atrial systole)

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SYSTOLE

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DIASTOLE

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ECG

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ECG Recording

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ECG Intervals and Segments

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Normal ECG Record

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ECG Leads

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ECG LEADS

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Normal ECG Recording

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ECG Abnormalities

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HEART SOUNDS

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 CARDIAC MUSCLE CELLS Elongated branching cells with one or two centrally located nuclei. Striated Intercalated discs Desmosomes Gap Junctions Autorhythmicity - cardiac muscle has the ability to depolarize spontaneously. only 1% of the cells have this ability
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Cardiac muscle

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Intercalated discs

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CONDUCTION SYSTEM
Sinoatrial node (SA Node): is medial to the opening of the superior vena cava. Action potentials originate here and travel across the wall of the atrium to the atrioventricular node (AV Node) located medial to the right atrioventricular valve. Action potentials pass through the AV node and along the atrioventricular bundle, which extends from the AV node into the interventricular septum.
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 The AV bundle divides into right and left bundle branches, the action potential descends to the apex of the heart along the bundle branches. Action potentials are carried by Purkinje fibers from the bundle branches up along the ventricular walls.

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The cardiac conduction system

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CONDUCTION SYSTEM

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On the left, the action potential of a contractile cell. On the right is the action potential of an autorhythmic cell

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Ionic changes in autorhythmic cells

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Ionic changes in ventricular muscle

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Heart sounds

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Mitral Area
located about the apex beat, which is usually in the fifth intercostal space. It is also called the apical, or the left ventricular area. The systolic murmur of Mitral Regurgitation and the diastolic murmurs of Mitral Stenosis and Increased Valvular Flow.
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Tricuspid Area
located at the lower left sternal border (LLSB). The diastolic murmur of Tricuspid Stenosis.

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Pulmonary Area
located in the second intercostal space at the left sternal border. The systolic murmur of Pulmonic Stenosis and the diastolic murmur of Pulmonic Regurgitation.
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Aortic Area
located in the second intercostal space at the right sternal margin. The systolic murmurs of Aortic Stenosis and Increased Aortic Valve flow.

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Electrocardiography (ECG)
It is a recording of electrical activity of the cardiac muscle from the surface of the skin of the thoracic cage where the body fluid act as a good conductor from cardiac muscle to electrodes placed on the skin.. The electrical activity proceed the heart contraction.
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Basis of the ECG

When the excitation wave begins to spread in the heart. The surface of the cells in the heart depolarized and becomes negative in relative to the surrounding region. Thus there are two areas in the heart one excited and the other is notexcited, and both of them act as two terminals of the battery, one negative and the other is positive. This generates an electrical field throughout the body fluid.
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Basis of the ECG

The electrical activity of the heart starts at the SAN then spread to the both atria and then to the both ventricles and the surrounding tissues. ECG is used to evaluate some heart problems such as arrhythmias, ischemia, necrosisand hypertrophy of the heart.
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 The used apparatus for recording called electrocardiograph which has an electrode placed on the skin and the recording obtained from a specific point called (a lead), the standard ECG has 12 different leads that record the same electric events but from different views. The leads are of 3 types:Bipolar limb leads. Unipolar leads. Augmented unipolar leads.
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Bipolar limb leads:

These leads measure the potential difference between 2 limbs by applying active electrodes from ECG apparatus anywhere on the limbs (wrist or ankle). 3 different leads are recorded: Lead I: It measures the potential difference between the left arm (LA) and right arm (RA). Lead II: It measures the potential difference between the left (LL) and right arm (RA). Lead III: It measures the potential difference between the left leg (LL) and left arm (LA).

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Unipolar leads:
These measure the absolute (actual) potential at a certain point. This is done by applying one electrode from electrocardiograph to the desired point while the other electrode is made indifference (-ve), this means that the unipolar leads measures the potential difference between active potential and zero potential.
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Unipolar limb leads: It measures the absolute potential at right arm (VR), left arm (VL) and left leg (VF). Unipolar (V) leads: It measures the absolute potential at 6 standard points on the anterior chest wall (V1, V2, V3, V4, V5 andV6).
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V1: At right margin of the sternum in the 4th intercostals space. V2: At left margin of the sternum in the 4th intercostals space. V3: Midway between V2 and V4. V4: At the left midclavicular line in the 5th intercostals space. V5: At the left anterior axillary line at the 5th intercostals space. V6: At the left mid axillary line at the 5th intercostals space.
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Augmented Unipolar limb Leads: In this case there is magnification of amplitudes by about 50%. The leads called aVR, aVL and aVF, where a= augmented. The augmented leads are easier to interpret and recorded by ECG machines.
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Normal ECG
Normal ECG consists of 5 main waves called P Q R S T waves. These waves are separated by segments. Each waves start and ends at the isoelectric line. The QRS waves from a complex called QRS complex. This normal ECG can be recorded in aVl, aVF, V5 and V6 because the exploring electrode faces the left ventricle.

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ECG

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ECG Components Diagram

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The P wave Represents atrial activation (atrial depolarization). Small +ve wave. Its amplitude 0.1 (up to 0.25) mv. Its duration 0.08 (up t0 0.11) seconds.

