Cardiovascular Physiology PDF

Cardiovascular Physiology Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology Cardiac Cycle Cardiac Output Controls & Blood Pressure Cardiovascular System Function Functional components of the cardiovascular system: – Heart...

Cardiovascular Physiology Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology Cardiac Cycle Cardiac Output Controls & Blood Pressure Cardiovascular System Function Functional components of the cardiovascular system: – Heart – Blood Vessels – Blood General functions these provide – Transportation Everything transported by the blood – Regulation Of the cardiovascular system – Intrinsic v extrinsic – Protection Against blood loss – Production/Synthesis Cardiovascular System Function To create the “pump” we have to examine the Functional Anatomy – Cardiac muscle – Chambers – Valves – Intrinsic Conduction System Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology Cardiac Cycle Cardiac Output Controls & Blood Pressure Functional Anatomy of the Heart Cardiac Muscle Characteristics – Striated – Short branched cells – Uninucleate – Intercalated discs – T-tubules larger and over z-discs Functional Anatomy of the Heart Chambers 4 chambers – 2 Atria – 2 Ventricles 2 systems – Pulmonary – Systemic Functional Anatomy of the Heart Valves Function is to prevent backflow – Atrioventricular Valves Prevent backflow to the atria Prolapse is prevented by the chordae tendinae – Tensioned by the papillary muscles – Semilunar Valves Prevent backflow into ventricles Functional Anatomy of the Heart Intrinsic Conduction System Consists of “pacemaker” cells and conduction pathways – Coordinate the contraction of the atria and ventricles Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology – Autorhythmic Cells (Pacemaker cells) – Contractile cells Cardiac Cycle Cardiac Output Controls & Blood Pressure Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Characteristics of Pacemaker Cells – Smaller than conduction myofibers contractile cells – Don’t contain many normal contractile myocardial cell myofibrils – No organized sarcomere structure do not contribute to SA node cell the contractile force AV node cells of the heart Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Characteristics of Pacemaker Cells – Unstable membrane potential “bottoms out” at -60mV “drifts upward” to -40mV, forming a pacemaker potential – Myogenic The upward “drift” allows the membrane to reach threshold potential (-40mV) by itself This is due to 1. Slow leakage of K+ out & faster leakage Na+ in » Causes slow depolarization » Occurs through If channels (f=funny) that open at negative membrane potentials and start closing as membrane approaches threshold potential 2. Ca2+ channels opening as membrane approaches threshold » At threshold additional Ca2+ ion channels open causing more rapid depolarization » These deactivate shortly after and 3. Slow K+ channels open as membrane depolarizes causing an efflux of K+ and a repolarization of membrane Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Characteristics of Pacemaker Cells  Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Altering Activity of Pacemaker Cells – Sympathetic activity NE and E increase If channel activity – Binds to β1 adrenergic receptors which activate cAMP and increase If channel open time – Causes more rapid pacemaker potential and faster rate of action potentials Sympathetic Activity Summary: increased chronotropic effects heart rate increased dromotropic effects conduction of APs increased inotropic effects contractility  Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Altering Activity of Pacemaker Cells – Parasympathetic activity ACh binds to muscarinic receptors – Increases K+ permeability and decreases Ca2+ permeability = hyperpolarizing the membrane » Longer time to threshold = slower rate of action potentials Parasympathetic Activity Summary: decreased chronotropic effects heart rate decreased dromotropic effects  conduction of APs decreased inotropic effects  contractility Myocardial Physiology Contractile Cells Special aspects – Intercalated discs Highly convoluted and interdigitated junctions – Joint adjacent cells with » Desmosomes & fascia adherens – Allow for synticial activity » With gap junctions – More mitochondria than skeletal muscle – Less sarcoplasmic reticulum Ca2+ also influxes from ECF reducing storage need – Larger t-tubules Internally branching – Myocardial contractions are graded! Myocardial Physiology Contractile Cells Special aspects – The action potential of a contractile cell Ca2+ plays a major role again Action potential is longer in duration than a “normal” action potential due to Ca2+ entry Phases 4 – resting membrane potential @ -90mV 0 – depolarization » Due to gap junctions or conduction fiber action » Voltage gated Na+ channels open… close at 20mV 1 – temporary repolarization » Open K+ channels allow some K+ to leave the cell 2 – plateau phase » Voltage gated Ca2+ channels are fully open (started during initial