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75 Cards in this Set
- Front
- Back
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Three circulations |
Pulmonary, systemic, lymphatic |
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Chambers of the Heart (4) |
Right atrium Right ventricle Left atrium Left ventricle |
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Atria (left and right) |
Thin-walled, receive blood from veins |
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Ventricles (left and right) |
Thick-walled, forcefully pump blood out of the heart (contraction) |
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Valves |
Blood flows bidirectionally Valve disease- mitral stenosis, mitral insufficiency |
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Cardiac Muscle Tissue |
Conducting system 1. Network of specialized tissue that stimulates contraction 2. Modified cardiac myocytes 3. Heart can contracted without any innervation |
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Cardiomyocytes |
1. Consists of multiple parallel myofibrils surrounded by mitochondria 2. T tubules, invaginations of cell membrane (sarcolemma), increase SA for ion transport 3. SR houses intracellular Ca2+ and abuts T tubules 4. Actin, myosin, tropomyosin, troponin |
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Gap junction (intercalated disks) |
Protein-based tubes, allow ions to pass from one cell to another without having to pass through the plasma membrane, direct communication
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Demosome, adherens junction (intercalated disks) |
Hold cells together, allow passage of some substances between cells |
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Tight junctions (intercalated disks) |
Mainly exist in epithelial cells |
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Major functions of intercalated disks |
Connect individual cells into an organized tissue, provide substance/signal exchange between adjacent cells |
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Cardiac Conducting Tissue |
Propagate the action potential (AP) through different parts of the heart, appropriate temporal and spatial distribution |
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Nodal Cells (SA, AV nodes) |
Relatively small Dense connective tissue Few myofibrils Rich in glycogen, mitochondria |
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Parking cell (fiber) |
Larger cell Little connective tissue Tightly packed No t tubules |
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Pacemaker cells (P) |
Where the heartbeat originates |
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Bradycardia |
Heart rate too slow (<60 bpm, resting) Fatigue, weakness, dizziness Reduced automaticity of SA node, slow heart rate, pauses Cardia impulse is prevented from activating the ventricles normally, blocked conduction |
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Tachycardia |
Heart rate too fast (>100 bpm, resting) Shortness of breath, lightheadedness, chest pain Increased automaticity of SA node, rapid heart rate Developing spontaneous depolarization, early reactivation of Na or Ca channels Re-entrant circuit of conductive system |
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Properties of Cell Membrane |
1. Selectively permeable 2. Ion gradients- Na/K, Ca ATPase 3. Sensitive to changing physical conditions- temp, pH, voltage 4. Sensitive to extracellular signals- receptors |
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Principles of Membrane Potential |
1. Permeable to K+, Cl- 2. Impermeable to Na+ 3. Results from charge separation between inside/outside of cell due to semipermeability 4. Depends on ion concen. and permeabilities 5. Resting state, inside of cell is - relative to outside |
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Cell Membrane Channels |
Voltage gate channels- open/close with specific changes in potential (membrane voltage, time), electrical Ligand-gated channels- depend on activation of a chemical transmitter, chemical |
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Membrane Currents (flow of ions) |
-Imbalance of Na+ concentrations across plasma membrane -Inside of the cell is electrically negative relative to outside |
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Resting membrane potential (RMP) |
The difference in potential across the membrane of a cardiomyocyte when its at rest (fully depolarized) |
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Threshold potential (TP) |
The level of membrane potential at which sufficient depolarization has occurred to initiate an action potential; not fixed value, influenced by various factors |
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Depolarization |
The cell membrane potential becomes less polarized, less negative |
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Repolarization |
The cell membrane potential becomes polarized again, moves to a more negative membrane potential |
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Hyperpolarization |
The cell membrane potential become more polarization (negative) than the original resting membrane potential level |
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Action Potential (AP) |
