Basic Cardiac Structure and Function Flashcards
Right-sided structures lie mostly _______ to their______ counterparts.
anterior………left-sided
Both _____ chambers located mostly to the ____ of their corresponding ________.
atrial…..right…..ventricles
What is the function of the pericardium?
- Allows heart to beat without friction
2. Allows for room to expand
How much fluid fills the pericardial cavity?
5-30 ml
What keeps the pericardium attached?
- Central tendon of diaphram
- Sternopericardial ligament
- Vertebropericardial ligaments
What are the 3 sections of the heart’s layers from outermost to innermost?
- Pericardium (heart sac)
- Myocardium (muscle layer)
- Subendocardium
- Endocardium (inner lining)
What layers make up the pericardium from outermost to innermost?
- Parietal pericardium (outermost)
2. Visceral pericardium or epicardium (innermost)
What is the endocardium?
endothelial cell layer covering trabeculae
What is the subendocardial layer?
The layer between the endocardium and myocardium
What structures are contained in the subendocardial layer?
fibroblasts, elastic & collagenous fibers, nerves, Purkinje fibers, blood vessels (Thebesian veins)
Describe the flow of blood through the right side of the heart.
- Right atrium receives deoxygenated blood from the body (IVC & SVC) and heart (coronary sinus).
- Right ventricle pumps deoxygenated blood through the lungs via the pulmonary artery
What are the structures in the right ventricle?
- Inner wall
- Moderator Band
- Papillary muscles
- Outflow tract
What covers the inner wall of the right ventricle?
Trabeculae canreae
What is the Moderator Band?
Large trabecula and crosses right ventricle cavity
Is the Moderator Band a component of a RBB or LBB?
RBB
How many papillary muscles are in the right ventricle?
Three on the tricuspid valve
What is the outflow tract called in right ventricle? How does it promote laminar flow?
- Conus arteriosus
- Smooth surface
Describe the flow of blood through the left side of the heart.
- Left atrium received oxygenated blood from the lungs via pulmonary veins.
- Left ventricle pumps oxygenated blood to systemic circulation via the aorta
How does the left ventricle compare to the right ventricle?
- Left ventricle has a thicker wall 9-11 mm
- Left ventricle has 2 papillary muscles (mitral valve) when right has 3
- Both smooth walled for laminar flow
What is the name of the smooth wall in left ventricle?
Aortic Vestibule
What is the origin of the RCA & LCA?
Just above the aortic valve cusps
What is the cardiac conduction system pathway?
- SA node
- Internodal bundles (RA) and Interartial bundle to LA
- AV node
- AV bundle of His
- Right and Left branches of AV bundle of His
- Subendocardial fibers (Purkinje fibers)
The subendocardial plexus of purkinje fibers allow what to happen?
-Papillary muscles to contract before ventricle wall
What is prevented by the papillary muscles?
valve regurgitation
What sympathetic fibers innervate the cardiac nerves and where do they terminate?
- Sympathetic fibers from T1-T6
- In the heart and great vessels
What parasympathetic fibers innervate the heart and where?
- CN X (vagus nerve)
- SA node, AV node, and Purkinje fibers
What occurs when the vagus nerve is stimulated?
- From medulla Vagus fiber is (long) preganglionic and releases Ach at nicotinic receptor in ganglia
- Postganglionic fiber (short) releases Ach and binds to M2 receptors on nodal/muscle tissue (Purkinje fibers)
- Effects are inhibitory
What are the cardiac effects of vagal stimulation?
- decreased heart rate
- increased AV node ERP (decreased conduction)
- increased PR
What occurs with sympathetic stimulation in the heart?
- From spinal column preganglionic fibers (short) release Ach at nicotinic receptors in ganglia
- Postganglionic adrenergic fiber (long) releases NE at alpha/beta receptors on heart and great vessels
What are the cardiac effects of sympathetic stimulation?
- increased heart rate
- decreased AVN ERP (increased conduction)
- decreased PR
- increased contractility (SV)
What cardiac vessels branch of the LCA (left coronary artery)?
- AIV, anterior interventricular artery (LAD)
- Circumflex artery
What cardiac vessels branch of the RCA (right coronary artery)?
- PIV, posterior interventricular artery (PDA)
- Right marginal artery
Muscle fibers below endocardium in subendocardium are supplied by coronary artery terminal branch or _______?
-Thebesian veins (particularly in papillary muscles and left vent. wall)
What is a myocyte?
- individual cardiac muscle cell
- 25 microns x 100 microns
What is a myofibril?
a group of sacromeres
What is a sarcomere?
individual contractile unit of the cell (striations)
What is a sarcolemma?
an excitable cell membrane of the muscle cell
What are the functions of intercalated discs?
they are gap junctions between myocytes and coordinate muscle contraction
What is the function of the sacroplasmic reticulum?
