Phys Exam 3 Quiz 2

Identify the 3 layers of the wall of the heart.

endocardium

myocardium

epicardium

endocardium

innermost layer

myocardium

thickest layer

middle layer

epicardium

thin outer layer

AKA visceral pericardium

visceral pericardium

contains pericardial space with small amount of serous fluid helps lubricate the surface to decrease friction as the heart beats

pericardial effusion

pericardial space between parietal and visceral layers of the pericardium is largely empty

fluid can collect in this space and compromise cardiac function because of interference with chamber filling → cardiac tamponade

myocardium consists of what two types of cells

contractile cells

pacemaker and conducting cells

contractile cells

atrial and ventricular cells

their contraction does the work of ejecting blood

pacemaker and conducting cells

generate and propagate the electrical rhythm that coordinates the action of the contractile cells

spontaneously depolarize

little contractile activity

autorhythmic

pacemaker and conducting cells spontaneously depolarize

cardiac contractile cells vs skeletal

both are striated, regularly arranged actin and myosin

cardiac are shorter, narrower, branched and connected end to end

intercalated discs

tightly bind myocytes together of the heart

what do intercalated discs contain

gap junctions

gap junctions

allow passage of small molecules including ions

electrical synapses

syncytium

individual fibers are connected electrically so that an AP spreads between the cells

atrial and ventricular syncitia are electrically isolated except at the AV node

Compare and contrast the makeup of contractile cells of the heart and cells of skeletal muscle, and explain how the arrangement of cells, their function and control differ between the two tissues

• Cardiac muscle: Intercalated discs mechanically hold cells together and allow electrical signals to spread between them through gap junctions. This allows the heart muscle to contract in a coordinated manner as a functional syncytium, even though the cells remain separate. Some cardiac cells are autorhythmic, meaning they can spontaneously generate electrical impulses.

• Skeletal muscle: Each muscle fiber contracts when stimulated by a somatic motor neuron. A motor unit consists of one motor neuron and all the muscle fibers it innervates. Recruiting different motor units allows the body to control the strength of a contraction.

Explain the abundance of mitochondria in cardiac cells.

depend on aerobic metabolism but can adapt to different fuel sources such as FA, glucose, ketones, or lactic acid

not prone to fatigue

have sarcoplasmic reticula to supply Ca2+

identify the difference between the sources of calcium for contraction in cardiac muscle and in skeletal muscle.

• Skeletal muscle: Calcium comes from the sarcoplasmic reticulum, which releases stored Ca²⁺ when stimulated by an action potential.

• Cardiac muscle: Calcium comes from both the extracellular fluid and the sarcoplasmic reticulum. The incoming Ca²⁺ triggers additional Ca²⁺ release from the SR, called calcium-induced calcium release

excitation contraction coupling

is the process by which an electrical signal (action potential) causes a muscle fiber to contract.

excitation contraction coupling in skeletal muscle

• Action potential travels along the sarcolemma and down the T-tubules.

• Voltage sensors (DHPR) activate ryanodine receptors (RyR) on the sarcoplasmic reticulum (SR).

• The SR releases Ca²⁺ into the cytoplasm.

• Ca²⁺ binds to troponin, moving tropomyosin away from actin's binding sites.

• Myosin binds actin, producing contraction.

excitation contraction coupling in cardiac muscle

• Action potential travels along the sarcolemma and into the T-tubules.

• Voltage-gated L-type Ca²⁺ channels open, allowing extracellular Ca²⁺ to enter.

• Incoming Ca²⁺ triggers the SR to release more Ca²⁺ through ryanodine receptors (calcium-induced calcium release).

• Ca²⁺ binds to troponin, moving tropomyosin away from actin's binding sites.

• Myosin binds actin, producing contraction.

three kinds of tropnin

T

C

I

what kinds of troponin differ from cardiac muscle to skeletal muscle

TnT

TnI

what may be used to diagnose MI

assays of cTnT and cTnI

how does cardiac troponin diagnosis MI

constituents of cardiomyocytes are released into the blood after cell injury

assays of these constituents have been used as biomarkers in the diagnosis of MI

troponin is specific for myocardial injury

Explain the diagnostic usefulness of cardiac troponin levels, including the utility of a test for myocardial infarction with a high negative predictive value

A test with a high NPV is very good at ruling out a condition when the result is negative. A negative high-sensitivity troponin test, interpreted with the patient's symptoms, ECG, timing, and sometimes repeat testing, makes an MI unlikely.

