Physiology Cardiovascular System Cardiac Muscle and the Heart
- Slides: 88
Physiology Cardiovascular System
Cardiac Muscle and the Heart n Myocardium n n n Heart muscle Sits in the media stinum of the thoracic cavity Left Axis Deviation n n May have a right axis deviation with obesity and/or pregnancy May hang in the middle of the thoracic cavity if the individual is very tall
The Heart n The heart has four chambers n Right and left atrium n Atria n is plural Right and left ventricle
Blood Flow Through the Heart n Deoxygenated blood enters the right atrium of the heart through the superior and inferior vena cava n Deoxygenated blood n Has less than 50% oxygen saturation on hemoglobin
Hemoglobin n Quaternary Structure n Four Globin proteins n n Four Heme attach to each Globin n n Globin carries CO 2, H+, PO 4 Heme binds O 2 and CO Heme contains an Iron ion About 1 million hemoglobin molecules per red blood cell Oxygen carrying capacity of approximately 5 minutes
Heart Valves Ensure One-Way Flow of Blood in the Heart n Atrioventricular Valves Located between the atria and the ventricle n Labeled Right and Left n Right Valve is also called Tricuspid n Left Valve is also called Bicuspid or Mitral n
Heart Valves n n Papillary muscles are attached to the chordae tendinae Chordae tendinae are also connected to the AV valves Just prior to ventricular contraction the papillary muscles contract and pull downward on the chordae tendinae The chordae tendinae pull downward on the AV valves n This prevents the valves from prolapsing and blood regurgitating back into the atria.
Follow Path of Blood through Heart
Blood Flow n n Due to gravity deoxygenated blood enters the right/left atrium (by way of the pulmonary veins) and flows through the open AV valve directly into the ventricles The filling of the ventricles with blood pushes the AV valve upward n n They are held in place by the chordae tendinae Right before the valves shuts completely the atria contract from the base towards the apex of the heart in order to squeeze more blood into the ventricle n The AV valves snapping shut creates the “Lub” sound of the heart beat
Blood Flow n When the AV valves are shut the Pulmonary and Aortic semi-lunar valves are also shut Diastole n Quiescence of the heart n
Myocardial Contraction (Systole) n n n After Diastole occurs the ventricles begin to contract from the apex towards the base of the heart The deoxygenated blood on the right side of the heart is pushed through the pulmonary trunk after opening the semi-lunar valve to the pulmonary arteries into the lungs to become oxygenated. The oxygenated blood on the left side of the heart is pushed through the aorta after opening the semi-lunar valve into the systemic circulation
Blood Flow n The Ventricles do not have enough pressure to push all of the blood out of the pulmonary trunk and aorta The blood falls back down due to gravity n The semi-lunar valves snap shut n n The “Dup” sound of the heart beat
Blood Flow n Blood is always flowing from a region of higher pressure to a region of lower pressure
Atrial and Ventricular Diastole The heart at rest n The atria are filling with blood from the veins n The ventricles have just completed contraction n AV valves are open n Blood flow due to gravity n
Atrial Systole: Completion of Ventricular Filling n The last 20% of the blood fills the ventricles due to atrial contraction
Early Ventricular Contraction n As the atria are contracting n Depolarization wave moves through the conducting cells of the AV node down to the Purkinje fibers to the apex of the heart Ventricular systole begins n AV Valves close due to Ventricular pressure n n First Heart Sound n S 1 = Lub of Lub-Dup
Isovolumic Ventricular Contraction AV and Semilunar Valves closed n Ventricles continue to contract n Atrial muscles are repolarizing and relaxing n Blood flows into the atria again n
Ventricular Ejection n The pressure in the ventricles pushes the blood through the pulmonary trunk and aorta Semi-lunar valves open n Blood is ejected from the heart n