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Abnormalities of P- wave
In left atrial hypertrophy (due to mitral stenosis), the P wave become broad and notched. In right atrial hypertrophy (due to pulmonary hypertension) P wave become tall. In AV nodal rhythm: P wave inverted. In atrial fibrillation: P wave disappear.
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The QRS complex

Represents ventricular activation (depolarization). The QRS duration is the duration of ventricular activation (0.06-0.1). Q wave: is ve wave due to depolarization of interventricular septum. R wave: is a large +ve wave, its amplitude is 10 mm (1 mv), caused by depolarization of the apex and ventricular wall, it is + ve wave. S wave: is a ve wave, caused by depolarization of the posterobasal part of the left ventricle and pulmonary conus.
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Abnormalities of QRS complex In ventricular hypertrophy. Infarction. Extrasystole. Bundle branch block. Electrolyte disturbance.

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T wave
It is a +ve large blunt wave. Represents ventricular activation (ventricular repolarization). Its amplitude 0.2 (up to 0.4) mv. Its duration 0.2 (up to 0.25) second.

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Abnormalities of T wave
Inverted:
Myocardial infraction. Ventricular hypertrophy. Extrasystole. Bundle branch block. Digitals overdosage.

Increase amplitude:
Sympathetic overactivity. Muscular exercise. Hyperkalmia.

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ECG Intervals and Segments

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P-R interval
- From the start of P-wave to the start of R wave. - Its range from 0.12 to 0.21 second. - It means conduction of cardiac impulse through A-V node. Abnormalities of P-R interval: 1- Prolonged: - First degree of heart block. - Increased vagal tone. 2 - Shortened: - A- V nodal rhythm. - Sympathetic overactivity. - Wolff- Parkinson- white syndrome.
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Q-T interval
Start from the onset of Q wave to the end of T wave. Its duration 0.36- 0.24 second. It is called electrical systole of the heart. T- Q interval: Start from the end of the T wave to the onset of the next Q wave. It is called electrical diastole. Its duration is about 0-4 second. Abnormalities of T-Q interval: It is shortened before atrial and ventricular extrasystole. It is prolonged after ventricular extrasystole.

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S-T segment
- Start from the end of S wave to start of T wave. Its duration is about 0.12. Abnormalities of S-T segment: Its deviation upward or downward indicates myocardial damage.

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ECG changes in myocardial infraction

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The Normal Heart - Coronary Artery Anatomy

Left Main CA Layers of the Arterial Wall Circumflex

Adventitia
Right CA Left Anterior Descending CA
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Media Intima
Marginal Branch

Intima composed of endothelial cells 125

Left Ventricular Volumes - Definitions

End Diastolic Volume (EDV)
Volume at the end of diastole (end of ventricular filling)

End Systolic Volume (ESV)

Volume at the end of systole (end of ventricular contraction)

Stroke Volume (SV) = EDV - ESV Ejection Fraction(EF) = SV EDV

Left ventricular norm for EF: 62%

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Ejection Fraction is the best indicator of heart performance and disease prognosis 126

Changes in Ventricular Volumes with Exercise

120 110 100 90 80 Left Ventricular 70 Volume (ml) 60 50 40 30 20 10 Rest
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LVEDV

LVEDV - LVESV = SV

SV

LVESV

300

600 - 750

Kg meters / min

Peak Exercise

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Definitions

Cardiac Output: (Q) = HR X SV Cardiac Index = Q / body surface area Preload: (EDV)volume of the left ventricle at the end of diastole Afterload: resistance to ventricular emptying during systole Frank Starling Law of the Heart:

(dependent on venous return & stretch of the cardiac muscle cells) (the amount of pressure the left ventricle must generate to squeeze blood into the aorta)

the heart will contract with greater force when preload (EDV) is increased

Myocardial Contractility: the squeezing contractile force that the heart

can develop at a given preload

regulated by: sympathetic nerve activity (most influential) catecholamines (epinephrine norepinephrine) amount of contractile mass drugs

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Starlings Law of the Heart and Contractility

SV
(left ventricular performance)

u contractility normal contractility

d contractility (heart failure)

Preload
(venous return)
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Influences on Myocardial Contractility

u Contractility related to :
b sympathetic adrenergic nerves catecholamines: - epinephrine - norepinephrine drugs: - digitalis - sympathomimetics

d Contractility related to:

- loss of contractile mass (may be due to heart attack) - myocardial muscle disease (cardiomyopathy) - drugs (anesthetics, barbiturates)
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Definitions

Arteriovenous Oxygen Difference (AVO2D)

energy production and metabolism

the difference in oxygen

content between arterial and venous blood- ml O / 100 ml blood 2 measured in ml%

Oxygen Consumption (VO2) - the rate at which oxygen can be used in

absolute measures: L O2 / min , ml O2 / min relative measures: ml O2 / kg body wt. / min Fick equation: VO2 = Q X AVO2D defined as plateau of consumption rate increase often estimated with VO2peak

Maximum Oxygen Consumption (VO2max ) maximum rate at which a

person can take in and utilize oxygen to create usable energy heart Myocardial Oxygen Consumption VO2 of the X SBPmuscle (myocardium) "estimated" by RPP: HR Aerobic Impairment: FunctionalVO - attained VO predicted
2m ax 2m ax

