Cardiac Muscle Flashcards
Two types of cardiac muscle cells
- contractile
- conducting
Contractile Cells
- 99%
- they are the cells that contract
- majority of atrial and ventricular tissues
What generates pressure?
Contractions
Conducting cells
- do not contract
- SA node, AV node, Bundle of His and Purkinje
SA node
- able to generate action potentials spontaneously
- pacemaker
- fastest electrical activity in the heart
- unstable resting membrane potential
- rapid upstroke, but no sustained plateau
- exhibits automaticity
- innervated by parasympathetic and sympathetic
Cardiac Muscle Characteristics
- not symmetrically in one line (skeletal muscle is, smooth muscle is)
- intercalated disks (also present in smooth)
- form a functional syncytium
- desmosome, gap junction, T-tubles, SR, intercalated disk, thin & thick myofilaments
Desmosomes
- within intercalated disks
- transfer force from cell to cell
- gap junctions which allow electrical signals to pass rapidly
Intercalated disk
- allows the signal to be passed very quickly
- allows the cells to function together in a coordinated manner called functional syncytium
Contraction of cardiac muscle is similar to what?
-skeletal muscle!
Gap Junctions
- allow rapid passage of electrical impulses from one cell to the next
- physical attachment of cardiac cells for contraction
Resting Potential
- negatively charged
- difference in K+ (potassium) concentration across the cell membrane is the primary determinate
- -85 mV
Role of Na+K+ pump?
- maintain the [Na+] and [K+] gradients
- the exchange between sodium and potassium starts the mechanism
Action Potential Phase 0
- upstroke
- begins when membrane potential approaches threshold and sodium (Na+) channels open
- rapid depolarization
Action Potential Phase 1
- initial repolarization
- brief period of repolarization due to inactivation of Na+ channels
- outward flow of K+, because inside cell is more positively charged
- very short, very minimal
Action Potential Phase 2
- plateau
- little change in membrane potential occurs
- calcium comes in
- potassium goes out
Where does the calcium come from for cardiac action potential?
-both the sarcoplasmic reticulum and from outside the cell
Action Potential Phase 3
- repolarization
- rapid return to resting membrane potential
- close calcium channels
- efflux of potassium
- the loss of potassium means the cell becomes more negative
Action Potential Phase 4
- resting membrane potential
- membrane fully repolarizes
- returns to resting level of -85mV
Latent Pacemakers
- AV node
- SA node (have shortest action potentials and shortest refractory periods)
- bundle of His
- Purkinje fibers
Which pacemaker controls heart rate?
-the one with fastest rate of phase 4 depolarization
-and shortest action potential
=SA nodal cells
Ectopic Pacemakers Become Active
- when the SA node firing is depressed/reduced or stopped
- intrinsic rate of latent pacemaker becomes faster than SA node
- conduction pathway from SA node to the rest of the heart is blocked
Excitation-Contraction Coupling
- phenomenon called the calcium-induced calcium release from the SR
- conduction of calcium ions into the cell trigger further release of ions into the cytoplasm
- ventricles will all contract as a unit
Contractility
- correlates with intracellular [Ca++]
- depends on the amount released from SR which depends on the size of trigger and the amount of calcium previously stored in the SR
Effect of Heart Rate on Contractility
-if heart rate increase - contractility increases
(there will be more action potential per unit time, and an increase in total trigger calcium that enters cell during plateau phase, which increase the release of calcium from the SR)
Main determinant of cardiac muscle length?
- the degree of diastolic filling
- length corresponds to the end-diastolic volume
- increase fiber length = increase contractile tension of the heart following systole
- increase heart rate = decrease filling time of blood
Cardiac vs Skeletal
- both are striated, composed of sarcomeres, thin & thick filaments (myosin, actin, troponin C, and tropomyosin)
- contraction = sliding filament model (has an abundance of mitochondria, myoglobin, and T-tubules, SR)
- exhibit length-tension relationship/curve
Cardiac vs Smooth
- connected by gap junctions (and desmosomes)
- contract as a unit or functional syncytium
- pacemaker activity and capable of self-excitation
- calcium enters from ECF and SR
- innervated by ANS (modifies rate and strength of contraction
Cardiac mechanism of excitation
- pacemaker potentials
- electrotonic depolarizations via gap junctions
Cardiac activity of muscle cell
-action potential plateaus
Cardiac Calcium Sensor
Troponin
What terminates cardiac contraction?
-action potential repolarization
Cardiac regulation of force
-regulation of calcium entry
Heart is under what control?
-Autonomic
How to slow down heart rate?
- the parasympathetic fibers release Ach which binds to muscarinic receptor of the SA node
- this stimulation slows HR and conduction velocity is decreased
Increase heart rate
- sympathetic fibers to the heart release norephinephrine which binds to B1-adrenergic receptors at the SA node, AV node, specialized conducting tissues, and cardiac muscle
- stimulation of these fibers cause increased HR, conduction velocity, and contractility
Bulb
- external and internal bifurcation
- there is a carotid sinus where nerve comes off and goes to the brain - this brings an afferent signal
Cardiac autonomic plexus
- has easy influence to access the cardiac muscle cells to influence changes if they are needed
- standard autonomic reflex
Afferent (GVA)
- when the afferent nerve traffic from the cardiac receptors is integrated with other afferent information, this leads to activity in sympathetic and parasympathetic nerves
- this adjusts cardiac output and systemic vascular resistance
- helps to maintain arterial blood pressure
- happens below conscious level
Efferent (GVE)
- sympathetic nerve activity
- hormones (argine vasopressin, angiotensn, aldosteron) serve as effectors for regulation of salt and water balance and blood volume
moment-by-moment regulation of arterial pressure
-is neural control of cardiac output and SVR
long-term regulation of arterial pressure
-hormones
