Cardiovascular Physiology

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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

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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

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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: a double layered closed sac that surrounds the heart: 1- Fibrous 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.

Pericardium

Pericardial cavity: between the parietal and visceral pericardium is filled with a thin layer of serous Pericardial fluid: reduces friction of the beating heart. 30/03/10 13

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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• 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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THE CARDIAC MUSCLE

• 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 PERIOD due 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)
• STARLING’s 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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• 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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3- RHYTHMICITY

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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 70-80/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.
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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 pressureAV 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 30/03/10 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, necrosis and 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 125 endothelial cells

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 126 disease prognosis

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
• regulated by: • sympathetic nerve activity (most influential) • catecholamines (epinephrine norepinephrine) • amount of contractile mass • drugs 30/03/10
can develop at a given preload

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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 :
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 (AVO D)
2

the difference in oxygen content between arterial and venous blood

• measured in ml% - ml O
2

2

/ 100 ml blood

• Oxygen Consumption (VO ) - the rate at which oxygen can be used in
energy production and metabolism
2 2

• “absolute” measures: L O / min , ml O / min • “relative” measures: ml O / kg body wt. / min • Fick equation: VO = Q X AVO D
2
2 2

• Maximum Oxygen Consumption (VO • often estimated with VO
2ek pa

) maximum rate at which a person can take in and utilize oxygen to create usable energy
2a mx

• defined as plateau of consumption rate increase

the • Myocardial Oxygen Consumption VO of mild heart muscle (myocardium) 27% - 40% "estimated" by RPP: HR X SBP • moderate 41% - 54%
2

predicted VO2mx - attained VO2max a
2a mx

Aerobic Impairment: • Functional predicted VO

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marked severe >

55% - 68% 69%

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Definitions

• Systolic Blood Pressure (SBP) pressure measured in brachial
artery during systole (ventricular emptying and ventricular contraction period)

• Diastolic Blood Pressure (DBP) pressure measured

in brachial artery during diastole (ventricular filling and ventricular relaxation)

• Mean Arterial Pressure (MAP) "average" pressure throughout the
cardiac cycle against the walls of the proximal systemic arteries (aorta)

• estimated as: • • •

.33(SBP - DBP) + DBP

• Total Peripheral Resistance (TPR) - the sum of all forces that
oppose blood flow
length of vasculature (L) blood viscosity (V) vessel radius (r) TPR = ( 8 ) ( V ) ( L ) (  ) ( r4 )
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Cardiovascular Hemodynamic Basics

Flow (Q) =

Pressure (MAP) = Resistance (TPR)

P aorta – 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 ) - amount of air passing through the
E

lungs in one minute

• Dyspnea - breathing difficulty • Respiratory Exchange Ratio - amount of CO
RER = .7 RER = .85 RER = 1.0

expired by the lungs divided by the amount of O2 extracted from the air in the lungs (VCO2 / VO2 ).
2

r 100% fat 0% carb r 50% fat 50% carb 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

 1 stimulation r constriction of:
blood vessels visceral sphincters bronchioles bladder



stimulation: vasodilatation bronchiole constriction

 1 stimulation:  2 stimulation:
u HR and contractility u renin secretion vasodilatation bronchiole dilation urinary tract relaxation relaxation of visceral smooth muscle
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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

7

6

Central Venous Pressure (mm Hg)
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0

1

5

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)

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

LUNGS

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

SYSTEMIC ARTERIES
low compliance

(92)

VEINS (CAPACITANCE VESSELS) (2)
high compliance 64% of blood volume PO2 = 40 PCO2 = 46

13% of blood volume

(20) CAPILLARY BEDS

(40) ARTERIOLES

7% of blood volume Systemic Circulation = 100 mmHg – 0 mmHg 30/03/10 Flow (Q) 1 mmHg sec / ml = 100 ml / sec = 6 liters / min
138

