Physiology - Part 2A PDF

[Part 2A] Physiology  Aorta branches into many arteries that travel to organs  Arteries branch into many arterioles in tissue  Arterioles branch into thin-walled capillaries for exchange of gases and nutrients  Deoxygenated blo...

[Part 2A] Physiology  Aorta branches into many arteries that travel to organs  Arteries branch into many arterioles in tissue  Arterioles branch into thin-walled capillaries for exchange of gases and nutrients  Deoxygenated blood begins its return in venules  Venules merge into veins and return to right atrium. Pulmonary circulation Right side of heart pumps deoxygenated blood to lungs Right ventricle pumps blood to pulmonary trunk pulmonary trunk branches into pulmonary arteries pulmonary arteries carry blood to lungs for exchange of gases Oxygenated blood returns to heart in pulmonary veins. There are 5 Phases of cardiac action potential:  Depolarization phase (phase 0): in which large number of Na+ enter inside the cell & causes the membrane potential to reverse from its resting potential (-90 to +30mV).  Early repolarization phase (phase 1): membrane potential return toward 0 mV as a result of closing Na+ channels & outward K+ current.  Plateau phase (2): a slow inward of Ca++ take place through opening of Ca++ channels for contraction & outflux of K+. Ventricular Contraction Phase.  Phase 3: it’s late phase of repolarization slow Ca++ channels close & rate of K+ outflux increases.  Phase 4: pacemaker potential for SA, AV node & Purkinje fiber in which there influx of Ca++, some Na+ influx but no K+ outflux resulting in depolarization. it’s the ability of cardiac muscle to contract isotonically & isometrically. Mechanism of cardiac cotraction:  During depolarization & plateau phase both Na+ & Ca++ enter the cardiac muscle cells & Ca++ triggers the release of additional Ca++ from sarcoplasmic reticulum & increases free Ca++➔Ca++ interacts with troponin-C leading to activation of cross-bridging or sliding between actin and myocin➔ cardiac muscle contraction. 1  [Part 2A] Physiology Factors affecting contractility: 1) Sympathetic stimulation: Stimulate B1 receptors in myocardium & increase contractility. 2) Increased Ca++ ions: increase cardiac contraction (excess Ca ion Stop heart during systole). 3) Increased Concentration: increase in cardiac diastole (excess K+ stop heart in relaxed state). 4) Alcohol & Ether: (organic solvents) decrease myocardial contractility.  Stroke volume: is the amount of blood pumped by ventricles in single contraction Increase in contractility ➔ increase in SV.  Cardiac output: is the amount of blood pumped by the heart / minute.  C.O.= HR ΧSV. ‫ حجم الضربة‬x ‫انتاج القلب = معدل ضربات القلب‬  which is the ability of cardiac muscle to initiate impulses within it self which make it beat regularly (myogenic in nature).  SA node has the highest rate of impulses (80-120/ minute) so it’s the normal pacemaker of the heart.  which is the ability of the cardiac muscle to conduct the impulses initiated in the SA node (normal pacemaker) in the form of depolarization. : it’s the period during which the heart cannot respond to usual stimuli. Sino-atrial node: It’s the pacemaker of the heart.  Its present in the upper part of the right atrium.  Radiate and send electricity to all parts of the heart in the following sequence (from sinoatrial node (SAN) ➔ atrial wall ➔Atrioventricular (AVN) ➔ Atrioventricular bundle (AVB) ➔Right & Left bundle branches ➔Purkinje fiber and so to ventricular wall).  It has a B1 receptor that stimulated by sympathetic stimulation.  Also contain parasympathetic stimulation receptor. Resting stage potential of individual cardiac muscle cell; inside negative & outside positive. 2  [Part 2A] Physiology  It’s the Recording of electrical events in myocardium.  P wave: depolarization of atrial myocardium half for RT. & LT. Signals onset of atrial contraction. (amplitude of wave 0.1mV, duration 0.1 second & normal positive).  R wave: ventricular depolarization. Signals onset of ventricular contraction. (amplitude of R wave 1mV, duration 0.06- 0.1 second & normal positive).  T wave: repolarization of ventricles (amplitude of wave 0.2 – 0.4 mV, duration 0.2 – 0.25 second & normal positive). ☺ Heart beat is called a cardiac cycle. ☺ In cardiac cycle: both atria contract together, then two ventricles contract; then whole heart relaxes. ☺ Systole: is the contraction of heart chambers; While diastole is their relaxation. ☺ The heart sounds, lub-dup, are due to closing of atrio-ventricular valves, followed by closing of semilunar valves. ‫البطينية متبوعة بانغالق الصمامات الهاللية‬-‫تنتج عن انغالق الصمامات االذينية‬ Heart Rate & its Regulation: [normally 60-90]  Pulse = effect of blood pressure on the artery:  infants have HR of 120 bpm or more.  young adult 60 - 90 bpm.  HR rises again in the elderly.  Tachycardia: resting adult HR above 100:  Physiological causes e. g. stress, anxiety.  Pathological causes e. g. heart disease , drugs or increase body temp.  Bradycardia: resting adult HR < 60:  Physiological causes e. g. sleep and athletes.  Pathological causes e. g. with some Heart diseases. (Autonomic N. S., other centers in CNS & Afferent reflexes )  Parasympathetic stimulation: - a negative chronotropic factor. Supplied by Vagus nerve, decreases heart rate, through release of acetylcholine.  Sympathetic stimulation: - a positive chronotropic factor Supplied by cardiac nerves. Due to release of Noradrenaline lead to increase heart rate. 3  [Part 2A] Physiology ☺ Cerebral cortex, limbic system: stress, fear & emotion increase HR. ☺ Hypothalamic stimulation: (posterior hypothalamic nuclei stimulation lead to increase in HR while anterior hypothalamic nuclei stimulation lead to decrease in HR ) ☺ Medulla Oblongata:  Cardiac inhibitory center: decrease HR.  Cardio-acceleratory center: increase HR.  Inspiratory center:increase HR while expiration decrease HR. 1- Bainbridge reflexes: increase venous return to heart ➔ stimulate stretch receptors in right atrium ➔ increase sympathetic activity & respiratory center lead to increase rate of respiration (Harrison reflex) &increase HR. 2- Baroreceptor Afferents: there are many baroreceptors in carotid sinus & aortic arch ➔ inhibition of vasomotor center (VMC) & stimulation of Cardiac Inhibitory Center., ➔ vagal over activity & decrease in HR. N. B.: Mary´s Law: HR rate is inversely proportional to arterial blood pressure 3- skeletal muscle contraction: send impulse to medulla and stimulate cardio-acceleratory center leading to increase in HR. 4- Moderate painful stimuli: increase HR while sever pain decrease HR can lead to SHOCK. 1- Para-sympathomimetic: e. g. Acetyl choline & physiostimine stimulate M2 receptors in SA node & to decrease HR While Para-sympatholytic block M2 receptors & increase HR. 2- sympathomimetic: e. g. noradrenaline & stimulate B1 receptors in SA node & to increase HR While sympatholytic e. g. propranolol block B receptors & decrease HR. 3- Intra- and extracellular ion concentrations: must be maintained for normal heart function e. g. Increase CO2 ➔ increase HR while increase O2 ➔ Decrease.  Hypothermia: decrease heart rate.  Fever: each increase in body temperature by 1C ➔ Increase HR by 15 /b/m except in typhoid fever due to the effect of typhoid toxin. 4