Heart: Electrophysiology and muscle contraction Flashcards
conducting and contractile cells
-contractile cells- majority, working cells of the heart -> contraction
-conducting cells- tissue of SA, atrial internodal tracts, AV node, bundle of his, purkinje system
-conducting cells have capacity to generate action potentials but it is usually suppressed (except in SA)
electrical path
-SA node- pacemaker
-atrial internodal tracts and atria- right and left atria
-AV node- slow conduction so ventricles can fill before activated to contract (increased AV conductance -> decreased SV, CO)
-bundle of his, purkinje, and ventricles- to bundle of his via common bundle -> right and left purkinje bundles
-action potential to one ventricle muscle cell to next via low resistance pathways
-rapid conduction here
normal sinus rhythm
-1. action potential originates in SA
-2. SA nodal impulses occur regularly 60-100
-3. activation of myocardium must occur in correct sequence with correct timing and delays
cardiac action potential steps
-0. Phase 0: QRS complex- sodium coming into the cell -> rapid upstroke
-Upstroke= caused by Na+= action potential
begins by rapid depolarization in the
ventricular, atrial, and Purkinje fibers
-1. Phase 1, initial repolarization: T Segment- goes back to isoelectric flat line
-Repolarization immediately follows upstroke
-Occurs because once it gets depolarized, the Na+ gates close, K+ continues to leave
-2. Phase 2, plateau: long period of stable,
depolarized membrane potential- inward and outward currents are equal so there’s no current flowing across
-Occurs because there is an increased inward Ca 2+ current= slow inward current
-3. Phase 3, repolarization: T wave- mainly driven by potassium (rapid repolarization all has to do with potassium)
-Occurs due to decrease in the inward Ca2+ current and increase in the outward K+ current
-At the end, K+ outward current is reduced bc the membrane potential is closer to the K+ equilibrium potential
-4. Phase 4, Resting membrane potential, or electrical diastole- the membrane potential is stable again, and inward and outward currents are equal
SA node
-no neural input
-unstable resting membrane potential
-no sustained plateau
laten pacemakers
-myocardial cells with intrinsic automaticity
-spontaneous phase 4 depolarization
-AV node, bundle of His, purkinje fiber cells
-not normally expressed
-pacemaker with the fastest rate of phase 4 depolarization controls heart rate (SA NODE)
-when SA drive heart rate -> suppressed latent pacemakers -> overdrive suppression
conduction velocity
-determines how long it takes the action potential to spread to various location in the myocardium
-Slow conduction velocity of AV ensures that the ventricles do not activate too early
-rapid conduction of the Purkinje fibers ensures that the ventricles can be activated quickly and in a smooth sequence for efficient ejection of blood
absolute refractory period (ARP)
even with a large stimulus, no action potential can occur because the gates are closed
effective refractory period (ERP)
at the end of ERP, Na+ channels start to recover
-ARP vs ERP: absolute means absolutely no stimulus is large enough to generate an action potential; effective means that a conducted action potential can’t be generated
relative refractory period (RRP)
Na+ gates are recovering to the closed but available state and a second action potential can be generated with a greater than normal stimulus
-if one is generated -> abnormal
chronotropic effects
-affects of the ANS on heart rate
-Stimulation of the sympathetic nervous system -> increases conduction velocity through the AV node -> increases the rate
that action potentials are conducted from the atria to the ventricle
-Stimulation of the parasympathetic nervous system -> decreases conduction velocity through the AV nodes ->
decreases the rate that action potentials are conducted from atria to ventricles
supranormal period (SNP)
-less inward current required to depolarize the cell to the threshold potential
-Na channels recovered (inactivation open) bc membrane potential is closer to threshold than at rest -> Easier to fire action potential than when resting
ECG/EKG
-1. P wave: atrial depolarization= the 2 atria are contracting
-2. QRS complex: ventricular depolarization, ventricles are contracting (looks like a V, so V for ventricles at the QRS complex)
-Atrial repolarization and relaxation also take place here- covered by the QRS complex can’t see it but it does exist (masked by the QRS complex)
-**depolarization of atria= P wave, ventricles= QRS complex
-3. T wave: ventricular Repolarization, ventricles are RELAXING
-PR interval: distance from beginning of P wave to beginning of QRS complex -> Correlates with the conduction time through the AV node
-QT interval: first ventricular depolarization to last ventricular repolarization.