Sites of Cardiorespiratory Control 30/03/10

139

Cardiorespiratory Control

•Heart Rate – CNS (medulla) and neurohormone regulation • Parasympathetic vagus control (Neurotransmitter: acetlycholine) • Vagal control dominant at rest – withdrawn during exercise • Sympathetic cardio–acceleration (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 30/03/10 u O or d CO r u parasympathetic discharge r d HR •
2 2

140

Cardiorespiratory Control
Stroke Volume – regulated by Frank Starling mechanism

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

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141

Cardiorespiratory Control
Blood Pressure – influenced by 3 major factors

• Total peripheral resistance
• Baroreceptor (BR) and CNS Influences

• u BP r u • d BP r d
2 2

BR firing rate r vasodilation r d BP BR firing rate r u sympathetics r u BP

• Chemoreceptor influences
• dO , u CO , d pH r
CNS stim. r vasoconstriction

• Circulating catecholamine influences • E and NE have varying effects on TP • E and NE usually activate α receptors r u • Fight or flight response •Q
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TPR

• Blood Volume

Renin – Angiotensin system

142

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

2

O

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 30/03/10 Mechanisms

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 30/03/10 • Gastrointestinal blood loss: bleeding from ulcers or colorectal cancer 144

• Signs & Symptoms of dehydration:

Dehydration

• 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 (NH 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 )
4

2

• Treating Dehydration

• Sip small amounts of water 30/03/10 carbohydrate / electrolyte solutions: Gatorade, Pedialyte.etc • Drink
0

145

Cardiorespiratory Control
Skeletal Muscle Blood Flow – autoregulated – 2 mechanisms

• Mechanism 1: Metabolic by-product vasodilation • Usually overrides neurohormone control • Mediated by vasodilator metabolite (VDM) buildup & removal • Adenosine (ATP by-product), CO , H , prostaglandins
2 +

• Exercise Example – negative feedback control

• Muscle exercises r VDM’s released r u vasodilation • u blood flow r VDM’s removed r vasoconstriction • Mechanism 2: Myogenic response • Involves stretch activated Ca++ channels 30/03/10 • u blood flow r vessel stretch r channel activation

146

Cardiorespiratory Control

Exercise Systemic Blood Flow: Autonomic influences

• Sympathetic outflow & circulating catecholamines • α activation r vasoconstriction in non - exercising tissue • Redistribution of blood flow during maximal exercise
- NC in brain blood flow - 11,300 ml/min u to muscle - 500 ml/min d to kidneys - 500 ml/min u to heart - 400 ml/min u to skin - 800 ml/min d to viscera - 200 ml/min d to various other parts of the body

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147

Cardiorespiratory Control
Respiration: VE = Tidal Volume X Respiratory Rate

• Controlled via the medulla respiratory center • Peripheral chemoreceptors – not a big influence
• u blood CO content r receptor activation r u V • d blood O content r receptor activation r u V
2 2 E 2 E

• Central chemoreceptors – dominant influence
a 2 3 ¯ + +

• u blood CO & lactate r receptor activation r u V • P CO r u HCO + H r H activates receptor r u V
E

E

• Respiratory control during exercise – no consensus
• u venous return r mechanoreceptor activation r u V • proprioceptor activation r u V • intrapulmonary receptor activation r u V
E E E

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• Minute ventilation control during exercise

148

Acute Responses to Aerobic Exercise

Oxygen Consumption (VO2)

• u VO in direct proportion to u workload (power requirement of exercise)
• Expressed in both relative and absolute terms • Relative: ml O /kg/min Absolute: ml/min or L/min • average VO for 40 year old male 37 ml/kg/min • Oxygen consumption linked to caloric expenditure (1 liter of O
2 2a mx 2

2

consumed = 5 kcal)

• Heart Rate
Heart Rate

• u 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
149

30/03/10

Workloads (Watts)

• Stroke Volume
• • • •

• u up to 1.5 resting value at peak exercise increase levels off at 40% - 50% VO2 max 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%
Stroke Volume 110 (ml/beat) 70
120

