Heart 2 Flashcards
Intercalated disc
Specialized region of intercellular connections between cardiac cells
Three types of adhering junctions within an intercalated disc
Fascia adherens, macula adherens, and gap junctions
Fascia adherens
Anchoring sites for actin that connect to the closest sarcomere
Macula adherens
Holds cells together during contraction by binding intermediate filaments, joining the cells together (desmosomes)
Gap junctions
Low-resistance connections that allow current (AP’s) to conduct between cardiac cells
How close are cell membranes in heart cells?
2-4 nanometers
Connexon channels
Create intracellular connections
Primary determinant of internal resistance in cardiac tissue
Gap junctions
“Healing over”
Increase in internal resistance that results from a decrease in the number of open gap junctions
What causes healing over?
Increase in intracellular (cytosolic) calcium and/or hydrogen ions
Clinical application of healing over
Damaged tissue from a myocardial infarction will become electrically isolated
Three factors that determine cardiac conduction
Length constant, and rate of rise AND amplitude of action potential
Membrane resistance is inversely related to __ __.
potassium permeability
Internal resistance is inversely related to . . .
the number of gap junction connections AND to cell diameter
What is shown on a graph showing the relationship between the number of available fast Na+ channels and the membrane potential before stimulation of an action potential?
Shows that all the sodium channels have already been activated during depolarization and are no longer open to continue working. The number hits zero around -50mV, which is right about where the depolarization happens
Conditions that influence the AP upstroke due to changes in the RMP
Hyperkalemia, premature excitation during relative refractory period, ischemia/myocardial injury
What effect does hyperkalemia have on the upstroke of the AP waveform?
The fast upstroke will not be present, as the sodium channels have been deactivated already from the membrane potential being so close to threshold. Creates a slow waveform
Other than elevated blood levels of potassium, how else can hyperkalemia be stimulated?
If there is an infarct in an area of the heart, the injured cells can leak out potassium and increase the concentration of potassium in the local ECF
During infarction, how high can the local potassium concentration reach?
Up to 20 mEq/L
P-R interval
Conduction time from atria to ventricular muscle
QRS interval
Intraventricular conduction time (i.e., conduction through ventricles)
Why does the AV node delay?
To allow time for optimal ventricular filling
Why is AP slow at the AV node
Due to slow inward calcium current
How is the long refractory period of the AV node beneficial?
Protects the ventricles from abnormally high atrial rates (i.e., atrial fibrillation or atrial flutter)
Clinical determinant of AV nodal conduction time
P-R interval
First degree heart block
Abnormal prolongation in P-R interval greater than 0.20 seconds
Second degree heart block
Some atrial impulses fail to activate ventricles; not all P waves are followed by a QRS complex
Third degree heart block
Complete AV nodal block; no consistent P-R interval
Typical method of travel through the His-Purkinje system
Rapid conduction that brings the electrical impulse to the endocardial surface, resulting in endocardial and epicardial activation of the ventricles
How long is the QRS complex normally?
Less than 100 msec in duration; narrow
Clinical determinant of intraventricular conduction time
Duration of QRS complex
Why does the QRS complex need to be so short?
Syncrhonized ventricular activation to give a concise and strong contraction
Possible causes of slurred QRS complexes
Hyperkalemia, ischemia, ventricular tachycardia
Notched QRS complex
Indicates asynchronous electrical activation of the left and right ventricles
Possible causes of a notched QRS complex
Right and/or left bundle branch blocks
Supraventricular tachycardia
Conduction through the ventricles is normal, just rapid; the impulse still comes from the atria and travels through the AV node into the His-Purkinje system.
Ventricular wall motion and QRS during supraventricular tachycardia
QRS duration is normal because ventricles are firing normally, just more frequently. Ventricular wall motion is normal
Ventricular tachycardia
Conduction through the ventricles is not normal, because the impulse originates within the ventricular muscle and not through the His-Purkinje system
EKG findings and ventricular wall motion during ventricular tachycardia
QRS duration is prolonged (slurred) and the wall motion is abnormal. This causes a compromise in stroke volume
What determines atrial conduction?
The shape of the P wave of an EKG
Which is more fatal: a-fib or v-fib?
V-fib, since that is what is responsible for getting the blood oxygenated and perfused to the body. Atrial dysrhythmia will still get enough blood through to sustain life
What is the life-threatening secondary effect of atrial fibrillation?
Clotting due to pooling of blood in the atrial appendages, increasing potential for stroke, MI, or PE
How does acetylcholine act in the heart?
Via muscarinic receptors
What is the effect of the ACh release in the heart?
Increases K permeability directly via G-proteins, hyperpolarizing the membrane and decreasing the chance for action potential
What is the other secondary effect of ACh release on the heart?
Inhibition of adenylate cyclase activity and cAMP synthesis, decreasing slow inward calcium current indirectly
ACh directly inhibits these structures in the heart
Atrial muscle, SA node, and AV node
What are the effects of ACh on an EKG?
Lengthened P-R interval, lengthened R-R interval
What does ACh not directly effect?
Basal ventricular muscle function
Atropine
Pharmaceutical agent that blocks the muscarinic ACh receptors
What areas of the heart does norepinephrine affect?
All areas
What is the primary receptor acted on by norepinephrine in the heart?
Beta-1 adrenergic receptors
When NE binds its receptors, what intracellular signal is released?
cAMP
On what gradient does NE have an effect?
Positive effect on slow inward calcium current
EKG changes seen after NE release
Decreased R-R interval, decreased P-R interval
Inotropic effect
Hormonal reaction that changes contractility of the heart