depolarization) 3 – repolarization » Ca2+ channels close and K+ permeability increases as slower activated K+ channels open, causing a quick repolarization – What is the significance of the plateau phase? Myocardial Physiology Contractile Cells Skeletal Action Potential vs Contractile Myocardial Action Potential Myocardial Physiology Contractile Cells Plateau phase prevents summation due to the elongated refractory period No summation capacity = no tetanus – Which would be fatal Summary of Action Potentials Skeletal Muscle vs Cardiac Muscle Myocardial Physiology Contractile Cells Initiation – Action potential via pacemaker cells to conduction fibers Excitation-Contraction Coupling 1. Starts with CICR (Ca2+ induced Ca2+ release) AP spreads along sarcolemma T-tubules contain voltage gated L-type Ca2+ channels which open upon depolarization Ca2+ entrance into myocardial cell and opens RyR (ryanodine receptors) Ca2+ release channels Release of Ca2+ from SR causes a Ca2+ “spark” Multiple sparks form a Ca2+ signal Myocardial Physiology Contractile Cells Excitation-Contraction Coupling cont… 2. Ca2+ signal (Ca2+ from SR and ECF) binds to troponin to initiate myosin head attachment to actin Contraction – Same as skeletal muscle, but… – Strength of contraction varies Sarcomeres are not “all or none” as it is in skeletal muscle – The response is graded! » Low levels of cytosolic Ca2+ will not activate as many myosin/actin interactions and the opposite is true Length tension relationships exist – Strongest contraction generated when stretched between 80 & 100% of maximum (physiological range) – What causes stretching? » The filling of chambers with blood Myocardial Physiology Contractile Cells Relaxation – Ca2+ is transported back into the SR and – Ca2+ is transported out of the cell by a facilitated Na+/Ca2+ exchanger (NCX) – As ICF Ca2+ levels drop, interactions between myosin/actin are stopped – Sarcomere lengthens Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology – Autorhythmic Cells (Pacemaker cells) – Contractile cells Cardiac Cycle Cardiac Output Controls & Blood Pressure Cardiac Cycle Coordinating the activity Cardiac cycle is the sequence of events as blood enters the atria, leaves the ventricles and then starts over Synchronizing this is the Intrinsic Electrical Conduction System Influencing the rate (chronotropy & dromotropy) is done by the sympathetic and parasympathetic divisions of the ANS Cardiac Cycle Coordinating the activity Electrical Conduction Pathway – Initiated by the Sino-Atrial node (SA node) which is myogenic at 70-80 action potentials/minute – Depolarization is spread through the atria via gap junctions and internodal pathways to the Atrio-Ventricular node (AV node) The fibrous connective tissue matrix of the heart prevents further spread of APs to the ventricles A slight delay at the AV node occurs – Due to slower formation of action potentials – Allows further emptying of the atria – Action potentials travel down the Atrioventricular bundle (Bundle of His) which splits into left and right atrioventricular bundles (bundle branches) and then into the conduction myofibers (Purkinje cells) Purkinje cells are larger in diameter & conduct impulse very rapidly – Causes the cells at the apex to contract nearly simultaneously » Good for ventricular ejection Cardiac Cycle Coordinating the activity Electrical Conduction Pathway Cardiac Cycle Coordinating the activity The electrical system gives rise to electrical changes (depolarization/repolarization) that is transmitted through isotonic body fluids and is recordable – The ECG! A recording of electrical activity Can be mapped to the cardiac cycle Cardiac Cycle Phases Systole = period of contraction Diastole = period of relaxation Cardiac Cycle is alternating periods of systole and diastole Phases of the cardiac cycle 1. Rest Both atria and ventricles in diastole Blood is filling both atria and ventricles due to low pressure conditions 2. Atrial Systole Completes ventricular filling 3. Isovolumetric Ventricular Contraction Increased pressure in the ventricles causes the AV valves to close… why? – Creates the first heart sound (lub) Atria go back to diastole No blood flow as semilunar valves are closed as well Cardiac Cycle Phases Phases of the cardiac cycle 4. Ventricular Ejection Intraventricular pressure overcomes aortic pressure – Semilunar valves open – Blood is ejected 5. Isovolumetric Ventricular Relaxation Intraventricular pressure drops below aortic pressure – Semilunar valves close = second heart sound (dup) Pressure still hasn’t dropped enough to open AV valves so volume remains same (isovolumetric) Back to Atrial & Ventricular Diastole Cardiac Cycle Phases Cardiac Cycle Blood Volumes & Pressure  Cardiac Cycle Putting it all together! Stroke volume: The amount of blood pumped by the left ventricle of the heart in one contraction. The stroke volume is not all the blood contained in the left ventricle; normally, only about two- thirds of the blood in the ventricle is expelled with each beat.