Acute Responses to Aerobic Exercise

25% 50% 75% Percentage of VO2 max

•Cardiac Output (Q)
• • • • •

off) u Q r u venous return Venous return mediated by and related to: sympathetic venoconstriction muscle pump 30/03/10 u inspiration r d thoracic pressure

• u up to 4 times resting value at peak exercise (u is rapid at onset, then levels

150

Arteriovenous oxygen difference
2

• Difference in [O ] between arterial and mixed venous blood
2

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

Blood Pressures and Resistance to Flow

to Aerobic Exercise

• SBP: u - failure to u signifies heart failure

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

• •

Coronary (Myocardial) Blood Flow

• 4.5% of Q goes to myocardium at rest and at peak exercise • this increase is due to u MAP and CA vasodilation • u as exercise duration u to allow for heat dissipation • d at max exercise to meet exercising muscle demands
151

Blood Flow to the Skin
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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

• Plasma Volumeu in the interstitum of exercising muscle blood plasma

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

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152

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: Oxygen Debt due to:

EXERCISE TIME AT CONSTANT WORKLOAD

Termination

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

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153

P P P

a

O O C

OBLA
2

Respiratory Compensation (hyperventilation)

A

2

A

&

O

2

P

a

C

O

2

No Change in

Ventilatory and Metabolic Changes During Exercise

V V V H

VE
E

VCO2

C O 2 C

2

O

V

Om 2

a

x

3

O

p H
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Increasing workload

154

• Resting

NC VO2

=

HR

x

SV

x

NC AVO2diff

due to: u time in diastole

due to: 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 VO2 = HR x SV x NC AVO2diff note: a d in afterload (mentioned above)
accompanied by a d in HR response translates into a d myocardial VO2 at rest or at any workload

• Max Workload (measured at peak exercise)
NC

VO2
30/03/10

=

HR

x

SV

x

AVO2diff
155

some studies show a slight decrease

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

Training Adaptations

Peripheral • TotalcapillarizationResistance and Afterload u (more parallel circuits) r d TPR

• • possible d at submaximal workload • may d at rest in borderline hypertensives • some studies report a mean d of about 9 mmHg • • d TPR r d Afterload (slight – not of major significance) • Rest: NC • Submax exercise: d • Max exercise: slight u

• Respiratory Variables • Respiratory Rate

• Occurs at a higher percentage of VO max 30/03/10 • Pre-training: 50% VO max Post-training: 80% VO max
2 2 2

• Tidal Volume • Rest: NC • Submax exercise: NC or slight u • Max exercise: slight u • Anaerobic Threshold

156

• Mitochondria • u number, size and membrane surface area • Aerobic Enzymes in Exercising Muscle • Fatty Acid & Glycogen Utilization

Training Adaptations

• u Krebs cycle enzymes (succinate dehydrogenase) • u β oxidation enzymes (carnitine acyltransferase) • u electron transport enzymes (cytochrome oxydase) • u utilization of β oxidative pathways to produce ATP • Called the “glycogen sparring” effect • d RER for any given submaximal workload • u muscle glycogen stores (with high carbohydrate diet)
Exception: training induced u in lean muscle mass

• No Appreciable Change in Resting Metabolic Rate • d Platelet Aggregation • u Fibrinolytic Activity • d Circulating Catecholamines • u vagal tone r d risk of arrhythmia • Resistance to Pathological Events

• smaller infarct size and quicker recovery 30/03/10 • Less of a d in ventricular function during ischemia

157

"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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158

"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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159

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

30 22

5

5

sedentary-rest

sedentary-max

trained-rest

trained-max

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160

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

6

sedentary-rest

sedentary-max

trained-rest

trained-max

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161

"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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162

"Average" Values for Sedentary and Trained Individuals Oxygen Consumption ( ml / kg / minute)
55 38

60 50 40 30 20 10 0 3.5 sedentary-rest sedentary-max 3.5 trained-rest

trained-max

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163

"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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164

"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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165

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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166

HEART ANATOMY (CROSSECTION VIEW)

The heart has four chambers. Two atria act as collecting reservoirs. Two ventricles pumps. act as

The heart has four valves for:  Pumping action of the heart.  Maintaining 30/03/10 unidirectional blood flow.

