Cardiovascular System. Week 10 Dr. Walid Daoud A. Professor. Cardiovascular System ____________________________________________________________________________________________________________________________________________. Functions: 1-Supplies O 2 , hormones & nutrients to cells.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
Dr. Walid Daoud
1-Supplies O2, hormones & nutrients to cells.
2-Collects CO2 and waste products of tissues.
4-Allows blood to pass in a forward direction.
Anatomy of the Heart:
It pumps blood distributes it allover the body according to pressure gradient.
It is a muscular pump that contracts and relaxes continuously.
It is of the size of the fist of the hand.
It is located in and protected by the thoracic bony cage.
Right side of the heart:
Right atrium, right ventricle and a tricuspid valve in between.
. Contains venous blood (70% oxygenated).
. Receives blood from superior and inferior vena cavae that open into the right atrium (venous return).
In between right ventricle and pulmonary artery there is a pulmonary valve.
Left side of the heart:
Left atrium, left ventricle with a mitral valve in between.
. Left atrium receives arterial oxygenated blood from the lungs via 4 pulmonary veins.
. In between the left ventricle and aorta there is an aortic valve.
A membranous double layer sac formed of inner visceral and outer parietal layers with a thin film of fluid (30 cc)in between them to avoid friction.
Striated muscle formed of many sarcomeres (dark and light bands) and rich in mitochondria.
Muscle fibers have no protoplasmic continuity but there are intercalated discs so the heart is a functional syncytium (one unit) i,e. contracts instantaneously.
Properties of Cardiac Muscle____________________________________________________________________________________________________________________________________________
It is the ability of cardiac muscle to contract
day and night. It obeys 2 laws:
1-All or non law: either contract to threshold stimulus or not contract at all to subthreshold stimulus.
2-Frank Starling law (length-tension relationship)
↑ in end-diastolic volume causes ↑ in fiber length, which causes ↑ in developed tension with powerful contractility within limit.
Factors ↑ Contractility:
-Increased heart rate e.g., exercise.
-Sympathetic stimulation via B receptors.
-Drugs e.g., digitalis.
-Frank Starling law.
Factors ↓ Contractility:
-Parasympathetic (vagus nerve) stimulation (atrial not ventricular muscle).
-Bleeding and decrease venous return.
It is the ability of the heart to initiate an action potential in response to own depolarizing current.
The heart is regular all the time with phases of refractory periods of excitability:
1-Absolute refractory period:
Cardiac muscle does not respond to any stimulus whatever its intensity.
2-Relative refractory period:
Cardiac muscle can respond to action potential due to strong stimulus and leads to extrasystole.
This result from ectopic focus in the cardiac muscle that competes with SAN (topic focus)
1-Atrial ectopic focus.
2-A-V nodal focus.
3-Ventricular ectopic focus.
Causes of ectopic foci:
Smoking, caffeine, myocadial ischemia or infarction, mitral stenosis & hyperthyroidism.
Cardiac action potentials:
Threshold stimulus causes depolarization:
Phase 0: Upstroke of action potential (Na+ influx).
Phase 1: initial repolarization (K+ efflux).
Phase 2: plateau (Ca++ influx and Na+ influx).
Phase 3: repolarization (K+ efflux).
Phase 4: resting membrane potential.
It is the ability of cardiac muscle to spread excitatory impulses in the heart tissue via a specialized conductive system in the cardiac muscle:
1-Sino-atrial node (SA node)
It is the pace maker of heart.
3-Bundle of Hiss.
4-Right and left bundle branches.
Spread of Cardiac Excitation____________________________________________________________________________________________________________________________________________
Depolarization is initiated in SAN, impulses spread in atria and converge on A-V node where impulse is delayed in it to avoid irregularity of impulses coming from atria. Then wave of depolarization spread from cardiac septum rapidly to Purkinje sustem to all parts of ventricles.
Sympathetic stimulation ↑ cardiac conductivity while vagal stimulation lengthened and slow conductivity in SAN, AVN & atrial fibers.
It is the ability of cardiac muscle to initiate an action potential of its own regularly. Normally SAN has the highest rhythmicity, therefore the SAN is the normal pace maker of the heart, i.e its rate determine the heart rate.
It is recording of electrical events during the cardiac cycle i.e., systole and diastole.
1- Measures the heart rate/min.
2- Identifies normal sinus rhythm (regularity).
3- Diagnosis of arrhythmias.
4- Diagnosis of ischemia and infarction.
5- Diagnosis of electrolytes imbalance.
The electrical changes in the cardiac muscle are recorded by electrodes of a special instrument called electrocardiography.
The record is the electrocardiogram (ECG)
Waves of normal ECG:
P-wave: atrial depolarization.
QRS-complex: ventricular depolarization.
T-wave: ventricular repolarization.
Intervals of ECG:
P-R interval: 0.12-0.2 sec.
Interval between atrial depolarization and ventricular depolarization (A-V conduction).
Interval from beginning of Q wave to end of
T wave (Whole period of depolarization and repolarization of the ventricle).
From end of S wave to end of T wave.