Ventricular Relaxation and Second Heart Sound n At the end of ventricular ejection Ventricles begin to repolarize and relax n Ventricular pressure decreases n Blood falls backward into the heart n Blood is caught in cusps of the semi-lunar valve n n Valves snap shut n S 2 – Dup of lub-dup
Isovolumetric Ventricular Relaxation Semilunar valves close n AV valves closed n The volume of blood in the ventricles is not changing n When ventricular pressure is less than atrial pressure the AV valves open again n n The Cardiac Cycle begins again
Cardiac Circulation Blood flowing through the heart has a high fat content n Curvature as well as diameter of the arteries is important to blood flow through the heart n n Vasoconstriction due to sympathetic nervous system input n Norepinephrine/Epinephrine n Alpha Receptors not Beta
Myocardial Infarction n Heart Attack n Due to plaque build up in the arteries n Decrease in blood flow to myocardium Depolarization of muscle cannot occur due to myocardial death n Myocardium doesn’t work as a syncytium any longer n Destruction of gap junction or “connexons” n
Atherosclerosis n Plaque in the arteries n n Elevated Cholesterol in the blood Cholesterol is cleared by the liver n HDL – High Density Lipoprotein n. H n LDL – Low Density Lipoprotein n. L n for healthy for Lethal Omega 3 fatty acids n “Rotorooter” for the arteries
If a Patient Has a Left Atrial Infarction Then n What happens to heart contraction and blood flow through the heart? What type of symptoms might your patient have? What recommendations might you give the patient to live a better life? n There are some things they better not do or they will die. What are these things (in general)?
Angioplasty/Open Heart Surgery
Cardiac Muscle & Heart n Heart muscle cells: n 99% contractile n 1% autorrhythmic
Cardiac Muscle Cells Contract Without Nervous Stimulation n Autorhythmic Cells n Pacemaker Cells set the rate of the heartbeat n Sinoatrial Node n Atriventricular Node n Distinct from contractile myocardial cells n Smaller n Contain few contractile proteins n http: //www. youtube. com/watch? v=7 K 2 icszdx. Qc
Excitation-Contraction (EC) Coupling in Cardiac Muscle n Contraction occurs by same sliding filament activity as in skeletal muscle some differences: n n AP is from pacemaker (SA node) AP opens voltage-gated Ca 2+ channels in cell membrane Ca 2+ induces Ca 2+ release from SR stores Relaxation similar to skeletal muscle Ca 2+ removal requires Ca 2 -ATPase (into SR) & Na+/Ca 2+ antiport (into ECF) [Na+] restored via? http: //www. youtube. com/watch? v=r. IVCu. C-Etc 0 n
Cardiac Contraction n Action Potentials originate in Autorhythmic Cells n AP spreads through gap junction n Protein tunnels that connect myocardial cells n AP moves across the sarcolemma and into the ttubules n Voltage-gated Ca +2 channels in the cell membrane open n Ca +2 enters the cell which then opens ryanodine receptor-channels n Ryanodine receptor channels are located on the sarcoplasmic reticulum and Ca +2 diffuses into the cells to “spark” muscle contraction n Cross bridge formation and contraction occurs
Myocardial Contractile Cells n In the myocardial cells there is a lengthening of the action potential due to Ca +2 entry http: //www. youtube. com/watch? v=OQp. FFi. Ld. E 0 E
AP’s in Contractile Myocardial Cells n n n Phase 4: Resting Membrane Potential is -90 m. V Phase 0: Depolarization moves through gap junctions n Membrane potential reaches +20 m. V Phase 1: Initial Repolarization n Na+ channels close; K + channels open Phase 2: Plateau n Repolarization flattens into a plateau due to n A decrease in K + permeability and an increase in Ca +2 permeability n Voltage regulated Ca +2 channels activated by depolarization have been slowly opening during phases 0 and 1 n When they finally open, Ca +2 enter the cell n At the same time K + channels close n This lengthens contraction of the cells n AP = 200 m. Sec or more Phase 3: Rapid Repolarization n Plateau ends when Ca +2 gates close and K + permeability increases again