167

HEART (PHYSIOLOGY)

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.

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168

VASCULAR FLUID MECHANICS
 Velocity and

pressure are inversely related to the cross sectional area of blood vessels.
 These parameters

30/03/10

drop in the capillaries where the cross-sectional area is more. 169

JUST BEFORE I LEAVE……

One of the Keys Happiness is having a

to

good health and a bad memory…

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170

•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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171

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172

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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173

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 30/03/10 muscle daily.” (Clark, 119)

174

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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175

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176

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177

Signs and Symptoms

None

Chest Pain

Signs & Symptoms

Shortness Of Breath

Heart Attack

None: This is referred to as silent ischemia. Blood to your heart may be restricted due to CAD, but you don’t feel any effects. Chest pain: If your coronary arteries can’t 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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30/03/10

can, and does, occur in almost any artery in the body. But in the heart it’s 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)

179

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180

• • • • •

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

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181

Risk Factors
Uncontrollable Uncontrollable

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

•Sex •Hereditary •Race •Age

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182

Screening and Diagnosis
me as ur es

blo od

sp ec i fi c

me asu res

shows

to he ar t

Electrocardiogram
s lse pu im

Stress Test
su pp ly

Coronary Angiography
ng in Narrowi

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183

coronaries

ele ctrical

of of es es St Siit

•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 heart’s movement •Ejection fraction (EF): determines how well your heart pumps with each beat. 30/03/10

184

• 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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185

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186

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 30/03/10 187

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.
30/03/10 188

• 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.
30/03/10 189

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.
30/03/10 190

Age:

Physiological factors affecting Arterial Blood pressure

• 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
30/03/10 increase A.B.P.

191

Factors that Affect Blood Pressure
• Blood pressure is affected by several factors:

• • • •

1- Cardiac output. 2- Peripheral resistance 3- Vessel elasticity 4- Blood volume
30/03/10 192

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.
30/03/10 193

Regulation of Cardiac Output
• The cardiac output is regulated by two forces:

• Intrinsic (Frank-starling mechanism). • Extrinsic (autonomic nervous system).
30/03/10 194

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 30/03/10 195

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196

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
30/03/10 197

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
30/03/10 199

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.

30/03/10 200

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 bloodborne vasoconstrictors. • (Epinephrine, Angiotensin II, Vasopressin)

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201

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. 30/03/10 202

b- Viscosity of blood

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.
30/03/10 203

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
30/03/10 204

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.
30/03/10 205

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.
30/03/10 206

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 a 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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210

Control of blood pressure

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211

2- intermediately acting mechanisms.
• • • • Starts: within half of hour. Lasts: hours to 3-4 days. Type: Mechanism:
– Fluid shift mechanism. – Stress relaxation mechanism.

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212

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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213

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214

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
sinus nerve to CN IX

Carotid sinus baroreceptor

vagus nerve CN X

Integrated nerve activity % maximum

sinus nerve

vagus nerve

Aortic arch baroreceptor

30/03/1060

0

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. When activated:

Receptor afferents

Medullary cardiovascular centres sympathetic parasympathetic

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 30/03/10

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 Vasoconstriction arterioles Tachycardia Reduced vagal tone to s.a. node 30/03/10 Increased myocardial sympathetic tone Raised stroke work Tend to restore arterial blood 217 pressure Effect of gravity on venous return Preload diminished - Starling’s Law Subject possibly feels faint as cerebral flow is reduced Due to reduced arterial B.P.

