Cardiac Physiology PDF

**The sino atrial node (SA node) exhibits the greatest degree of self excitation and inherent discharge rate** **For this reason the SA node is the pacemaker of the heart** Sinoatrial node (SA node) - "pacemaker"; located in right atrium AV node and Purkinje fibers are secondary pacemakers of ect...

**The sino atrial node (SA node) exhibits the greatest degree of self excitation and inherent discharge rate** **For this reason the SA node is the pacemaker of the heart** Sinoatrial node (SA node) - "pacemaker"; located in right atrium AV node and Purkinje fibers are secondary pacemakers of ectopic pacemakers; slower rate than the "sinus rhythm" **[Conducting tissues of the heart]** a. Action potentials spread via intercalated discs (gap junctions). b. SA node to AV node to stimulate atrial contraction c. AV node at base of right atrium and bundle of His *(a collection of heart muscle cells specialized for electrical conduction)* conduct stimulation to ventricles. d. In the interventricular septum, the bundle of His divides into right and left bundle branches. e. Branch bundles become Purkinje fibers, which stimulate ventricular contraction. **Self excitation of nodal fibres** - **Na+ ions naturally tend to leak into sinus nodal fibres-multiple membrane channels** - **Membrane potential rises to a threshold voltage of -40 millivolts the Ca+ Na+ channels open** **Monophasic Action Potential (MAP) in Cardiac Pacemaker Cells** A monophasic action potential (MAP) is a specific type of electrical activity observed in cardiac pacemaker cells, primarily those located in the sinoatrial (SA) node. It\'s characterized by a single, smooth depolarization phase followed by a repolarization phase. Key Features of a Monophasic Action Potential: Phase 4 (Pacemaker Potential): Spontaneous, slow depolarization due to the influx of sodium ions (Na+) and the gradual decrease in potassium ion (K+) permeability. This phase is responsible for the inherent rhythmicity of the heart, allowing for continuous electrical impulses. Phase 0 (Rapid Depolarization): - **The potential of the SA fibre between discharges is -55 to -60 millivolts** - **The potential of the ventricular fibre between discharges is -85 to -90 millivolts** - **The reason for this difference is the that the sinus fibres are naturally leaky to sodium ions** Rapid influx of calcium ions (Ca2+) through voltage-gated calcium channels. This leads to a steep rise in the membrane potential. Phase 3 (Repolarization): Efflux of potassium ions (K+) through voltage-gated potassium channels. This brings the membrane potential back to its resting state. **Action Potentials in Cardiac Muscle** - **Resting membrane potential of cardiac muscle is -85 to -90 millivolts** - **Ventricular membrane potential moves from -85 to +20 millivolts (overshoot potential)** - **The plateau phase in cardiac muscle 3-15 times the duration of the plateau phase of skeletal muscle** - **Cardiac muscle** fast sodium channels as well as slow calcium Sodium channels (slow calcium-sodium channels T TYPE calcium channels) open - The L-TYPE calcium-sodium channels open slower but remain opened for longer. Both sodium and calcium flow in for a prolonged period causing the extended plateau phase - **Secondly** onset of the AP decreases the muscle permeability to potassium by about 5 fold - Decreased potassium permeability decreases the outflux of potassium ions during the AP and prevents early recovery - The cessation of calcium and sodium influx into the muscle is followed by increased potassium membrane permeability which returns the muscle to its resting potential **[Excitation-contraction Coupling]** a. Ca^2+^-stimulated Ca^2+^ release b. Action potentials conducted along the sarcolemma and T tubules, open voltage-gated Ca^2+^ channels c. Ca^2+^ diffuses into cells and stimulates the opening of calcium release channels of the SR d. Ca^2+^ (mostly from SR) binds to troponin to stimulate contraction e. These events occur at signaling complexes on the sarcolemma where it is close to the SR **[Repolarization]** a. Ca^2+^ concentration in cytoplasm reduced by active transport back into the SR and extrusion of Ca^2+^ through the plasma membrane by the Na^+^-Ca^2+^ exchanger b. Myocardium relaxes **Differences in the conduction of the AP in cardiac muscle vs skeletal muscle cont..