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mild moderate marked severe >

27% - 40% 41% - 54% 55% - 68% 69%

predicted VO2max

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Definitions

Systolic Blood Pressure (SBP) pressure measured in brachial

artery during systole (ventricular emptying and ventricular contraction period) artery during diastole (ventricular filling and ventricular

Diastolic Blood Pressure (DBP) pressure measured in brachial

cardiac cycle against the walls of the proximal systemic arteries (aorta)

relaxation)

Mean Arterial Pressure (MAP) "average" pressure throughout the Total Peripheral Resistance (TPR) - the sum of all forces that
oppose blood flow

estimated as:

.33(SBP - DBP) + DBP

length of vasculature (L) blood viscosity (V) vessel radius (r)

TPR = ( 8 ) ( V ) ( L )

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( p ) ( r4 )

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Cardiovascular Hemodynamic Basics

Flow (Q) =

= Resistance (TPR) =

Pressure (MAP)

Paorta P vena cava (8) (V) (L) () (r 4)

Normally Resting Q is about 5 - 6 liters / minute

Flow (Q)

() (Pa Pv) (r 4) (8) (V) (L)

V = viscosity of fluid (blood) flowing through the pipe L = length of pipe (blood vessel) r = radius of the pipe (blood vessel) Pa = aortic pressure Pv = venous pressure
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Respiratory Physiology - Definitions

Minute Ventilation (V E) - amount of air passing through the

lungs in one minute

Dyspnea - breathing difficulty Respiratory Exchange Ratio - amount of CO2 expired by

the air 1.0

lungs divided by the amount of O2 extracted from the in the lungs (VCO2 / VO2). RER = .7 r 100% fat 0% carb RER = .85 r 50% fat 50% carb RER = r 0% fat 100% carb

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Neurophysiology - Definitions & Concepts

Afferent - sensory nerves - going toward spinal column Efferent - effector nerves - going away from spinal column

Adrenergic Receptor Types

a 1 stimulation r a2

constriction of: blood vessels visceral sphincters bronchioles bladder

stimulation: vasodilatation bronchiole constriction u HR and contractility u renin secretion vasodilatation bronchiole dilation urinary tract relaxation relaxation of visceral smooth muscle

b 1 stimulation: b 2 stimulation:

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Microcirculatory Anatomy a Capillary Bed

Smooth Muscle Arteriole

Precaillary Sphincter Anastomosis (Shunt) True Capillary With Single Layer of Endothelium

Metarteriole
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Venule

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Development of the Driving Pressure in the Human Cardiovascular System

Arterial 100 Pressure (mm Hg)
Mean Circulatory Filling Pressure

102 26 7
Normal Resting Pressure Driving the Blood from Left Ventricle to Vena Cava: 102 - 2 = 100 mmHg

7 0 7

Central Venous Pressure (mm Hg)

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Cardiac Output (Q) (Liters / min)

Normal Resting Cardiac Output

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The Closed Cardiovascular Hemodynamic System RV RA (0) (13)

Mean arterial pressures in red

PO2 = 160 PCO2 = .3

LV LA AORTA (100)

LUNGS
PO2 = 100 (3) PCO2 = 40 9% of blood volume

(7)
Ohms Law: Flow (Q) = upstream pressure downstream pressure resistance

SYSTEMIC ARTERIES

(92)

VEINS (CAPACITANCE VESSELS) (2)

high compliance 64% of blood volume PO2 = 40 PCO2 = 46

low compliance 13% of blood volume

(20) CAPILLARY BEDS

(40) ARTERIOLES

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Sites of Cardiorespiratory Control

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Cardiorespiratory Control

Heart Rate CNS (medulla) and neurohormone regulation Parasympathetic vagus control (Neurotransmitter: acetlycholine) Vagal control dominant at rest withdrawn during exercise Sympathetic cardioacceleration (Neurotransmitter: E and NE) Baroreceptor influences Sympathetic discharge indirectly proportional to firing rate Parasympathetics are directly proportional to firing rate d pressure r d receptor firing r u sympathetics r u HR u pressure r u receptor firing r u parasympath. r d HR Chemoreceptor influences Main function: protect brain from poor perfusion u O2 or d CO2 r u parasympathetic discharge r d HR 06/12/11 d O2 or u CO2 r d pH r pressor area stimulation r u HR

140

Cardiorespiratory Control
Stroke Volume regulated by Frank Starling mechanism

venous return r u EDV r u

stroke volume

Cardiac Output (Q) main determinant: body O2 needs

Autoregulated by intrinsic changes in preload, & SV u afterload r initial d in Q r u EDV r u SV back to

normal u venous return r u

Autoregulated by extrinsic hormonal influences Norepinephrine release r u HR and SV

preload r u SV

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Cardiorespiratory Control
Blood Pressure influenced by 3 major factors

Total peripheral resistance

u BP

Baroreceptor (BR) and CNS Influences u BP r u BR firing rate r vasodilation r d BP d BP r d BR firing rate r u sympathetics r dO2, u CO2, d pH r CNS stim. r vasoconstriction Circulating catecholamine influences E and NE have varying effects on TP E and NE usually activate receptors r u TPR Fight or flight response