Myocardial Autorhythmic Cells n Anatomically distinct from contractile cells – Also called pacemaker cells n Membrane Potential = – 60 m. V n Spontaneous AP generation as gradual depolarization reaches threshold n Unstable resting membrane potential (= pacemaker potential) n The cell membranes are “leaky”
Myocardial Autorhythmic Cells, cont’d. If-channel Causes Mem. Pot. Instability n Autorhythmic cells have different membrane channel: If - channel allow current (= I ) to flow n If n n f = “funny”: researchers didn’t understand initially channels let K+ & Na+ through at -60 m. V Na+ influx > K+ efflux Slow depolarization to threshold
Myocardial Autorhythmic Cells, cont’d. “Pacemaker potential” starts at ~ -60 m. V, slowly drifts to threshold AP
Myocardial Autorhythmic Cells, cont’d. Channels involved in APs of Cardiac Autorhythmic Cells n Slow depolarization due to If channels n As cell slowly depolarizes: If -channels close & Ca 2+ channels start opening n At threshold: lots of Ca 2+ channels open AP to + 20 m. V n Repolarization due to efflux of K+
Autorhythmic Cells n n No nervous system input needed Unstable membrane potential n -60 m. V Ca +2 channels open n Calcium influx creates the steep depolarization phase of the action potential n At the peak of the action potential Ca +2 channels close and slow K+ channels open n Repolarization of the autorhythmic action potential is due to the efflux of K + n Pacemaker potential not called resting membrane potential At -60 m. V If (funny) channels permeable to K + and Na + open Na + influx exceed K + efflux n The net influx of positive charge slowly depolarizes the autorhythmic cells n As the membrane becomes more positive the If channels gradually close and some Ca +2 channels open n The influx of Ca +2 continues the depolarization until the membrane reaches threshold http: //www. youtube. com/watch? v=3 Hv. IKs. Qb 6 es
Autonomic Neurotransmitters Modulate Heart Rate n n The speed at which pacemaker cells depolarize determines the rate at which the heart contracts The interval between action potentials can be altered by changing the permeability of the autorhythmic cells to different ions n n Increase Na + and Ca +2 permeability speeds up depolarization and heart rate Decrease Ca +2 permeability or increase K + permeability slow depolarization and slows heart rate http: //www. youtube. com/watch? v=OQp. FFi. Ld. E 0 E http: //www. youtube. com/watch? v=j 2 i. Y 1 c. T 2 g. EE
Autonomic Neurotransmitters Modulate Heart Rate n The Catecholamines: norepi and epi increases ion flow through If and Ca+2 channels n More rapid cation entry speeds up the rate of the pacemaker depolarization n n Β 1 -adrenergic receptors are on autorhythmic cells c. AMP second messenger system causes If channels to remain open longer http: //www. youtube. com/watch? v=3 Hv. IKs. Qb 6 es
Autonomic Neurotransmitters Modulate Heart Rate n Parasympathetic neurotransmitter (Acetylcholine) slows heart rate n Ach activates muscarinic cholinergic receptors that n Increase K+ permeability and n Decrease Ca+2 permeability
Electrical Conduction in the Heart Coordinates Contraction n n n Action potential in an autorhythmic cell Depolarization spread rapidly to adjacent cells through gap junctions Depolarization wave is followed by a wave of contraction across the atria from the sinoatrial node on the right side of the heart across to the left side of the heart and then from the base to the apex From AV nodes to the atrioventricular bundle in the septum (Bundle of His) Left and right bundle branches to the apex Purkinje Fibers through the ventricles branches from apex to base and stopping at the atrioventricular septum
Pacemakers Set the Heart Rate n SA Node is the fastest pacemaker n n Approximately 72 bpm AV node approximately 50 bpm Bundle Branch Block n Complete Heart Block n