what does depolarization of cardiomyocyte cause

opening voltage gated L type Ca2+ channels in the T tubules so Ca2+ enters the cytosol

what does the Ca2+ that has entered the cardiomyocyte do

binds an opens ryanodine receptor Ca2+ channels in the SR

when does cardiac contraction end

when cytosolic [Ca2+] returns to baseline

lusitropy

the rate of heart muscle relaxation

depends on the removal of Ca2+ fromt he cytosol

Ca2+ ATPase pumps

return calcium to the SR

activity increases by sympathetic stimulation

Na+/Ca2+ exchangers/antiporters

pump Ca2+ out of the cell using the energy of Na+ moving down ins electrochemical gradient into the cell

digoxin

blocks the Na+/K+ ATPase pumps

digoxin in practice

only oral inotropic support agent currently used in clinical practice for heart failure

how does digoxin work

inhibits Na+/K+ ATPase → increases intracellular Na+ → decreaes Na+ electrochemical gradient → decreases Na+/Ca+ antiporters → increases intracellular Ca2+

digoxin is what kind of drug

parasympathomimetic

decreases chronotropic and dromotropic

good for A fib

lusitropic

affecting the rate of myocardial relaxation

chronotropic

affecting the heart rate

dromotropic

affecting myocardial conductivity

inotropic

affecting the force of myocardial contraction

calcium channel blockers that inhibit Ca2+ entry via L type Ca2+ channels

used as antihypertensives and have negative chronotropic, dromotropic, and inotropic effects on the heart and relax smooth muscle

no effect on skeletal muscle

how do calcium channel blockers affect smooth muscle

relaxes smooth muscle of artery walls to decrease SVR and BP

how do calcium channel blockers affect cardiac muscle

decrease cardiac contractility and heart rate

what does the strength of cardiac contraction depend on

concentration of cytosolic Ca2+

more Ca2+ → more binding of troponin → all cells of a single syncytium contract together

length tension relationship in cardiac muscle

increase of cell stretch induces more vigorous contraction

AKA Frank-Starling law

steps of Frank-Starling law

increase ventricular filling → increase stretch of cells → increase contractility → increase amount of blood ejected

when is the strongest contraction of a myocyte achieved

when the myocyte is stretched to 80-100% of maximum

3 most important types of membrane ion channels in contractile cardiomyocytes

fast Na+, K+, and L-type Ca2+ channels

Na+ channels job in cardiac contractile cells

opening of fast Na+ channels depolarize the cell

K+ channels job in cardiac muscle

allow the efflux of K+ to repolarize the cell

plateau of AP in cardiac contractile cells

due to

• entry of Ca2+ through L-type Ca2+ channels because they remain open for an extended period of time

• the slowed efflux of K+ balancing the influx of Ca2+

end of plateau caused by what

when the Ca2+ channels finally close and the K+ efflux increases the the cell repolarizes

what does the prolonged Ca2+ influx cause

a long refractory period which limits the maximum frequency of cell depolarization and increases intracellular Ca2+ which increases contractility

how many phases of cardiac AP

5

phase 0

depolarization

fast voltage gated Na+ channels open and depolarize the cell

phase 1

initial repolarization

Na+ channels close while K+ channels briefly open

phase 2

plateau

K+ efflux slows and L-type Ca+ channels become fully open

phase 3

rapid repolarization

Ca2+ channels close and slow K+ channels are opens so K+ efflux repolarizes the cell

phase 4

return to resting membrane potential 90 mV

membrane remains somewhat permeable to K+

Identify the main ion fluxes occurring during each of the 5 phases of the action potential of contractile cardiac cells

• Fast Na⁺ channels: Cause the rapid depolarization during phase 0.

• L-type Ca²⁺ channels: Cause the plateau during phase 2 and allow Ca²⁺ entry that triggers calcium release from the sarcoplasmic reticulum for contraction.

• K⁺ channels: Help repolarize the cell during phases 1 and 3 and maintain the resting membrane potential during phase 4.

antiarrhythmic agents

act on ion channels

Class I-IV

class I antiarrhythmic agents

Na+ channel blockers

class II antiarrhythmic agents

beta blockers

class III antiarrhythmic agents

K+ channel blockers

class IV antiarrhythmic agents

Ca2+ blockers

Explain how tension generated by cardiomyocytes is regulated and why the two ways the brain can instantaneously increase tension generated by skeletal muscle won’t work in cardiac muscle.

Cardiac muscle increases tension mainly by increasing intracellular Ca²⁺, rather than recruiting motor units or summing contractions as in skeletal muscle

ion fluxes for each phase

• Phase 0: Na⁺ moves into the cell.

• Phase 1: K⁺ moves out of the cell.

• Phase 2: Ca²⁺ moves into the cell, while K⁺ moves out.

• Phase 3: K⁺ moves out of the cell; Ca²⁺ influx decreases.

• Phase 4: K⁺ movement through inward-rectifier channels maintains the resting membrane potential.

how do APs spread through contractile cells of the heart

through the conduction of ions through gap junctions in the intercalated discs

velocity of conduction along atrial and ventricular muscle fibers

relatively slow for a desirable contraction to be slow and sustained

velocity of perkinje fibers

faster in these conduction fibers

when are cardiomyoctyes refractory to restimulation

during the action potential

the refractory period

why is the refractory period prolonged in cardiac tissue

helps to prevent excessively rapid depolarizations and ineffective contractions

skeletal vs cardiac muscle refractory period

skeletal muscle has a much shorter period which allows for summation and tetanus

cardiac muscle does not allow for this

what produces the long refractory period in cardiac cells

The long refractory period in cardiac contractile cells is caused by the prolonged plateau phase (phase 2) of the action potential.