Chemoreceptor influences

Q Blood Volume Angiotensin system Renin

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H H
r e n a l

y p o t e n s i o n y p o v o l e m i aH

r e a b s o

p e r f u s s y i m n p a t h e t i cA o

D o H n e( v a s o p t

a f f e r e n t a r t e N i oa C a l r d e l i v e r y r l s t r e t c h i n J Gm a c u l s a d e n s a c e l l r e n i n a n g i o t e n s i n

t o m e s s a n g i a c c e e l l l sl c o n t r a c G F R

stretch receptor I activation in atria, aorta, and carotid sinuses

Renin - Angiotensin System of Body Fluid Balance and other Body Fluid Regulation Mechanisms 06/12/11

B L O O D P R E Sa S g i Ro E e n s i n n U t I I t h i r s t ( v a s o c o n s t r i c t i o n ) ( t h i r s t i s m o r e s r e g u l a t e d b y o r e c e p t o r s i n a l d o s t e r o n e h y p o t h a l a m u n e g f e e d b a c k N +a r e a b s o r p t i o n + ( a n d K e x c r e t i o n ) E C F v o l u m e

n e g r e n i n

f e e d b a c k
143

Dehydration

Dehydration: the loss of body water and associated electrolytes Causes:

Gastroenteritis (viral / bacterial infection r vomiting & diarrhea) most common Diseases: yellow fever, cholera, Excessive alcohol consumption Most liquors have Congeners which are toxins.they must be removed The clearer & better quality your liquor (vodka & gin) the less congeners more distillation cycles r better quality This removal is done by the liver (liver glucose is broken down r lethargy) The excess fluid is flushed out by the kidneys (u water usage r dehydration) Prolonged exercise without fluid replacement (heat exhaustion & heat stroke risk) Diabetes: hyperglycemia r u glucose excretion r u water loss r dehydration Shock: blood loss due to some hypotensive state Gastrointestinal blood loss: bleeding from ulcers or colorectal
cancer
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Dehydration

Signs & Symptoms of dehydration:

Treating Dehydration of water Sip small amounts

Dry mouth, dry swollen tongue, rapid heart rate (possible chest palpitations) Lethargy (sluggishness), confusion Poor skin turgor (a pinch of skin does not spring back into position) Good test for ailing elderly folks Elevated BUN (NH4 metabolized in liver & excreted by kidneys (renal function test) Elevated creatinine r d GFR (kidney clearance of waste products) Low blood viscosity Headache Fluid loss r low blood pressure r dizziness upon standing up A high urinary specific gravity (comparison of density to water: 1 gram / cm 2 )

Drink carbohydrate / electrolyte 0solutions: Gatorade, Pedialyte.etc If core body temperature > 104 + d BP or u HR r consider IV fluid replacemen

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Cardiorespiratory Control
Skeletal Muscle Blood Flow autoregulated 2 mechanisms Metabolic by-product vasodilation Mechanism 1: overrides neurohormone control Usually

Mediated by vasodilator metabolite (VDM) buildup & removal Adenosine (ATP by-product), CO2, H+,
prostaglandins

Exercise Example negative feedback control Muscle exercises r VDMs released r u vasodilation u blood flow r VDMs removed r
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vasoconstriction

Myogenic response Mechanism 2: stretch activated Ca++ channels Involves

u u

blood flow r vessel stretch r channel activation [Ca++ ] in smooth muscle r vasoconstriction r d flow

146

Cardiorespiratory Control

Exercise Systemic Blood Flow: Autonomic influences Sympathetic outflow & circulating catecholamines

Redistribution of blood flow during maximal exercise

- NC in brain blood flow - 500 ml/min u to heart - 11,300 ml/min u to muscle - 400 ml/min u to skin - 500 ml/min d to kidneys - 800 ml/min d to viscera - 200 ml/min d to various other parts of the body

activation r vasoconstriction in non - exercising tissue

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Cardiorespiratory Control
Respiration: VE = Tidal Volume X Respiratory Rate

Controlled via the medulla respiratory center

chemoreceptors not a big influence Peripheralblood CO content r receptor activation r u V u
d
blood O2 content r receptor activation r u VE
2 E

chemoreceptors dominant influence Central u blood CO & lactate r receptor activation r u V

PaCO2 r u HCO3 + H+ r
2

H+ activates receptor r u VE

Respiratory control during exercise no consensus u V u venous return r mechanoreceptor activation r Minute ventilation control duringuexerciseu TV and u RR Low exercise intensity: V by both
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proprioceptor activation r u VE intrapulmonary receptor activation r u

VE
148

Acute Responses to Aerobic Exercise

Oxygen Consumption (VO2)

u VO2 in direct proportion to u workload (power requirement of exercise) Expressed in both relative and absolute terms Relative: ml O2/kg/min Absolute: ml/min or L/min average VO2max for 40 year old male 37 ml/kg/min Oxygen consumption linked to caloric expenditure (1 liter of O2consumed = 5
kcal)

Heart Rate
u
Heart Rate

up to 3 times resting value at peak exercise (d time spent in diastole) 180 160 140 100 1.0 2.0 3.0 Oxygen Uptake (L / min) 50 150 250