Electrocardiogram n Einthoven’s triangle n n Electrodes are attached to both arms and left leg to form a triangle Lead I- negative electrode attached to right arm Lead II – positive electrode attached to left arm Lead III – Ground attached to the left leg
Electrocardiogram ECG (EKG) • Surface electrodes record electrical activity deep within body - How possible? • Reflects electrical activity of whole heart not of single cell! EC fluid = “salt solution” (Na. Cl) good conductor of electricity to skin surface Signal very weak by time it gets to skin • • n n n ventricular AP = ? m. V ECG signal amplitude = 1 m. V EKG tracing = of all electrical potentials generated by all cells of heart at any given moment
ECG n P wave n Depolarization of the atria n n QRS complex n Ventricular depolarization n n Atrial contraction begins almost at the end of the P wave Ventricular contraction begins just after the Q wave and continues through the T wave n Ventricular repolarization
ECG n PQ or PR segment n n Q wave n n n Conduction through bundle branches R wave n n Conduction through AV node and AV bundle Conduction beginning up the Purkinje Fibers S wave Conduction continue up half way ST segment n Conduction up the second half of Ventricles
ECG When an electrical wave moving through the heart is directed toward the positive electrode, the ECG waves goes up from the baseline n If net charge movement through the heart is toward the negative electrode, the wave points downward n
Einthoven’s Triangle and the 3 Limb Leads: + I RA – – II III + + LA –
Why neg. tracing for depolarization ? ? Net electrical current in heart moves towards + electrode EKG tracing goes up from baseline Net electrical current in heart moves towards - electrode EKG tracing goes Down from baseline
Info provided by EKG: 1. 2. 3. HR Rhythm Relationships of EKG components each P wave followed by QRS complex? PR segment constant in length? etc.
For the Expert: Find subtle changes in shape or duration of various waves or segments. Indicates for example: n Change in conduction velocity n Enlargement of heart n Tissue damage due to ischemia (infarct!)
Prolonged QRS complex Injury to AV bundle can increase duration of QRS complex (takes longer for impulse to spread throughout ventricular walls).
Heart Sounds (HS) n 1 st HS: during early ventricular contraction AV valves close n 2 nd HS: during early ventricular relaxation semilunar valves close
Gallops, Clicks and Murmurs Turbulent blood flow produces heart murmurs upon auscultation
Plumbing 101: Resistance Opposes Flow 3 parameters determine resistance (R): Tube length (L) 1. Constant in body Tube radius (r) 2. 1. Poiseuille’s law 8 L R= r 4 Can radius change? Fluid viscosity ( (eta)) 3. 1. Can blood viscosity change? ? Blood Flow Rate P/ R R 1 / r 4
Velocity (v) of Flow Depends on Flow Rate and Cross-Sectional Area: n Flow rate (Q) = volume of blood passing one point in the system per unit of time (e. g. , ml/min) n n If flow rate velocity Cross-Sectional area (A) (or tube diameter) n If cross sectional area velocity v=Q/A
Blood Flow n Mechanistic: Because the contractions of the heart produce a hydrostatic pressure gradient and the blood wants to flow to the region of lesser pressure. Therefore, the Pressure gradient ( P) is main driving force for flow through the vessels Blood Flow Rate P/ R
Pressure n Hydrostatic pressure is in all directions n Measured in mm. Hg: The pressure to raise a 1 cm column of Hg 1 mm n Sphygmomanometer n Flow is produce by Driving Pressure n Pressure of fluid in motion decreases over distance because of energy loss due to friction Blood Flow Rate P/ R
Unique Microanatomy of Cardiac Muscle Cells n 1% of cardiac cells are autorhythmic n n Intercalated discs with gap junctions and desmosomes n n Electrical link and strength SR smaller than in skeletal muscle n n Signal to contract is myogenic Extracelllar Ca 2+ initiates contraction (like smooth muscle) Abundant mitochondria extract about 80% of O 2