A short-lasting event, electrical membrane potential of a cardiomyocytes rapidly rises and slowly falls, consistent trajectory |
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Inward Currents (negative currents) |
Postive charge (Na+, Ca2+) flowing into the cell, or negative charge flowing out of the cell |
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Outward Current (positive currents) |
Positive charge (K+) flowing out of the cell, or negative charge (Cl-) flowing into the cell |
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Refractory period (RP) |
The amount of time it takes for an excitable membrane to be ready for a second stimulus once it returns to its resting state following excitation |
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AP in excitable cells |
-Excitable cells have AP -Opening and closing of Na+, Ca2+, K+ channels -AP occurs because of sequential increases in the permeability -Time dependent, voltage dependent -All or none |
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Type 1: fast response cells |
Atrial myocardial cells Ventricular myocardial cells Purkinje fiber cells |
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Type II: slow response cells |
SA node cells AV node cells |
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Cardiac Action Potential (AP) |
Different cells serve different functions, all are electrically active Different tissues uniquely combine ionic currents to produce distinctive AP Cardiac AP have distinctive phases |
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Phases of Fast Cardiac Cell Membrane AP |
1. Resting potential 2. Depolarization of Na+ influx, rapid upstroke 3. Outward K+ current creates partial depolarization, results in decrease of Na+ conductance 4. Slow Ca2+ influx, low K+ flux, plateau of previous phase 5. Rapid repolarization, K+ efflux |
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Phases of Slow Cardiac Cell Membrane AP |
1. Resting membrane polarization is less in fast response cells, lower K+ permeability 2. No plateau phase 3. Slower upstroke is Ca2+ dependent (rather than Na+ dependent) |
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T type Ca2+ channels |
Open at a more negative voltage (-60 to -50 mV) Rapid inactivation, normally not found in fast responding atrial cells |
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L type Ca2+ channels |
Open at a higher voltage (-40 mV) Slow inactivation |
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Refractory Period (RP) |
The period of time after AP during which another AP cannot be initiated 250-300 ms (ventricles) 150 ms (atrium) |
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Effective/Absolute refractory period (ERP/ARP) |
Begins when NA+ channels are inactivated during AP, lasts until Na+ channels return to resting state Ventricles ARP ~200-250 ms Atrium ~100 ms No response to any stimuli Second AP cannot be initiated regardless of the strength of the stimuli Unexcitable |
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Relative refractory period (RRP) |
Always immediately follows ARP Second AP can be triggered Some Na+ channels have returned to resting state, available for activation 50 ms Strong stimuli require for premature bears formation Upstroke is less steep, lower amplitude, slower velocity |
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Significance of Refractory Period |
Protects heart from too rapid re-excitation Protects the rhythmic excitation-relaxation recycling of the heart RP of the excited myocardial cells is longer than time taken for spread of excitation over atria and ventricles Wave of excitation originating from SA node can cover the heart only once at most, then dies out |
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Heart Pump |
Electrical impulse-->Ca2+ signaling-->Contraction |
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Contractile Tissue |
Maintain trans-sarcolemma ionic gradient balance Translate biochemical signals |
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T Tubule |
Conduction of exciting electrical impulses from cell membrane into depth of cell (contractile system) Activate myofibrils Distribution/removal of substances to and from interior of cell |
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Sarcoplasmic Reticulum (SR) |
Contains ion channels, pump, receptors Majority of intercellular Ca2+ Not continuous with sarcolemma membrane Belongs to smooth, ER, exists in muscle cells Contains large stores of Ca2+, sequesters and releases when muscle cell is stimulated |
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Endoplasmic Reticulum (ER) |
Smooth ER Rough ER Protein modifications (folding, transporting) |
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Ryanodine Receptor (RyRs) |
Skeletal, heart, brain Intercellular Ca2+ channels |
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Inositol Trosphosphate Receptor (IP3R) |
Abundant in brain, atrial and ventricular myocytes Ca2+ channels on ER, release Ca2+ to cytoplasm when activated with IP3 |
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Cardiac Cycle |
Includes all events related to the flow of blood through one complete heartbeat 1. Filling 2. Isovolumic contraction 3. Ejection 4. Isovolumic relaxation |
