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30 Cards in this Set
- Front
- Back
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ECG vs. AP
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ECG: electrode on surface of skin
-measure electrical events developed in heart that dissipate to surface of skin AP: individual muscle cell, electrical measurement |
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Myofilaments
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Thick = Myosin
-head regions interact w/ actin -form cross bridge -attach & slide to shorten (contract) Thin = Actin, Tropomyosin & Troponin |
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Excitation-Contraction Coupling
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Skeletal muscle
-excite & contract -innervate by neurons from CNS -NT = Ach -binds to nicotinic cholinergic receptors -Na movies in K moves out create AP -propagates membrane to T-tubule to SR to release Ca -Ca binds to troponin (thin filament) in intracellular matrix -triggers mvmt of tropomyosin from actin so myosin can bind -in cardiac once ICF Ca is raised, cross bridge cycle is the SAME in skeletal -difference is initial point of what triggers the AP |
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Cardiac Muscle vs. Skeletal Muscle
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Skeletal
-striated -voluntary -thick & thin filament -SR = more dense -mitochondria = many (can rest) -cells independent of one another Cardiac Muscle -striated -involuntary -thick & thin filaments -SR = less dense -mitochondria = tremendously numerous (no resting) -intercalated disks: inter locking jxn, fxning all cells as 1 big unit |
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Intercalated discs
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1. Desmosomes
-prevent adj cardiac cells from separating during contraction 2. Gap jxn: -allow ion to pass free from cell to cell -directly transmit depolarizing current across entire heart |
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Functional Syncytium
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myocardial wall behaves as single unit
-cardiac fibers electrically coupled by gap jxn |
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Cardiac Conduction System
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-buried w/in myocardial walls
-microscopic, cannot be seen w/ naked eye -2 jobs: 1. create electrical current 2. propagate (spread current) -Pathway: 1. SA Node: where superior vena cava dumps into R atrium -spontaneous on/off rhythm -can be influenced by autonomic NS 2a. Interatrial Tracts (left atrium) - stops here, dissipates at L Atrium 2b. Internodal Tracts (right atrium) 3. AV Node: bottom of R Atrium (from internodal tract) 4. AV Bundle (bundle of His) -inside interventricular septum -bifurcate to: 5. Bundle Branches R/L 6. Purkinje Fibers -hairpin turns -deliver current to ventricular muscle cells (ventricular myocytes) - travel to other cells via intercalated discs upward *NOT NEURONS* -modified muscle tissue (part neuron part muscle tissue) -highway: begins electrical current & spreads to rest of road |
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Membrane Potential
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-cells in body that generate current (excitable cells):
>neurons & muscle cells >electrical pot. diff across bio mem are basis of the electrical activity of excitable cells -measure indiv. cell w/ electrode to get current -inside cell = negative (K, Cl) -outside cell = positive (Na) |
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Neuronal AP
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-depolarization: Na enters (raise mem pot)
-repolarization: close Na channels & open K channels flow out -re-est. conc. gradient |
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Cardiac AP
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-DEPENDS on where it is measured
-cannot measure w/ ECG (just electrodes on surface of skin, not measuring single cell - need microelectrode) 2 types: 1. Non-pacemaker (fast response) -occur in atria, ventricles & purkinje fibers -undergo rapid depolarization 2. Pacemaker (slow response) -occur in SA & AV node -undergo "slow" depolarization |
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AP speed of:
1. neurons 2. skeletal 3. cardiac |
AP duration:
-neurons = 1 msec -skeletal = 2-5 msec -cardiac = 200-400 msec |
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Non-Pacemaker Cardiac AP
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-fast response
1. PHASE 0: rapid depolarization -upstroke of AP -fast Na channels open up >have activation M gate & inactivation H gate -K channels close 2. PHASE 1: Early/Initial Repolarization -transient out current as K channels open -fast Na channels closed (h gates close) 3. PHASE 2: Plateau Phase -Ca channels open lead to inward Ca mvmt -cardiac = REQUIRE Ca influx during AP -efflux of K: same amt of Ca enter as K leaving 4. PHASE 3: Late/Final Repolarization -Ca channels close (no more + in) -K channels still open (+ leave cell) AP repolarizes 5. PHASE 4: resting mem pot -K channel remain open -Na/K pumps restore -Ca extrusion mxn highly active |
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ECF Ca Influx
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-amt Ca enter cardiac muscle during AP = small & does NOT promote actin-myosin interaction
-triggers to induce Ca release from SR -promotes contraction -Ca from 2 sources in cardiac -HIGHLY regulated: NT (ANS) >norepi = symp >Ach = parasymp >drugs: beta blockers, Ca channel blockers *MORE Ca = GREATER FORCE OF CONTRACTION |
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Ca Extrusion Mxns
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1. SR Ca pumps (SERCA)
-surface of SR have pumps -need ATP 2. Sarcolemmal Ca pumps 3. 3Na/1Ca antiporters *1 & 2 most important* -if don't rid of Ca, Ca binds to troponin over & over again, muscle constantly contracting |
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Clinical Application of Troponin