IMBALANCE OF FORCES AT A CAPILLARY - OEDEMA Osmotic imbalance
Reduction of Π c - Π i reduces absorption and increases net water loss from the plasma mmHg 35 Area 1 > Area 2

25

1 2
arteriolar venular

Πc-Πi

15

Pc - Pi

This may be due to: reduction of plasma protein (Π c) - e.g. reduced albumin production; raised urinary 30/03/10 218 loss

IMBALANCE OF FORCES AT A CAPILLARY - OEDEMA Hydraulic imbalance
Increase of Pc - Pi increases filtration and thereby net water loss from the plasma mmHg 35

Area 1 > Area 2 1 2

25

Πc-Πi

15 arteriolar venular

Pc - Pi

This is generally due to an increase of Pc.Note that the venular end rises more than the arteriolar end as postcapillary resistance is less than precapillary resistance Factors that raise venous pressures will therefore increase Pc - e.g. congestive heart 30/03/10 219 failure, venous compression

THE BALANCE OF FORCES AT A PULMONARY CAPILLARY
In a pulmonary capilllary hydraulic pressures are much less mmHg 35 The smaller value of Pc is due to the reduced pressure generated by the right ventricle. Pc - Pi < Π c - Π i along the entire capillary. Thus there is no filtration of fluid. This ensures that the extravascular space is relatively fluid free minimising the diffusion distance between alveolus and capillary.
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25 Absorption 15

Πc-Πi

5

arteriolar

Pc - Pi

venular

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Shock

• Shock is an abnormal reduction in cardiac output to the point that not enough blood is being circulated to supply all of the cells in the body with adequate oxygen and nutrients.
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• Shock is a severe condition that occurs when not enough blood flows through the body, causing very low blood pressure, a lack of urine, and finally cell and tissue damage.
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Types of shock

1- Cardiogenic. 2- Hypovolemic. 3- Distributive. 4- Obstructive.
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1- Cardiogenic Shock
This type of shock is caused by sever depression of myocardial contractility. • Cause: Myocardial infarct (MI; a “heart attack”). A myocardial infarct is an area of dead cardiac muscle fibers that were killed when their blood supply was interrupted, usually because the artery supplying them with blood became occluded (plugged).
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If more than about 40% of the left ventricle’s muscle fibers stop functioning, the remaining cardiac muscle fibers are unable to eject enough blood from the left ventricle to keep cardiac output within homeostatic limits, and the person will usually go into cardiogenic shock. • About 5 – 10% of all MI victims go into cardiogenic shock, which has a mortality rate of 80 – 90%.
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Manifestations of the cardiogenic shock

1- dyspnea, 2- cheyne-stock respiration. 3- edema. 4- confusion. 5- lack of concentration. 6- rapid week pulse. 7- low blood pressure. 8- pale cold skin. 9- sweating, 30/03/10

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2- Hypovolemic Shock Hypovolemic shock develops when the volume of blood in the circulatory system falls below normal limits. If the volume of blood in the cardiovascular system is reduced, there will be less blood for the heart to pump and, all else being equal, less blood for the heart to pump will result in less blood being pumped ( = reduced cardiac output).
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If the reduction in blood volume is great enough, cardiac output may be reduced enough to put a person into shock. A loss of 10 – 15 % of one’s total blood volume is sufficient to induce at least a mild state of hypovolemic shock in most persons.
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Examples of hypovolemic shock:

• • • •

a- Hemorrhagic Shock b- Burn shock C- Internal bleeding D- Dehydration
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Hemorrhagic Shock
• Hemorrhage – loss of blood – is probably the most obvious cause of hypovolemic shock. • A serious wound, especially one that severs a large artery, can result in loss of sufficient blood to put a person into shock. • The degree, or depth, of hypovolemic shock is directly related to the amount of blood loss, as are the symptoms and the hazards of remaining in a state of shock for a period of time.
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b- Burn shock