HR VO2 relationship is linear until about 90% VO2max

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Workloads (Watts)

Stroke Volume1.5 resting value at peak exercise u up to

Acute Responses increase levels off at 40% - 50% VO2 max to Aerobic Exercise u in venous return r u EDV (Starling mechanism) d ESV eluding to an u in myocardial contractility u ejection fraction rest: 58% max exercise: 83% 120
Stroke 110 Volume 70 (ml/beat)

25% 50% 75% Percentage of VO2 max (Q) CardiacuOutput times resting value at peak exercise (u is rapid at onset, then up to 4

levels off) u Q r u venous return Venous return mediated by and related to: sympathetic venoconstriction muscle pump 06/12/11 150 u inspiration r d thoracic pressure blood flows to an area of reduced pressure

difference Arteriovenous oxygenbetween arterial and mixed venous blood Difference in [O ]

Resistance to Blood Pressures andto u signifies heartFlow SBP: u - failure failure

2 Illustrated by the oxyhemoglobin desaturation curve u approximately 3 fold from rest to max exercise at rest, about 25% of arterial O2 is extracted at peak exercise 85% of arterial O2 is extracted Acute Responses to Aerobic

DBP: slight u or slight d or NC MAP: slight u TPR: d - mainly due to vasodilation in exercising muscle

Exercise

Coronary (Myocardial) Blood Flow

to the Blood Flow exerciseSkin u to allow for heat dissipation u as duration

4.5% of Q goes to myocardium at rest and at peak exercise this increase is due to u MAP and CA vasodilation
at max exercise to meet exercising muscle demands during exercise recovery, again for heat dissipation
151

d 06/12/11 u

Acute Responses to Aerobic Exercise

Minute Ventilation resting average:

6 Liters/min peak exercise average: 175 Liters/min respiratory rate: resting 12-18 peak exercise: 45-60 tidal volume: resting .5 liters peak exercise: 2.25 Liters

Volume Plasmablood plasma u in the interstitum of exercising muscle

fluid shift results in a 5% u in the hemoconcentration blood viscosity increases

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Oxygen Debt and DEFICIT Oxygen DEBT & OxygenDeficit

Steady State VO2 Oxygen Deficit Oxygen Debt (EPEOC)

VO2
Rest Onset

Untrained or people with certain cardiorespiratory diseases will have larger DEBTS and DEFICITS

Oxygen Deficit due to: delay in time for aerobic ATP production to supply energy Oxygen Debt due to: resynthesis of high energy pohosphates (CP, ATP) replace oxygen stores lactate conversion to glucose (gluconeogenesis) u HR, respiration, catecholamines, body temperature

EXERCISE TIME AT CONSTANT WORKLOAD

Termination

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P P P

O O C

OBLA
2

Respiratory Compensation (hyperventilation)

&

No Change in

Ventilatory and Metabolic Changes During Exercise

VE

V V V H

VCO2

C O 2 C

Om 2

p H
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Increasing workload

154

Resting NC

VO2 =

HR

NC SV x

AVO2diff

due to: due to: u time in diastole u preload d afterload u ventricle size u blood volume

Effects of Exercise Training on the Components of the Fick Relationship

Submax Workload (measured at same pre-training workload) NC NC

VO2 = HR x SV x AVO2diff
accompanied by a d in HR response translates into a d myocardial VO2 at rest or at any workload

note: a d in afterload (mentioned above)

(measured at peak exercise) Max Workload NC

VO2 = HR x SV x AVO2diff
some studies show a slight decrease

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Pressure Mean Arterialrest or during exercise NC at Systolic and Diastolic Blood Pressure usually NC at rest or during exercise

Training Adaptations

possible d at submaximal workload may d at rest in borderline hypertensives some studies report a mean d of about 9 mmHg Total Peripheral Resistance and Afterload d TPR u capillarization (more parallel circuits) r d TPR r d Afterload (slight not of major significance) Tidal Volume
Respiratory Rate Rest: NC Submax exercise: d Max exercise: slight u Rest: NC Submax exercise: NC or slight u Occurs at a percentage of VO max Pre-training: higherVO max Post-training: 80% VO max 50%

Respiratory Variables

Max exercise: slight u Anaerobic Threshold

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Training Adaptations Mitochondria size and membrane surface area u number, Aerobicu Enzymes in Exercising Muscle Krebs cycle enzymes (succinate dehydrogenase)

u oxidation enzymes (carnitine acyltransferase) u electron transport enzymes (cytochrome oxydase) Utilization Fatty Acid & Glycogenoxidative pathways to produce u utilization of ATP Called the glycogen sparring effect d RER for any given submaximal workload u muscle glycogen stores (with high carbohydrate
Change in Resting Metabolic Rate No Appreciabletraining induced u in lean muscle mass Exception:
diet)

d Platelet Aggregation u Fibrinolytic Activity d Circulating Catecholamines u vagal tone r d risk of arrhythmia Resistance to Pathological Eventsrecovery smaller infarct size and quicker
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Less of a d

in ventricular function during ischemia

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"Average" Values for Sedentary and Trained Individuals Heart Rate ( beats / minute )
200 150 100 50 0 75 60 185 185

