3.B Heart Flashcards
Shape size and location of the heart
Cone-shape, fist sized, 2/3 is left of midline, apex is 5th intercostal, oblique position in mediastinum of thorax
Auricles
Appendages of atria, very elastic to increase blood volume capacity of atria (slightly), they then sling-shot blood that collects in the auricles into the ventricles
Chordae tendinae and papillary muscles
When ventricle relaxes the papillary muscle relaxes, allowing the chordae tendinae to slacken (AV valve is opem)
When ventricle contracts, papillary muscles contract which makes chordae tendinae taut, closing the AV valve and therefore preventing blood flow back into atria
Heart murmur
Damage to any of the four valves, allowing blood to leak back into wrong chamber
Ascending Aorta to
RCA and LCA
RCA to posterior interventricular branch and marginal branch
LCA to anterior interventricular branch (LAD) and circumflex branch
Left Coronary Artery
Divides into LAD and circumflex
LAD perfuses anterior IV septum and anterior papillary muscle of L ventricle
Circumflex Artery perfuses left lateral wall of L ventricle
Right Coronary Artery
Divides into marginal and posterior descending artery
LAD perfuses
Anterior IV septum and anterior papillary muscle of L ventricle
Circumflex perfuses
L lateral wall of L ventricle
Marginal perfuses
R ventricle
Posterior descending artery perfuses
Posterior portion of heart, IV septum, SA and AV nodes and posterior papillary muscle
What perfuses posterior 3rd of septum
Either R posterior descending OR circumflex
In most cases it is RPDA (called right dominance)
Anastomoses
Interconnecting branches of arteries
Can provide collateral circulation in case of blockage
Overview of coronary venous circulation
Myocardial capillaries to coronary veins to coronary sinus to R atrium
Intrinsic stimulation of the heart
about 1% of heart fibers exhibit autorhythmicity
Self excitable
Ability to generate their own action potential
Form the cardiac conduction system
Extrinsic stimulation of the heart
Heart rate can be altered by nerve or hormonal stimulation
Fibrous skeleton of the heart
Dense connective tissue between the atria and ventricles. Stops electric current from traveling from atria to ventricles
Cardiac muscle intercalated discs
Ends of fibers connect by intercalated discs which have desmosomes to hold them together and gap junctions to allow action potentials to conduct from one to the next (allow coordination)
Ca2+ in the heart
Sarcoplasmic reticulum is smaller and therefore less calcium reserve
Depolarization
Resting membrane -90. Fast sodium channels open in response to threshold level depol
Close within a few milliseconds
Na+ flows in because of eletrical and chemical gradient
Plateau phase calcium
slow voltage gated Ca2+ in sarcolemma open in sarcolemma.
Ca2+ moves from interstitial into cytosol, causing more Ca2+ to pour out of sarcoplasmic reticulum to cytosol through more Ca2+ channels.
Increased Ca2+ triggers contraction
Plateau voltage gated K+
Just before plateau some K+ open, potassium leaves as Ca2+ enters to keep membrane potential at 0mV.
Lasts .25 in cardiac, 0.001 in skeletal muscle (lacks plateau phase)
Repol
After plateau more K+ opens, K+ moves out and restores negative resting membrane potential to -90mV (only for cardiac) Ca2+ closes
Mechanism of contraction
As Ca2+ rises in contractile fiber, Ca2+ binds to troponin which allows actin and myosin to slide past each other and tension develops.
Epi increases Ca2+ into cytosol
ATP in cardiac muscle
Mostly aerobic
60% fatty acids 35% glucose
Creatine kinase catalyzes transfer of a phosphate from creatine phosphate to ADP to form ATP.
Cells death leads to leakage of CK and is an indication of muscle damage
Ventricular conduction lined up with an ECG
Phase 4 (rest) up until QRS complex starts (phase 0) and continues through phase 1.
Phase 4
During diastole
Membrane potential slowly becomes more positive
Pacemaker potential is either due to HCN channels which open at very negative voltages allowing both K+ and Na+ into the cell for depol
The other pacemaker potential theory is calcium clock. Calcium released from SR in cell, increasing sodium-caclium exchanger creating more positive MP (+3 charge being brought in by 3Na+, +2charge leaving as one Ca2+)
Phase 0
Ventricles:
Na+ fast sodium channels open when cell hits -70mV (through gap junctions from neighbor cell) causing depol to 50mV
SAN opens calcium channels when voltage is increased from phase 4 or oncoming action potential. It is 10/20ms in SAN cells (2ms in ventricular) because the calcium channels activate slower than sodium.