-ST segment correlates with the plateau of the ventricular action potential
components of cardiac muscle contraction parts
-composed of sarcomeres (thick and thin filaments)
-Thick filaments: composed of myosin, globular heads have actin binding sites and ATPase
-Thin filaments: composed of actin, tropomyosin, and troponin
-Actin has a myosin binding site
-Tropomyosin: BLOCKS the MYOSIN binding site
-Troponin: binds to Ca2+, removes the tropomyosin inhibition of the actin myosin interaction
-Transverse (T) tubules: carries action potentials to the cell interior
cardiac muscle contraction steps
-1. Ventricular action potential- cardiac action potential is initiated in the myocardial cell membrane, and the depolarization spreads to the interior of the cell via T Tubules
-2. Ca 2+ release from sarcoplasmic reticulum- increase in Ca2+ concentration is not enough to initiate contraction, but it triggers release of more Ca2+, which enters during the plateau phase
-3. Ca 2+ binds to troponin C
-4. Tension
a. 3+ 4 = Ca2+ now binds to troponin C , tropomyosin is moved out of the way, and interaction of actin and myosin can occur
b. Actin and myosin bind, cross bridges form and then break, the thin and thick filaments move past each other and tension is produced
-5. Ca 2+ accumulation by sarcoplasmic reticulum- The magnitude of the tension determined by myocardial cells is proportional to the intracellular Ca2+ concentration. Hormones, neurotransmitters, and drugs that alter the inward Ca2+ current during the action potential plateau or that alter sarcoplasmic reticulum Ca2+ stores would be expected to change the amount of tension produced by the myocardial cells
muscle relaxation
occurs when the Ca2+ is REACCUMULATED in the sarcoplasmic reticulum by the action of the Ca2+ ATPase- the intracellular Ca2+ concentration falls to resting levels, Ca2+ dissociates from troponin C, actin- myosin interaction is blocked, and RELAXATION OCCURS
ionotropism
-ability of myocardial cells to DEVELOP FORCE at a given muscle cell length
-Positive inotropic effects- agents that increase contractility-> increase rate of tension development and peak tension
-Negative inotropic effects- decrease contractility; decrease both the rate of tension development and the peak tension
force of contraction
-Contractility directly correlates with the intracellular Ca2+ concentration, which depends on the amount of Ca2+ released from sarcoplasmic reticulum stored during excitation- contraction coupling
-the larger the inward Ca2+ current and the larger the intracellular stores= the greater the increase in intracellular Ca2+ concentration= the greater the contractility
innervation HR
-Sympathetic nervous system- has a positive inotropic effect on myocardium= contract
-Parasympathetic nervous system- negative inotropic effect on atria= contraction decreases
-**HR increases= contractility increases
-HR decreases= contractility decreases
positive staircase effect
-tension rises stepwise
-with each beat, more Ca2+ is accumulated by the sarcoplasmic reticulum, until a maximal storage level is achieve
-bowditch staircase
postextrasystolic potentiation
-when an extra beat is generated, the very next beat has increased tension
-early beat- heart hasn’t had chance to reach full diastole -> next beat is not as forceful
-the following beat (postextrasystole) after that has a stronger force of contraction
-this is due to extra amount of Ca entering cell during extrasystole -> accumulation
-you get an early beat, and then the beat after that has a stronger force of contraction (after more relaxation, get a strong beat after)
staircase analogy
-as HR increases, tension increases
-early beat (extrasystole) -> less tension from that beat -> beat following will be delayed
-higher pressure at the postextrasystole
-people typically feel the after beat
-calcium gives you stronger muscle contraction -> during the delay the calcium is building up
-bow and arrow
-parasympathetic will reduce calcium movement -> decrease HR -> decrease contractility
cardiac glycosides
-POSITIVE IONOTROPIC DRUG
-Digoxin: drug used to treat heart failure and abnormal heart rhythms (arrhythmias)
-Helps the heart work better and control your heart rate
-patients with afib: have an irregular heart beat, so a different volume of blood is pumped out each time
-the more relaxation= the higher consequent cardiac output (FRANK STARLING LAW)
-glycosides inhibit Na-K pump which kills Na gradient -> INCREASE INTRACELLULAR NA -> no gradient for Ca-Na pump -> stops pumping Ca out -> Ca build up -> increase contraction force
-Cardiac glycosides like digoxin have POSITIVE INOTROPIC AGENTS= increase in tension by increasing intracellular Ca2+ concentration= inc contractility
-Used mainly for congestive heart failure- by increasing the intracellular Ca2+ concentration
-cardiac glycosides have a positive inotropic action, which counteract the negative inotropism of the failed ventricle
negative ionotropic drug
-decreases contractility
-ex. calcium channel blocker -> indirectly block Na-K pump
-DO NOT give to pts with systolic heart failure