sedentary-rest

sedentary-max

trained-rest

trained-max

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"Average" Values for Sedentary and Trained Individuals Stroke Volume ( ml / beat )
160 150 100 50 0 120 60 80

sedentary-rest

sedentary-max

trained-rest

trained-max

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"Average" Values for Sedentary and Trained Individuals Cardiac Output ( liters / minute)
40 35 30 25 20 15 10 5 0 30 22

sedentary-rest

sedentary-max

trained-rest

trained-max

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"Average" Values for Sedentary and Trained Individuals A-V O2 Difference ( ml%)
20 15 10 5 0 6 14 16

sedentary-rest

sedentary-max

trained-rest

trained-max

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"Average" Values for Sedentary and Trained Individuals Oxygen Consumption ( liters / minute)
6 5 4 3 2 1 0 0.25 sedentary-rest sedentary-max 0.25 trained-rest trained-max 3 4.5

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"Average" Values for Sedentary and Trained Individuals Oxygen Consumption ( ml / kg / minute)
60 50 40 30 20 10 0 3.5 sedentary-rest sedentary-max 3.5 trained-rest trained-max 38 55

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"Average" Values for Sedentary and Trained Individuals Systolic Blood Pressure ( mm Hg)
210 200 150 100 50 0 sedentary-rest sedentary-max trained-rest trained-max 134 130 206

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"Average" Values for Sedentary and Trained Individuals Diastolic Blood Pressure ( mm Hg)
90 88 86 84 82 80 78 76 74

84 82 80 82

sedentary-rest

sedentary-max

trained-rest

trained-max

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HEART ANATOMY (EXTERNAL VIEW)

The heart is a complex muscular pump that maintains oxygen and blood circulation through the lungs and the rest of the body. The heart pumps about 7200 liters/day.

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HEART ANATOMY (CROSSECTION VIEW)

The heart has four chambers. nTwo atria act as collecting reservoirs.
n n

Two ventricles act as pumps. The heart has four valves for: Pumping action of the heart. Maintaining unidirectional blood flow.

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HEART (PHYSIOLOGY)
n

Deoxygenated blood returns to the heart via the superior and inferior vena cava, enters the right atrium, passes into the right ventricle, and from here it is ejected to the pulmonary artery. Oxygenated blood returning from the lungs enters the left atrium via the pulmonary veins, passes into the left ventricle, and is then ejected to the aorta.

n n

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VASCULAR FLUID MECHANICS

Velocity and

pressure are inversely related to the cross sectional area of blood vessels. These parameters drop in the capillaries where the crosssectional area is more.
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JUST BEFORE I LEAVE

One of the Keys Happiness is having a

to

good health and a bad memory

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The Heart

Is a muscle about the size of your fist Weighs approximately one pound Is located behind and slightly to the left of the breastbone Pumps about 5 quarts (4.7 liters) of blood every minute

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The function of the heart is to circulate blood throughout the body by:

Pumping blood through the lungs removes carbon dioxide and refreshes the blood with oxygen The oxygenated blood is pumped to the body to provide oxygen and nutrients and to remove waste products. The coronary arteries are the blood vessels that supply blood and oxygen to the heart muscle.

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Blood Supply To The Heart

2 coronary arteries branch from the main aorta just above the aortic valve. No larger than drinking straws, they divide and encircle the heart to cover its surface with a lacy network that reminded physicians of a slightly crooked crown (coronary comes from the Latin coronarius, belonging to a crown or wreath). They carry out about 130 gallons of blood through the heart muscle daily. (Clark, 119)
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Coronary Artery Disease

Coronary artery disease is one of the most common and serious effects of aging. Fatty deposits build up in blood vessel walls and narrow the passageway for the movement of blood. The resulting condition, called atherosclerosis often leads to eventual blockage of the coronary arteries and a heart attack.

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Signs and Symptoms

None

Chest Pain

Signs & Sympto ms

Shortn ess Of Breath

Heart Attack

None: This is referred to as silent ischemia. Blood to your heart may be restricted due to CAD, but you dont feel any effects. Chest pain: If your coronary arteries cant supply enough blood to meet the oxygen demands of your heart, the result may be chest pain called angina. Shortness of breath: Some people may not be aware they have CAD until they develop symptoms of congestive heart failure- extreme fatigue with exertion, shortness of breath and swelling in their feet and ankles. Heart attack: Results when an artery to your heart muscle becomes completely blocked and the party of your heart muscles fed by that artery dies.

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Atherosclerosis
can, and does, occur in almost any artery in the body. But in the heart its effects can be crucial. The body depends on a strong pumping heart to circulate life-giving blood, and this includes to the heart muscle itself. If the coronary arteries become blocked, the cardiac muscle begins to fail, and so the blood circulation decreases, which includes the circulation to the heart muscle itself. (Thibodeau, 494)

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Cause s

High blood cholesterol High blood pressure Smoking Obesity Lack of physical activity

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Risk Factors

Uncontrollable
Sex Hereditary Race Age

Controllable
High blood pressure High blood cholesterol Smoking Physical activity Obesity Diabetes Stress and anger

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Screening and Diagnosis

me as ur es

blo od

sp ec i fi c

me asu res

shows

to he art

es uls p im

su pp ly

ng in Narrowi

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coronaries

elec trical

of of es es St Siit

Other Tests Include...