** - **In cardiac muscle large amounts of Ca2+ diffuse into the sarcoplasm from the T-tubules- without this the cardiac muscle will not contract fully** - **The sarcoplasmic reticulum of cardiac muscle-less developed than skeletal muscle but:** **T tubule diameter in cardiac muscle -- 5 times that of skeletal muscle and 25 times greater volume** **[Electrocardiogram waves and intervals]** a. P wave - atrial depolarization b. P-Q interval -- atrial systole c. QRS wave - ventricular depolarization d. S-T segment - plateau phase, ventricular systole e. T wave - ventricular repolarization In hyperkalaemia, the T wave is "pulled upwards", creating tall "tented" T waves, and stretching the remainder of the ECG to cause P wave flattening, PR prolongation, and QRS widening **Hypokalaemia** creates the illusion that the T wave is "pushed down", with resultant T-wave flattening/inversion, ST depression, and prominent U waves **[Electrocardiograph leads]** a. Bipolar limb leads record voltage between electrodes placed on wrists and legs. 1. Lead I: between right arm and right leg 2. Lead II: between right arm and left leg 3. Lead III: between left arm and left leg a. *"Lub"* occurs after the QRS wave as the AV valves close "Dub" occurs at the beginning of the T wave as the SL valves close - Abnormal heart rhythms a. Bradycardia: slow heart rate, below 60 bpm b. Tachycardia: fast heart rate, above 100 bpm c. These heart rhythms are normal if the person is active, but not normal at rest. Abnormal tachycardia can occur due to drugs or fast ectopic pacemakers a. Ventricular tachycardia occurs when pacemakers in the ventricles make them contract out of synch with the atria. b. This condition is very dangerous and can lead to ventricular fibrillation and sudden death. **[Flutter and Fibrillation]** a. Flutter: extremely fast (200−300 bpm) but coordinated contractions b. Fibrillation: uncoordinated pumping between the atria and ventricles **[Types of Fibrillation]** a. Atrial fibrillation: 1. Can result from atrial flutter 2. Atrial muscles cannot effectively contract. 3. AV node can't keep pace with speed of atrial contractions, but some stimulation is passed on. 4. Only reduces cardiac output by 15% 5. Associated with increased risk of thrombi, stroke, and heart failure Ventricular fibrillation Ventricles can't pump blood, and victim dies without CPR and/or electrical defibrillation to reset the heart rhythm. Caused by circus rhythms -- continuous cycling of electrical waves Refractory period prevented Sudden death progresses from ventricular tachycardia, through ventricular fibrillation, ending in astole (straight-line ECG) **[AV Node Block]** a. Damage to the AV node can be seen in changes in the P-R interval of an ECG. b. First degree: Impulse conduction exceeds 0.2 secs. c. Second degree: Not every electrical wave can pass to ventricles d. Third degree/complete: No stimulation gets through. A pacemaker in the Purkinje fibers takes over, but this is slow (20−40 bpm). - Tunica interna - inner layer; composed of simple squamous endothelium on a basement membrane and elastic fibers a. Vasoconstriction and vasodilation of arterioles b. Precapillary sphincters: a band of smooth muscle that adjusts blood flow into a. Continuous capillaries: Adjacent cells are close together; found in muscles, adipose tissue, and central nervous system (add to blood-brain barrier) b. Fenestrated capillaries: have pores in vessel wall; found in kidneys, intestines, and endocrine glands c. Discontinuous: have gaps between cells; found in bone marrow, liver, and spleen; allow the passage of proteins. **[Veins]** - Most of the total blood volume is in veins - Lower pressure (2 mmHg compared to 100 mmHg average arterial pressure) - Thinner walls than arteries, larger lumen; collapse when cut Need help to return blood to the heart: Skeletal muscle pumps: Muscles surrounding the veins help pump blood. Venous valves: Ensure one-directional flow of blood Breathing: Flattening of the diaphragm at inhalation increases abdominal cavity pressure in relation to thoracic pressure and moves blood toward heart. **Atherosclerosis** - Most common form of arteriosclerosis (hardening of the arteries) a. Contributes to 50% of the deaths due to heart attack and stroke Damage the endothelial lining -Free Radicals ROS -endothelial adhesiveness for monocytes (platelets) =Nitric oxide decreased -Impairs endothelium-dependent relaxation to acetylcholine (EDR) c\. LDL+VLDL oxidised h\. rupture- forming a clot e\. Inflammatory cytokines CRP, TNF Alpha f\. Cell proliferation- smooth muscle cells start to migrate Out to the foam cells- release collagen Protein cap- to protect from blood g\. Ca+ \--hardens the foam cells **[Inflammation in Atherosclerosis]** a. Atherosclerosis is now believed to be an inflammatory disease. b. C-reactive protein (a measure of inflammation) is a better predictor for atherosclerosis than LDL levels. c. When endothelial cells engulf LDLs, they become oxidized LDLs that damage the endothelium d. Antioxidants may be future treatments for this condition. **[Cholesterol and Lipoproteins]** a. Low-density lipoproteins (LDLs) carry cholesterol to arteries. 