Cardiac Muscle Cell Contraction is Graded n Skeletal muscle cell: all-or-none contraction in any single fiber for a given fiber length. Graded contraction in skeletal muscle occurs through? n Cardiac muscle: n force to sarcomere length (up to a maximum) n force to # of Ca 2+ activated crossbridges (Function of intracellular Ca 2+: if [Ca 2+]in low not all crossbridges activated) http: //www. youtube. com/watch? v=OQp. FFi. Ld. E 0 E http: //www. youtube. com/watch? v=j 2 i. Y 1 c. T 2 g. EE
Length Tension Relationship
In order to increase heart rate at the SA node A. B. C. D. Potassium permeability across the membrane must increase Sodium permeability across the membrane must increase Potassium impermeability across the membrane must increase Sodium impermeability across the membrane must increase
The neurotransmitter responsible for increasing potassium permeability at the SA node is A. B. C. D. Norepinephrine Epinephrine Acetylcholine Serotonin
The initiation of the heartbeat normally originates from the A. B. C. D. Atrio-ventricular (A-V) node of the heart Sino-atrial (SA) node of the heart Central nervous system Thyroid
The systemic circulation A. B. C. D. E. Receives more blood than the pulmonary circulation does Receives blood from the left ventricle Is a high pressure system compared to the pulmonary circulation Both (b) and (c) above are correct All of the above are correct
The chordae tendinae A. B. C. D. E. Keep the AV valves from opening in the opposite direction during ventricular contraction Hold the AV valves during diastole Hold the right and left ventricles together Transmit the electrical impulse form the atria to the ventricles Contract when the ventricles contract
The aortic valve prevents backflow of blood from the aorta into the left ventricle during ventricular diastole A. True B. False
A mammalian heart has _____ chamber(s) A. B. C. D. One Two Three Four
Ectopic focus is the place where A. B. C. D. E. An abnormally excitable area of the heart initiates a premature action potential All of the electrical impulses of the heart normally terminate An ECG lead is attached on the outside of the chest A heart valve is attached The chordae tendineae attach to a valve
During isovolumetric ventricular contraction A. B. C. D. E. Rapid filling of the ventricles occurs No blood enters or leaves the ventricles The maximum volume of blood is ejected The maximum rate of ejection occurs None of the above is correct
The type of intercellular junction that connects cardiac muscle fibers and allows for direct, electrical synapsing is known as a A. Tight junction B. Desmosome C. Plasmodesmata D. Gap junction
Cardiac muscle A. B. C. D. E. Has a shortening velocity that is greater than that of glycolytic (white) skeletal muscle fibers Has a more extensive sarcoplasmic reticulum than skeletal muscle Is an electrical syncytium Has a resting potential that depends mainly on sodium distribution All of the above are correct
Spontaneous depolarization of the sinoatrial node is produced by A. An inward leak of sodium and an increase B. C. D. E. in the outward leak of potassium An inward leak of sodium and a decrease in the outward leak of potassium Opening of fast sodium channels and an increase in the outward leak of potassium Neural impulses from the sympathetic nerves
A heart murmur is characterized by A. B. C. D. Rapid heart contraction Irregular heart contraction Mitral valve prolapse Semilunar valve dysfunction
The P wave of a normal electrocardiogram indicates A. B. C. D. Atrial depolarization Ventricular depolarization Atrial repolarization Ventricular repolarization
Damage to the _______ is referred to as heart block A. B. C. D. SA node AV bundle AV valve
Stenosis of the mitral valve may initially cause a pressure increase in the A. B. C. D. Vena cava Pulmonary circulation Left ventricle Coronary circulation
The tricuspid valve is closed A. B. C. D. E. While the ventricle is in diastole By the movement of blood from the atrium to ventricle By the movement of blood from atrium to ventricle While the atrium is contracting When the ventricle is in systole
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