Blood tests: used to evaluate kidney and thyroid function as well as to check cholesterol levels and the presence of anemia. Chest X-ray: shows the size of your heart and whether there is fluid build up around the heart and lungs. Echocardiogram: shows a graphic outline of the hearts movement Ejection fraction (EF): determines how well your heart pumps with each beat.
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Treatment
Many people are able to manage coronary artery disease with lifestyle changes and medications.

Other people with severe coronary artery disease may need angioplasty or surgery.

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Arterial Blood Pressure It is the lateral pressure exerted by blood on the walls of aorta and arteries.
Ejection of blood into the aorta by the left ventricle results in a characteristic aortic pressure pulse. The peak of the aortic pressure pulse is termed the systolic pressure (Psystolic). The lowest pressure in the aorta is termed the diastolic pressure (Pdiastolic). The difference between the systolic and diastolic pressures is the aortic pulse pressure. The mean aortic pressure (MAP) is the average pressure (geometric mean) during the aortic pulse cycle
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As the aortic pressure pulse travels down the aorta and into distributing arteries, there are characteristic changes in the systolic and diastolic pressures, as well as in the mean pressure. As the pressure pulse moves away from the heart, the systolic pressure rises and the diastolic pressure fall. There is also a small decline in mean arterial pressure as the pressure pulse travels down distributing arteries due to the resistance of the arteries.

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 Therefore, when arterial pressure is measured using a sphygmomanometer (i.e., blood pressure cuff) on the upper arm, the pressure measurements represent the pressure within the brachial artery, which will be slightly different than the pressure measured in the aorta or the pressure measure in other distributing arteries.

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Measurements of Blood Pressure

1- Direct Method The most accurate means for measuring blood pressure is directly within an artery (intra-arterial) using a catheter. But because this method is invasive, it is neither practical nor appropriate for repeated measurements in non-hospital settings, or for large-scale public health screenings. 2- The mercury-filled sphygmomanometer The usual method of measurement, therefore, is a noninvasive means that uses a sphygmomanometer, which includes either a column of mercury or pressure-registering gauge.

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Physiological factors affecting Arterial Blood pressure

Age:

New born: 80/40 mmHg 4 years: 100/65 mmHg. Adults: 120/80 mmHg After that: Gradually increase due to increase elasticity of arteries. Sex: Children: have equal Blood pressure. Adults before 45 years: male more than female. Adults after 45 years: the diastolic B.P. is more in female than males. Race: ABP in oriental is less than in European and American. Gravity: B.P. in upper parts of the body is more than the lower parts especially during standing. Meals: Digestion increases the arterial blood pressure. Emotions and exercise: increase the arterial blood pressure. Sleep: Deep quiet sleep decrease A.B.P., while sleep with dreams increase A.B.P.
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Factors that Affect Blood Pressure

Blood pressure is affected by several factors:

1- Cardiac output. 2- Peripheral resistance 3- Vessel elasticity 4- Blood volume

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1- Cardiac Output
It is the amount of blood pumped by the left ventricle per minute. It keeps the arteries full of blood. An increase in cardiac output results in increased blood pressure. Anything that decreases cardiac output also decreases blood pressure, because there is less pressure on the vessel walls. Cardiac Output = Heart Rate X Stroke Volume Anything that affects heart rate or stroke volume affects cardiac output and thus blood pressure. 06/12/11 193

Regulation of Cardiac Output

The cardiac output is regulated by two forces:

Intrinsic (Frank-starling mechanism). Extrinsic (autonomic nervous system).

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Intrinsic control
Increased end-diastolic volume = increased strength of cardiac contraction and increased stroke volume This increase in strength of contraction due to an increase in end-diastolic volume (the volume of blood in the heart just before the ventricles begin to contract) is called the Frank-Starling law of the heart: Increased end-diastolic volume = increased stretching of cardiac muscle = increased strength of contraction = increased stroke volume
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Extrinsic control
Increased sympathetic stimulation, increased strength of contraction of cardiac muscle Mechanism sympathetic stimulation cause release of norepinephrine which increase permeability of muscle cell membranes to calcium and calcium diffuses through more cross-bridges and causes stronge contraction
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Extrinsic control

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198

2- Peripheral Resistance
One of the main factors that affect blood pressure is peripheral resistance. Blood cells and plasma encounter resistance when they contact blood vessel walls. If resistance increases, then more pressure is needed to keep blood moving. Three main sources of peripheral resistance: a. Blood vessel diameter b. Blood viscosity c. Total vessel length

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2 a)- Vessel Diameter

Vessel diameter affects peripheral resistance. As a diameter of a tube gets smaller, a greater proportion of the fluid is in contact with the wall of the tube. Therefore resistance to flow is increased and pressure rises. Larger diameter, same volume, less pressure. Smaller diameter, same volume, more pressure.

