Professional Documents
Culture Documents
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CVS consists of the heart and a series of blood vessels (arteries, veins and capillaries).
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CVS
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The circulatory system forms two circuits in series with each other:-
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Lungs
Left Atrium
Septum
Brain
Lungs
Muscle
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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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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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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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Mammalian 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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GAP JUNCTIONS
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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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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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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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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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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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m/sec 1 1m/sec
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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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SYSTOLE
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DIASTOLE
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ECG
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ECG Recording
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ECG Leads
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ECG LEADS
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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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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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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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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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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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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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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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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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Adventitia
Right CA Left Anterior Descending CA
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Media Intima
Marginal Branch
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Ejection Fraction is the best indicator of heart performance and disease prognosis 126
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
regulated by: sympathetic nerve activity (most influential) catecholamines (epinephrine norepinephrine) amount of contractile mass drugs
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SV
(left ventricular performance)
Preload
(venous return)
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u Contractility related to :
b sympathetic adrenergic nerves catecholamines: - epinephrine - norepinephrine drugs: - digitalis - sympathomimetics
Definitions
content between arterial and venous blood- ml O / 100 ml blood 2 measured in ml%
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predicted VO2max
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Definitions
relaxation)
Mean Arterial Pressure (MAP) "average" pressure throughout the Total Peripheral Resistance (TPR) - the sum of all forces that
oppose blood flow
estimated as:
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( p ) ( r4 )
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Flow (Q) =
= Resistance (TPR) =
Pressure (MAP)
Flow (Q)
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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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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a 1 stimulation r a2
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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Precaillary Sphincter Anastomosis (Shunt) True Capillary With Single Layer of Endothelium
Metarteriole
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Venule
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102 26 7
Normal Resting Pressure Driving the Blood from Left Ventricle to Vena Cava: 102 - 2 = 100 mmHg
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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)
(40) ARTERIOLES
7% of blood volume Systemic Circulation = 100 mmHg 0 mmHg 06/12/11 Flow (Q) 1 mmHg sec / ml = 100 ml / sec = 6 liters / min
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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
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Cardiorespiratory Control
Stroke Volume regulated by Frank Starling mechanism
stroke volume
preload r u SV
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Cardiorespiratory Control
Blood Pressure influenced by 3 major factors
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
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r e n a l
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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
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
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Dehydration
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
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
u u
blood flow r vessel stretch r channel activation [Ca++ ] in smooth muscle r vasoconstriction r d flow
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Cardiorespiratory Control
Exercise Systemic Blood Flow: Autonomic influences Sympathetic outflow & circulating catecholamines
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Cardiorespiratory Control
Respiration: VE = Tidal Volume X Respiratory Rate
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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VE
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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
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Workloads (Watts)
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
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
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
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d 06/12/11 u
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
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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
Termination
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P P P
O O C
OBLA
2
&
No Change in
VE
V V V H
VCO2
C O 2 C
Om 2
p H
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Increasing workload
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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
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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
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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
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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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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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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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to
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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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None
Chest Pain
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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coronaries
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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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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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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
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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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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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 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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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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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.
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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
sinus nerve
vagus nerve
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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
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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.
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