6/12/ :14 PM 1 Circulatory System

6/12/ :14 PM 2 Organization of CVS Heart Blood vessels

6/12/ :14 PM 3 Heart Consist of two pumps in series One propel blood through the lungs The other propel blood to all tissues of the body Unidirectional flow through the heart Is achieved by appropriately arranged cardiac valves.

6/12/ :14 PM 4 Organization of CVS Thus two systems Pulmonary circulatory system Systemic circulatory system

6/12/ :14 PM 5 Head &Arms Brain Lt Heart Rt Heart Spleen,GITLiver Lungs Kidneys Trunk, legs Hepatic artery Portal vein Coronary vessels

6/12/ :14 PM 6 Aorta and arteries Have strong vascular walls Allows flow of high pressure blood

6/12/ :14 PM 7 Arteriole Have thick muscular layer (smooth muscle) Acts as control valves

6/12/ :14 PM 8 Capillaries Extremely thin structures Single layer of highly permeable endothelium Allows exchange of material (solute and solvents) between plasma and ISF.

6/12/ :14 PM 9 Veins and Venae carvae Have thin walls which is muscular Acts as controllable reservoir

6/12/ :14 PM 10 BP in various portions of circulation Pressure in the aorta is high averaging 100mmHg Arterial pressure fluctuates between systolic level (120mmHg) and diastolic 80mmHg. Falls progressively to about O mmHg at the termination of venae carvae Systemic capillaries varies from as high as 35mmHg near arteriole end to as low as 10mmHg near venous end with average functional pressure of about 17mmHg

6/12/ :14 PM 11 BP in various portions of circulation. In pulmonary circulation Systolic ≈ 25mmHg Diastolic ≈ 8mmHg Mean pulmonary arterial pressure is about 16mmHg Pulmonary capillary pressure averages about 7mmHg.

6/12/ :14 PM 12 Impulse generation & conduction

6/12/ :14 PM 13 Impulse generation & conduction RMP of normal cardiac muscles is -85 to – 95 mV Purkinje fibers is –90 to –100mV SA + AV nodes is –55 to –65mV.

6/12/ :14 PM 14 Cardiac muscle AP Why plateau Slow Ca++ channels slow to open and remain open for several tenths of sec. Immediately after onset of AP muscle membrane permeability to K+ ↓

6/12/ :14 PM 15 Cardiac muscle AP When slow Ca2+ channels close at the end of 0.2 to 0.3 sec and the influx of Na+and Ca2+ cease the membrane permeability for K+ ↑ rapidly.

6/12/ :14 PM 16 Cardiac muscle The strength of contraction of cardiac muscles depends on [Ca2+] is ECF.

6/12/ :14 PM 17 Natural Excitation of the heart NS controls various aspects of the behavior of the heart However cardiac function certainly does not require intact nervous pathway The properties of automaticity and rhythmicity are intrinsic to cardiac tissues Apparently at least some cells in the walls of the 4 cardiac chambers are capable of initiating beats.

6/12/ :14 PM 18 Natural Excitation of the heart Such cells are in the nodal tissues or specialized conducting fibres of the heart The cardiac region that ordinarily generate impulse at the greatest frequency is the SA node it is called natural pacemaker of the heart

6/12/ :14 PM 19 Natural Excitation of the heart RMP of sinus node fibres is –55 to - 60mV Why: The cell membrane of sinus node fibres are naturally leaky to Na+ At this negativity level (-55 to -60) the fast Na+ channels have mainly become inactivated which means that they have become blocked

6/12/ :14 PM 20 Self Excitation of SA Fibres Influx of Na+ Increases membrane potential RMP gradually rises between 2 beats When it reaches a threshold voltage of ≈ -40mV the Ca2+ - Na+ channels become activated leading to rapid entry of both Ca2+ and Na+ causing AP Ca2+ - Na+ channels become inactivated after 100 –150ms At the same time greatly increased number of K+ channels open

6/12/ :14 PM 21 Self Excitation of SA Fibres Influx of Ca2+ and Na+ through Ca2+ - Na+ channel ceases at the same time large number of K+ diffuse out, i.e. terminating the AP K+ channels remain open for another few tenths of a Sec Causing hyperpolarization