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Systolic Phase (contraction) |
Mitral/ tricuspid valve closure Isovolumic contraction Rapid, reduced injection Aortic/pulmonic valve closure 1/3 of cycle ESV |
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Diastolic Phase (relaxation) |
Before mitral/ tricuspid valve open Isovolumic relaxation Rapid passive filling, reduced filling 2/3 of cycle EDV |
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Cardic Output (CO) |
Volume of blood pumped per minute by each ventricle of the heart (L/min)= stroke volume (SV) x heart rate (HR) Normal 4-8 L/min |
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Cardiac Index (CI) |
CO divided by body surface area CO/surface area Normal 2.6-4.2 L/min/m^2 Useful to see how well the heart is functioing as a pump |
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Rest vs. Exercise |
At rest, most blood goes to brain, kidney, GI, skeletal muscles Exercising, almost all blood goes to skeletal muscles |
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Bradycardia |
Low resting heart rate, CO can decrease below ability of system to compensate by increasing SV
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Tachycardia |
High resting heart rate, CO decreases because of inadequate time to complete filling of ventricles during diastole |
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Factors Affecting Heart Rate |
Cardiac pacemaker cell activity ANS activity Species Age Body weight/size/conditioning Endocrine, environ factors Disease factors |
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Parasympathetic innervations |
Restricted to atria Exert a negative chronotropic effect (slowing of heart rate) Hyperpolarizes cell |
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Sympathetic innervations |
Exert a postive chronotropic effect on nodes Because they reach the ventricles, produce a positive inotropic effect Increasing firing rate , lowering threshold for AP |
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Stroke Volume (SV) |
Volume ejected from the ventricle on each heart beat SV= EDV- ESV (starting v- ending v) |
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Factors Affecting SV |
Preload, venous return Disease Contractility Afterload, resistance |
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Starling Principle |
CO must be responsive to changes in venous return |
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Measurements of CO |
Invasive- Fick indicator, dilution techniques, blood flow probes *easier to use, after, can be repeated often, more accurate Non-invative- echocardiography, doppler, TEE, ICG |
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Ejection Factor (EF) |
Assess heart as a pump EF= SV/EDV Amount of blood pumped out during systole compared with the amount of blood loaded into ventricle before systole |
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Variability of EF |
Heart failure- lowers Hypertension- lowers Contractility- increases SNS stimulation- increases |
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Echocardiography |
Non-invasive, readily available in hospital, can provide additional information Dependent on endocardial visualization, less accurate if aortic regurgitation |
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Right ventricle |
Tricuspid valve- entrance, papillary muscle attached, prevents regurgitation of blood into right atrium during systole Pulmonary valve- exit, thicker and smaller, no papillary muscle attached, prevents regurgitation of blood during diastole |
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Left ventricle |
Mitral valve- entrance, ntrance, papillary muscle attached, prevents regurgitation of blood into left atrium during systole Aortic valve- exit, thicker and smaller, no papillary muscle attached, prevents regurgitation of blood during diastole |
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Normal/Abnormal Heart sounds |
Made by vibrations, caused by closure of valves |
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Murmurs |
Caused by high velocity and turbulent flow through a narrowed opening or changes in direction of blood flow Congenital/acquired lesions Systolic or diastolic phases Have higher audio frequency than normal heart sounds, last long, build up/die away more gradually |
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Blood Pressure Measurement: pressure gauge/stethoscope |
Cuff is inflated, stops arterial blood flow, no sound can be heard if stethoscope is place over brachial artery Korotkoff sounds created by pulsatile blood flow through compressed artery Blood flow is silent when artery is no longer compressed |
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Regulation of CO |
Cardiac current- spread by cell-cell transmission of AP Depolarization spreads across myocardium, increases pumping efficiency of heart |
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Biomedical Engineering |
Artificial organs Prostheses (fake hip) |
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Stem cells |
Undifferentiated cells, capable of self-renewal, can differentiate into specialized cell types |