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-troponin complex consists of 3 proteins:
1. cardiac troponin C -what Ca binds to 2. cardiac troponin I -inhibit part that hides from myosin 3. cardiac troponin T -binds to troponin -skeletal & cardiac isoforms (T&I) differ in aa sequence -ischemia: tissue receive poor amt of blood -coronary BV deliver blood to myocardium; when BF compromised (fat, plaque) -Angina: chest pain: referred to shoulder, arm, to jaw = no cell death >nitroglycerine relieves chest pain -Myocardial Infarction = cell death (lack of O2) -cell death = troponin spills out (marker for myocardial cell injury) -I & T: rise 2-6 hrs after injury -both peak in 12-16 hours -I stay elevated for 5-8 days -T elevated for 5-14 days |
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Coupling of Electrical &
Mechanical Activity |
-in cardiac they overlap
-in skeletal electrical is over before mxl events begin -thus impossible to produce summation & tetanus found in skeletal during high freq stim in cardiac muscle -tetany of heart = death -prolonged refractory periods (in part) allow ventricles to relax & fill w/ blood before next contraction |
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Refractory Periods
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1. effective (absolute) refractory period: 2nd AP absolutely cannot be initiated no matter how large a stim applied
2. relative refractory period -2nd AP may be evoked only when stim is suff. strong (supra-threshold) -long refractory prevents tetanus from occuring |
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Conduction Velocity
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-dromotropic = conduction velocity
-influenced by ANS -symp activation increases conduction velocity in nodal & non-nodal tissue by increase slope of phase 0 -> more rapid depolarization of adj cells (more Na channels open) -positive dromotropic effect of symp activat result from NE bind to Beta-1 receptros -drugs that block B1recepters decrease conduction velocity & produce AV block -negative dromotropy: parasymp: decrease slope, less Na channels open (Ach - muscarinic) -excess vagal activ produce AV block |
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Quinidine
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-anti-arrhythmic drug: block fast Na channels & cause decrease in conduction velocity in non-nodal tissue
-help restore normal rhythm |
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Chronotropy vs. Dromotropy
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Chronotropic: changes in heart rate
-negative = HR decreases, by decrease rate of SA node -positive: HR increases, by increase fire rate of SA node Dromotropic: changes in CV: in AV node -speed of spread of current -negative: decrease CV thru AV node, slow conduction of AP from atria to ventricles -positive: increase CV thru AV node, speed conduct of APs from atria to ventricles |
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SA Node
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-normally the pacemaker of the heart
-has unstable RMP (resting mem pot) -exhibits phase 4 depolarization or automaticity (ability to initiate its own depolarization) |
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Pacemaker Cardiac AP
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*no Phase I or II
PHASE 0: -upstroke of AP -caused by increase in Ca conductance PHASE 3: -repolarization -cause by increase in K conductance; increase results in outward K current cause repolarization of the mem pot PHASE 4: -slow depolarization -accounts for automaticity in SA node -cause by increase in Na conductance inward current (If) -turned on by repolartization of the mem pot during preceding AP -repeated automatically |
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Basic Electrocardiogram
ECG |
-none of the waveforms = AP
-electrical activty that dissipates to surface of skin waveforms segments intervals |
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ECG
Waveforms |
-P wave: depolarization of the atria (atria electrically stim)
-QRS complex: depolarization of the ventricles (vent elec. stim: spread to purkinje fibers) **DO NOT represent contractions** only electrical activity, contract occurs after wave -T wave: repolarization of the ventricles (cannot measure repol of atria bc ventricle repol is masking it) |
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ECG
Segments |
flat portions of ECG
-PQ segments: (end of P wave to begin of QRS complex) time when impulse is travel thru AV node, bundle of His, & bundle branches -ST segment: end of QRS complex to onset of T wave |
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ECG
Intervals |
include both wave form & flat line
-PR interval: include P wave to middle of QRS complex (PQ segment) -ST interval: end of QRS complex to end of T wave (include ST segment) -QT interval: onset of QRS complex to end of T wave |
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Label the ECG:
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X
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What is occuring at this part of the ECG?
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1. SA node generates impulse, atrial excitation begins
2. impulse delay at AV node 3. impulse passes to heart apex; ventricular excitation begins 4. ventricular excitation complete |
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1st degree AV block
2nd degree AV block |
1: extended PQ segment
-something is extending the conduction velocity to electrical current to ventricles -ex: scar tissue near bundle of His, covers & impedes speed of electrical activity 2: P wave but no QRS complex or T wave -electrical activity not reaching to ventricular area -P wave initiated by SA node but not traveling to target |
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Overdrive Suppression
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-SA node = king of pacemakers ~80 beats/min
-under normal conditions is pacemaker -if SA node fails we have back up: >AV Node (limited ANS control; 40-60 beats/min) no P wave just QRS-T >Purkinje Fibers (no ANS control; 15-40 beats/min) |