• It is a hypovolemic shock which follows extensive burns. • It is due to loss of plasma from the burned skin.
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C- Internal bleeding
Loss of blood from the body. Loss of blood from the cardiovascular system can occur internally, as well as externally. For example, hypovolemic shock is a serious risk following blunt force trauma to the chest or abdomen This is because the force of the blow can rupture the aorta, spleen, or liver.
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D- Dehydration 1
A reduction in blood volume sufficient to cause shock can occur in other ways that don't involve hemorrhage For example, dehydration resulting from any number of causes can reduce the blood volume enough to induce hypovolemic shock. Vomiting and/or diarrhea, particularly in infants, can quickly result in dangerous degrees of dehydration.
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D- Dehydration 2
This is why cholera is such a deadly disease. The cholera bacterium, to facilitate its spread to other hosts, produces a toxin that does nothing more than make the capillaries of the intestinal tract lining highly permeable to water. This results in massive efflux of water from the blood into the lumen of the intestine which, in turn, induces severe diarrhea. The resulting water losses are so rapid that it's very difficult to replace them quickly enough to prevent death due to dehydration.
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Signs and Symptoms Hemorrhagic Shock

1- Palpitations. 2- dizziness. 3- tachycardia. 4- Cold clammy skin. 5- Sweating. 6- oliguria. 7- breathing difficulty. 8- Anuria ( = no urine production) Deficient blood supply to brain and heart Brain and heart damage leading to death.
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• As the term “distributive” implies, this form of shock develops when the cardiac output (which is usually normal in this case) is not being distributed properly to the organs that need it. • There are a variety of causes of distributive shock, but they all have one thing in common: - a massive dilation of the blood vessels – especially the veins – throughout the body, with the result that blood tends to pool in the vessels an not reach the capillaries rapidly enough.
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3- Distributive Shock

• In addition, certain causes of distributive shock also trigger mechanisms that make the capillaries very leaky to plasma (the liquid fraction of the blood). • This results in a significant fraction of the plasma leaking out into the extracellular spaces ( = edema), where it’s no longer available for circulation by the heart. The resulting hypovolemia makes the situation even worse.
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Causes of Distributive shock
a- Septic Shock • The most common form of distributive shock is septic shock, which results directly from some sort of infection, usually bacterial (sepsis means “a toxic condition resulting from infection”). In some cases, the body responds to sepsis with a massive reaction that is essentially allergic in nature. Cells throughout the body release a variety of compounds that trigger the general vasodilatation and plasma loss that produce the shock state. •
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b- Anaphylactic Shock • Anaphylactic shock is similar to septic shock in that it also involves the generalized vasodilatation and increased capillary permeability that severely reduces blood supply to the tissues, but the cause is not a bacterial infection. • The most common causes of anaphylaxis and the resulting shock are foods (especially peanuts), drugs (especially penicillin and aspirin), insect stings (especially bees, wasps, and ants), blood transfusions, and even exercise. 30/03/10 239

c- Neurogenic Shock • This form of shock involves the nervous system. • The basic cause of neurogenic shock is generally a massive inhibition of both the Excitatory and Inhibitory portions of the Vasomotor Center. Now, • Well, the problem is that inhibition of the Excitatory Portion of the • Vasomotor Center also results in vasodilatation throughout the body, due to inactivation of the tonic vasoconstrictor neurons that are normally being stimulated by the Excitatory Vasomotor Center
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• This vasodilatation, coupled with the decreased cardiac output, typically results in a drastic reduction in blood flow to the brain, a reduction sufficient to lead to damage within a relatively short time. • The two principal causes of neurogenic shock are trauma to the medulla (say, from a head injury), spinal cord injuries, and general anesthetics.

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4- Obstructive Shock • This is an unusual form of shock that results when pressure on the heart prevents it from filling or pumping effectively. • The most common causes of obstructive shock are pneumothorax (air in the chest cavity) or cardiac tamponade (compression of the heart by fluid or blood in the pericardial space)

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