• L-type Ca²⁺ channels remain open, allowing Ca²⁺ to enter the cell.

• This keeps the membrane depolarized for longer.

• Fast Na⁺ channels remain inactivated until the membrane repolarizes sufficiently, so another action potential cannot be initiated normally.

how does a long refractory period prevent tetany in cardiomyocytes

In skeletal muscle, repeated stimuli can cause contractions to summate before the muscle relaxes, producing sustained contraction (tetany). Cardiac muscle cannot do this because its refractory period is so long.

This ensures the heart relaxes between beats so its chambers can refill with blood.

generation of AP in cardiac muscle is due to what

myogenic generation not neurogenic

automaticity

spontaneous depolarization

path of cardiac conduction

depolarization starts in right atrium is then conducted through the AV node to apex of the heart and then spreads through muscle cells back up towards the base

spreads between cells via gap junctions

what does the cardiac conduction system consist of

pacemaker cells and conduction pathways

they coordinate the contraction of the atria and venctricles

where is depolarization initiated

in the SA node in the right atrium

normally controls rhythm of whole heart

what happens to the signal while the atria depolarizes

the signal is carried by 3 internodal pathways to the AV node

why is it important that the atria and ventricles are not electrically isolated at the AV node

allows depolarization of the atria to occur before depolarization of the ventricles

atria contracts first pumping blood into ventricles

Describe the anatomy of the pacemaker and conductive system of the heart

SA node → atrial myocardium → AV node → AV bundle (His) → right and left bundle branches → Purkinje fibers → ventricular myocardium.

SA node

Located in the right atrium near the opening of the superior vena cava. It is the heart’s primary pacemaker and initiates each normal heartbeat.q

AV node

Located in the inferior right atrium near the interatrial septum. It briefly delays the electrical impulse, allowing the atria to finish contracting before the ventricles contract.

AV bundle (bundle of His)

Carries the impulse from the AV node into the interventricular septum. It is the normal electrical connection between the atria and ventricles.

Right and left bundle branches

Travel down the interventricular septum toward the apex, conducting impulses to each ventricle.

perkinje fibers

pread throughout the ventricular myocardium, rapidly distributing the impulse so the ventricles contract in a coordinated manner, generally from the apex upward.

how does depolarization spreads through the contractile cells.

Depolarization spreads between cardiac contractile cells through gap junctions in the intercalated discs.

1. One cardiac cell depolarizes, allowing positive ions (mainly Na⁺) to enter.

2. The positive electrical current spreads into neighboring cells through gap junctions.

3. The neighboring cells reach threshold and generate their own action potentials.

4. The depolarization spreads from cell to cell, allowing the myocardium to contract in a coordinated manner.

Discuss the purpose and function of the SA

• Purpose: Initiates the electrical impulses that determine the heart’s normal heart rate and rhythm.

• Function: SA node cells are autorhythmic, meaning they spontaneously depolarize and generate action potentials without needing an external nerve stimulus.

Discuss the purpose and function of the AV

• Purpose: Ensures the atria contract and finish emptying blood into the ventricles before the ventricles contract.

• Function: Receives the impulse from the atria and briefly delays it before passing it to the AV bundle (bundle of His).

ECG PR interval

atria depolarize and contract before the ventricles

why is AV node conduction slow

to produce a delay between depolarization of atria and ventricles

what is the slow AV node conduction caused by

fewer gap junctions

decremental conduction

refractory period are unidirectional

decremental conduction

at rest the shorter the time between impulses (higher frequency) the slower the conduction through the node

helps prevent transmission of very rapid impulses to ventricles in the event of an atrial tachdysrhythmia

progressively slower conduction through the AV node → delayed ventricular contraction.

explain decremental conduction clinical significance in a condition such as atrial fibrillation

• Decremental conduction in the AV node slows conduction and helps prevent every atrial impulse from reaching the ventricles.

• This protects the ventricles from contracting at the same extremely fast rate as the atria.

• However, enough impulses still pass through the AV node to cause an irregular ventricular rhythm, often with a rapid heart rate.

Clinical significance: The AV node acts as a filter, limiting how many rapid atrial impulses reach the ventricles. If too many impulses pass through, the ventricles beat too quickly, reducing filling time and potentially decreasing cardiac output.

purkinje fibers function

conducts electrical signal that stimualtes contraction by transmitting signals fromt eh AV node to the myocytes of the ventricles

bundle of his function

travels a short distance down the interventricular septum before dividing into left and right bundles that conducts the APs to the endocardium of the apex and up the free walls

intercalated discs function

convey the depolarization through the ventricular syncytium so the muscle can contract en masse

what layer of the heart depolarizes first

the endocardium first then spreads toward the epicardium