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Vasomotor Fibers Constriction of blood vessels raises blood pressure. Vessel diameter is actively regulated by vasomotor fibers, sympathetic nerve fibers that innervate the vessel's smooth muscle layer. Vasomotor fibers release norepinephrine, a powerful vasoconstrictor. A vasoconstrictor is a substance that causes blood vessels to constrict. Vasoconstrictors Blood vessel diameter is also regulated by blood-borne vasoconstrictors. (Epinephrine, Angiotensin II, Vasopressin)

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2 b)- Viscosity of blood

Blood viscosity affects peripheral resistance. Viscosity is related to the thickness of a fluid. The greater the viscosity, the less easily molecules slide past one another and the more difficult it is to get the fluid moving and keep it moving. Because of this greater resistance to flow, a greater pressure is required to pump the same volume of viscous fluid. The hematocrit is the percentage of red blood cells in the total blood volume. The hematocrit affects blood viscosity and therefore resistance to flow. The more viscous the blood, the greater resistance it encounters and the higher the blood pressure. The hematocrit can increase when there are more red blood cells or less plasma in the blood. The hematocrit can decrease when there are fewer red blood cells or more plasma.

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2 c)- Vessel Length Total vessel length affects peripheral resistance. Increased fatty tissue requires more blood vessels to service it and adds to the total vessel length in the body. The longer the total vessel length, the greater the resistance encountered, and the greater the blood pressure.
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3 - Vessel Elasticity
Besides peripheral resistance, blood vessel elasticity also affects blood pressure. A healthy elastic artery expands, absorbing the shock of systolic pressure. The elastic recoil of the vessel then maintains the continued flow of blood during diastole. When an individual has arteriosclerosis, arteries become calcified and rigid, so they can't expand when the pulse wave of systolic pressure passes through them

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4 - Blood Volume
Blood volume affects blood pressure. When there is a greater volume of fluid, more fluid presses against the walls of the arteries resulting in a greater pressure. When there is less volume there is less pressure. Reduced blood volume (for example due to excessive sweating) reduces blood pressure short term. Long term homeostatic mechanisms compensate, bringing blood volume and blood pressure back up to normal levels. Increased blood volume (for example due to water retention from excessive salt intake) increases blood pressure short term. Long term homeostatic mechanisms compensate, bringing blood volume and blood pressure back up to normal levels.

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Regulation of arterial blood pressure

Blood pressure is maintained at a constant level within a narrow limit to ensure an adequate flow of blood to the tissue especially the vital organs e.g. heart, brain and kidney.

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Regulation of arterial blood pressure 2

Blood pressure=cardiac output X peripheral resistance

Thus the regulation of arterial blood pressure depend upon the previous two factors through two mechanisms:1- Nervous 2- Hormonal

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Regulatory mechanisms
1- immediately acting mechanisms. 2- intermediately acting mechanisms.

3- Long term acting mechanisms.

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Immediately acting mechanisms

Starts: within seconds. Lasts: hours. Type: Nervous. Mechanism: Stimulation of baroreceptors in the aortic arch or carotid sinus by changes of blood pressure between 60mmHg and 200mmHg blood pressur. Stimulation of chemoreceptors in the aortic body or carotid body by changes of blood pressure between 40mmHg and 60mmHg blood pressure.
209

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1- immediately acting mechanisms

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Control of blood pressure

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2- intermediately acting mechanisms.

Starts: within half an hour. Lasts: hours to 3-4 days. Type: Mechanism:
Fluid shift mechanism. Stress relaxation mechanism.

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3- Long term acting mechanisms Starts: within half an hour. Lasts: days, months, or even years. Type: hormonal. Mechanisms:
1- Renin mechanism. 2- Aldosterone mechanism. 3- Antidiuretic hormone mechanism.

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SHORT-TERM CONTROL OF ARTERIAL BLOOD PRESSURE THE SENSORY ARM Arterial blood pressure is controlled by a negative feedback process Carotid sinus and aortic arch baroreceptors respond to changes of blood pressure.
100 Int carotid Ext carotid
Carotid sinus baroreceptor vagus nerve CN X sinus nerve to CN IX

Integrated nerve activity % maximum

sinus nerve

vagus nerve

Aortic arch baroreceptor

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110 200 arterial pressure, mm Hg

Afferent nerve firing reflects both the rate of change of blood pressure during the pulse and the 215 mean level

SHORT-TERM CONTROL OF ARTERIAL BLOOD PRESSURE THE EFFERENT ARM Medullary cardiovascular centres regulate the efferent arm via the autonomic nervous system.

Receptor afferents

When activated: Sympathetic fibres innervate arterioles - vasoconstriction the s.a. node - tachycardia myocardium - positive inotropy Parasympathetic (vagal) fibres innervate the s.a. node - bradycardia
Vagal tone to the s.a node predominates 06/12/11

Medullary cardiovascular centres sympathetic parasympathetic

216

THE BARORECEPTOR REFLEX - AN EXAMPLE CORRECTION OF POSTURAL HYPOTENSION On standing up venous return falls Cardiac output diminishes Arterial blood pressure is reduced Baroreceptor afferent firing reduced Medullary centres inhibition reduced Increased sympathetic tone to arterioles Tachycardia Reduced vagal tone to s.a. Raised stroke work node 06/12/11 Increased myocardial sympathetic tone Vasoconstriction Tend to restore arterial blood pressure 217 Effect of gravity on venous return Preload diminished - Starlings Law Subject possibly feels faint as cerebral flow is reduced Due to reduced arterial B.P.

THANK YOU
..

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