6/12/ :14 PM 22 Transmission of impulses SA node fibres fuse with the surrounding artrial muscle fibers From SA node → atrial muscle → eventually to AV node → Lt atrium through anterior interatrial band Other 3 small bands curve through atrial wall to terminate in AV node Anterior,Middle &Posterior internodal pathways

6/12/ :14 PM 23 Transmission of impulse SAN → AVN → AV bundle system. (0.03) (0.12) (0.16) ↓ Purkinje fibers (1.5-4m/s) ↓ ventricular muscle. (0.3 – 0.5m/s)

6/12/ :14 PM 24 Slow conduction in AV node Fibers are smaller than the size of normal atrial muscle fibers Few gap junctions connect the successive cells in the pathway so that there is great resistance of conduction

6/12/ :14 PM 25 Slow conduction in AV node Delay in impulse conduction from Atria to ventricles Allows atria to contract ahead of ventricles

6/12/ :14 PM 26 Purkinje system Fibers are very large Transmit AP at 1.5 – 4m/s believed to be due to high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up Purkinje fiber.

6/12/ :14 PM 27 Control of excitation & conduction in the heart. SA node ANS

6/12/ :14 PM 28 Control of excitation & conduction in the heart SAN initiates impulses at a rate of 60 – 100bpm AVN and the bundle of His has intrinsic firing rate of approximately 50 – 60bpm Cells of Purkinje system 30 – 40bpm Hence SAN controls heart rate Natural pacemaker

6/12/ :14 PM 29 Control of excitation & conduction in the heart AVN, the bundle of His and Cells of Purkinje system are latent pacemakers. These latent pacemakers may initiate impulses and take over the pacemaker function at their intrinsic firing rates if the faster pacemakers (i.e cells of the SAN) fail, or if the conduction abnormalities block the normal wave of depolarization from reaching the latent pacemaker sites.

6/12/ :14 PM 30 HR and Rhythm Arrhythmias may arise from Altered automatically of the SAN or latent pacemakers within the specialized conducting pathway. Development of abnormal automaticity by atrial or ventricular myocytes.

6/12/ :14 PM 31 Increased Sinus node automaticity The most important modulator is ANS Sympathetic stimulation or increased circulating catecholamines increases the permeability of the pacemaker channels This cause SAN to reach threshold and fire earlier than in the absence of sympathetic stimulation Sympathetic stimulation also shifts the AP threshold to more negative voltage, by increasing the probability that voltage- sensitive Ca++ channels are open.

6/12/ :14 PM 32 Decreased sinus node automaticity Mediated primarily by Parasympathetic NS Acetycholine reduce the permeability pacemaker channels to Na+ and Ca2+ Moves the AP threshold closer to zero. Increases permeability of K+ channels. If the sinus node becomes suppressed fires less frequently than normal, the site of impulse formation usually shifts to a latent pacemaker Escape beat

6/12/ :14 PM 33 Escape beats Persistent impairment of SAN will allow continued series of escape beats termed escape rhythm. Represent protective mechanism that prevent the heart rate from becoming too slow when SAN firing is impaired. latent pacemaker can develop an intrinsic rate of depolarization faster than that of SAN – Ectopic beat.

6/12/ :14 PM 34 Ectopic beats Impulse is premature in terms of normal rhythm When similar ectopic beats occur in series it is called ectopic rhythm. Induced during periods of hypoxemia, ischemia, electrolyte disturbances, certain drug toxicity.

6/12/ :14 PM 35 Abnormal automaticity Cardiac tissue injury may lead to pathological changes in impulse formation whereby myocardial cells outside the specialized conducting system acquire automaticity and sponteneously depolarize Can be source of abnormal ectopic rhythms.

6/12/ :14 PM 36 Altered impulse conduction May also lead to arrhythmias Mechanisms primary responsible Conduction block generally lead to slow HR A propagating impulse is blocked when it encounters a region of the heart that is electrically unexcitable Transient or permanent Unidirectional or bi-directional. Causes Ischemia, fibrosis(scarring), trauma temporarily by certain drugs.