1. People who consume or produce a lot of cholesterol have more LDLs. 2. This high LDL level is associated with increased development of atherosclerosis High-density lipoproteins (HDLs) carry cholesterol away from the arteries to the liver for metabolism. This takes cholesterol away from the macrophages in developing plaques (foam cells). Statin drugs (e.g., Lipitor), fibrates, and niacin increase HDL levels. Monitoring ones diet. Saturated fats increase LDL and unsaturated fats increase HDL **[Ischemic Heart Disease]** a. Ischemia is a condition characterized by inadequate oxygen due to reduced blood flow. 1. Atherosclerosis is the most common cause. 2. Associated with increased production of lactic acid and resulting pain, called angina pectoris (referred pain). 3. Eventually, necrosis of some areas of the heart occurs, leading to a myocardial infarction (heart attack). Nitroglycerin produces vasodilation Improves blood flow Reperfusion injury may cause death of neighboring cells to enlarge the infarct Ischaemia-Reperfusion injury (IRI) is defined as the paradoxical exacerbation of cellular dysfunction and death, following restoration of blood flow to previously ischaemic tissues. **[Detecting Ischemia]** 1. Depression of the S-T segment of an electrocardiogram Plasma concentration of blood enzymes Creatine phosphokinase -- 3-6 hours, return to normal in 3 days Lactate dehydrogenase -- 48-72 hours, elevated about 11 days Troponin I -- today's most sensitive test Troponin T **Maximum Heart Rate (MHR) = 220 -- age** - Stroke volume is the amount of blood pumped out of the left ventricle per beat. - Cardiac output is the amount of blood pumped out of the left ventricle of the heart per minute cardiac output = stroke volume x heart rate - Regular exercise causes changes to the heart. - The heart gets larger - The muscular wall become thicker and stronger - Stroke volume at rest increases, leading to a lower resting heart rate Having high blood pressure puts stress on the heart. It can lead to angina, heart attacks and strokes. 1. **Normal:** - Systolic: 100-119 mmHg - Diastolic: 60-79 mmHg 2. **Hypotension:** - Systolic: \ - Aldosterone increases the rate of reabsorption of salt and water by the tubules of the kidneys, thereby reducing the loss of these in the urine while at the same time causing an increase in blood volume and extracellular fluid volume **Stages of Shock** - A nonprogressive stage (sometimes called the compensated stage), in which the normal circulatory compensatory mechanisms eventually cause full recovery without help from outside therapy - A progressive stage*,* in which, without therapy, the shock becomes steadily worse until death - An irreversible stage*,* in which the shock has progressed to such an extent that all forms of known therapy are inadequate to save the person\'s life, even though, for the moment, the person is still alive Nonprogressive Shock-Compensated Shock The factors that cause a person to recover from moderate degrees of shock are: - Baroreceptor reflexes - Central nervous system ischemic response - Increased secretion of renin by the kidneys and formation of angiotensin II - Increased secretion by the posterior pituitary gland of vasopressin (antidiuretic hormone) - Increased secretion by the adrenal medullae of epinephrine and norepinephrine - Compensatory mechanisms that return the blood volume back toward normal Progressive Shock\" Is Caused by a Vicious Circle of Cardiovascular Deterioration - Cardiac Depression - Vasomotor Failure - Blockage of Very Small Vessels-\"Sludged Blood" - Increased Capillary Permeability - Release of Toxins by Ischemic Tissue - Generalized Cellular Deterioration - Tissue Necrosis Types of shock Hemorrhagic Shock Neurogenic Shock Anaphylactic Shock Septic Shock