Phase 1
Inactivation of fast Na+ channels reduce movement of sodium into cell, while also k+ channels open and close quickly allowing for K+ out and making cell more negative
(no phase 1 in pacemaker cells, phase 0 goes through it)
Phase 2
Plateau. Membrane is fairly constant and slowly beginning to repol
K+ leaves, calcium flows out of SR (responsible for contraction) and activates Cl- (Cl- enters cell)
Increased Ca2+ increases sodium calcium exchanger, sodium enters cell and increases Na+/K+ pump
Not present in pacemakers
Phase 3
Ca2+ channels close, slow k+ stay open allowing K+ out, as cell gets more negative more K+ open and flow out until cell hits -85mV
Ionic movements during action potential
K+ can flow inward during phase 4 (from inwardly rectifying K+ current)
Poons ionic basis of action potential
Phase 0 depol fast Na+ opens
Phase 1 Fast Na+ close, K+ efflux opens
Phase 2 is sustained contraction from Ca2+ channels
Phase 3 Ca2+ close, K+ efflux opens, cell begins to repol
QT prolonged during phase two if K+ cannot leave channel (efflux channel blockade)
Why does AV slow conduction
Fibers have smaller diameters and fewer gap junctions.
0.1 second delay allowing atria to contract
Conduction pathway
Endo outward to epi
Repols backwards because, causing T wave to be upright
Repol takes
0.2 seconds
Cardiac Cycle is
Events that occur in on heart beart: Systole and diastole Takes 0.8 seconds Avg 72-75BPM Has 3 phases
Atrial Systole
0.1 seconds, puts last 25mL (EDV is 130mL ) into ventricles
Ventricular systole
0.05 seconds of isometric contraction (both SL and AV valves close)
LVP 80 mmHg to open aorta
RVP 20mmHg to open pulm
Ventricular ejection is when SL valves are open
EDV is 60mL bilat as SV is 70mL
Ventricular relaxation
Aortic valve closes at 100mmHg as blood back flows
Ventricular pressure drops below atrial, AV valves open and ventricles fill (mostly just from AV valve opening)
At one point all 4 valves closed, called isovolumetric relaxation
Heart sounds overview
Come from turbulence of blood as valves close
Lubb S1 AV valves close
Dubb S2 SL close
Cardiac output
CO = SV X Rate = 5.2 L / min
Extrinsic factors to regulate heart
Autonomic nervous system and endocrine hormones adjust to meet an increase or decrease in O2 demands
What’s responsible for input to cardiovascular center in the brain
Higher brain centers: Cerebral cortex, limbic, hypothalamus Sensory receptors: Proprio (movement) Chemo (chemistry) Baro (pressure)
Sympathetic innervation
Nerves from medulla to thoracic region of spinal cord (cardiac accelerator nerves) extend to SA, AV and most portions of myocardium which can trigger norepi for B1 which speeds rate of contraction for SA and AV node, increases contractility by increasing Ca2+ entry
Parasympathetic innervation
R and L vagus nerves innervate SA, AV and atrial myocardium with acetyl choline which slows rate of depol in autorhythmic fiber
Not many go to ventricles so that doesn’t change
Broad chemical influences on the heart
hypoxia, acidosis, alkalosis all depress cardiac activity
Hormones on the heart
Thyroid, epi, nor epi all enhance the heart rate and contractility
Cations on the heart
Excess Na+ drops CO by blocking Ca2+ inflow during action potentials
Excess K+ drops CO by blocking action potentials
Increase in Ca2+ speed heart rate and strengthen contraction
Blood flow
Arteries to arterioles to capillaries to venules to veins
Artery wall characteristics
Elastic, able to relax and expand with passage of blood
Contractile : circular smooth muscle can change diameter
Anastomosis
AnastomosEs is plural
Connection between branches of two or more arteries that supply same body region, for collateral circulation
Capillaries
Precap sphincters relax to allow blood through cap bed, or contract to force it through thoroughfare channel
They connect arterioles and venules, allow waste and nutrients in or out
One cell thick, branched networks with increased surface area for rapid exchange
Sinusoids
Specialized capillaries in liver, vey wide and blood flow slows
How is blood flow achieved
Pressure gradient (veins have larger diameters so less resistance) Skeletal muscle milks veins and lymph Resps (inspiration drops thorax/abdo pressure) Velocity is lower in caps for better nutrition exchange
Systolic pressure
Amount, rate, force of blood leaving LV and elasticity of arteries
Blood will remain in arteries because of elasticity
Diastolic pressure
Representation of pressure created by closure of AV valve, blood volume, artery elasticity, resistance of (or lack of) arterioles
BP =
CO X PVR
CO = SV X HR
BP regulation
Occurs short term/long term
Has neuronal and hormonal controls
Hormonal BP reg
ADH, RAAS, catechols
Renin angiotensin aldosterone RAA
Decreased volume or flow to kidneys to secrete renin
Renin and ACE act to produce angiotensin II
Angiotensin II is potent vasoconstrictor, and stimulates aldosterone to reabsorb Na+ and water to increase volume
Epi and nor epi
Constriction in arteries and veins in skin, organs
Dilation in arteries in cardiac muscle and skeletal muscle
ADH (vasopressin)
Posterior pituitary from dehydration or decreased blood flow.
Vasoconstricts and retains solute free water
ANP
Atrial natruiretic peptide released by cells in atria causes vasodilation by promoting loss of salt and water in urine