Intracellular membrane network that releases Ca++ causing excitation contraction coupling
What is a T-tubule?
invagination of the sarcolemma that conduct impulses from cell surface down into the cell to the sarcoplasmic reticulum
Define action potential
- reversal of electrical potential across a semipermeable membrane caused by conformational changes in selective ion channels
- rhythmic, conducted appropriately, coupled to myocardial contraction
What are 3 major electrically excitable cell types?
- SA and AV nodes (pacemaker cells)
- Purkinje fibers
- Cardiac myocytes
Do pacemakers have neuromuscular junctions?
No, they have automaticity
What is the resting potential of pacemaker (nodal) cells?
-60 mV
What is the resting potential of myocytes?
-90 mV
Where does spontaneous discharge occur in pacemaker cells?
SA node
What is unique about pacemaker cells resting membrane potential?
-resting membrane potential -60 mV
slow voltage gate on Na+ channel cannot recover so Na+ channel remains inactivated
What is unique about pacemaker cells ion channel?
allows continuous slow inflow of Na+ until threshold is reached
Since Na+ channels are inactivated, upstroke of AP is dependent on ________?
Ca++ influx (slower)
Depolarization depends on ion transport and is governed by 2 characteristics?
- concentration gradients
- transmembrane potential
How does concentration gradients govern depolarization?
If extracellular Na+ is 142 mEq and intracellular is 14 mEq
-Strong force drives Na+ into cell, down it conc. gradient and causes depolarization
How does transmembrane potential govern depolarization?
- the resting potential inside cell is -90 mV
- a strong electrical attraction for Na+ to enter cell.
What type of Na+ channels do myocytes have?
Fast Na+ Channels
What happens when Fast Na++ Channels are activated?
- Open and close quickly
- Inactivated until membrane repolarized, providing refectory period
Are Fast Na++ Channels active on pacemaker cells?
No, only on myocytes
Why is the K+ conc. greater inside the cell?
Sodium-potassium pump
3 Na+ out
2 K+ in
What is the function of the inward rectifier channels?
- open in resting state allowing some K+ to flow out of cell
- overall negative interior charge slows K+ outflow
What is the K+ equilibrium potential?
-91 mV (zero net movement)
What is phase 4 of cardiac muscle AP?
- Resting state before depolarization
- rectifier channels leak K+ out to keep TMP at -90 mV
What is phase 0 of cardiac muscle AP?
-Rapid influx of Na+ through Fast Na+
What is phase 1 of cardiac muscle AP?
-transient K+ channels open and K+ efflux returns TMP to 0 mV
What is phase 2 of cardiac muscle AP?
- influx of Ca++ through L-type Ca++ channels
- electrically balanced through delayed rectifier K+ channels
What is phase 3 of cardiac muscle AP?
- Ca++ channels close
- delayed rectifier K+ channels remain open until TMP returns to -90mV
What is the “Fibrous Skeleton” of the heart?
- fibrous connective tissue surrounding AV valves
- serves as electrical insulator, isolates atria & ventricles
What is the only electrical conductor to the ventricles?
AV node
Why is there a delay at the AV node?
allows atria time to contract before ventricles
What is known as the “electrical gatekeeper”? Why?
AV node and limits ventricular stimulation during abnormal rapid atrial rhythms
What is excitation-coupling contraction?
electrical AP leads to physical contraction
What is regularly spaced on actin and has 3 subunits?
Troponin
What is the double helix that lies between actin filaments and blocks actin and myosin interactions?
Tropomysin
Thin filaments, a-helix?
actin
What is myosin?
- protein arranged in thick filaments
- globular heads contain myosin ATPase
What are contractile proteins in muscles contractions?
- myosin
- Actin
What are regulatory proteins in muscle contractions?
- Tropomyosin
- Troponin
Describe the process of calcium induced calcium release.
- L-Type Ca++ channels open during phase 2 of AP
- Ca++ enters cell via T tubule
- Ca++ triggers ryanodine receptorts on SR
- SR dumps its stores of Ca++
What is the MOA of Ca++ channel blockers?
- bind to L-type Ca++ channels
- once bound, causes reduction in the transmembrane Ca++ current
What are the effects of Ca++ channel blockers?
- decrease SA node rate
- decrease AV node rate
- decrease contractility
- increase vasodilation
What are the three classifications of Ca++ channel blockers?
- benzothiazepines (diltiazem)
- phenylalkylamines (verapamil)
- dihydropyridines (nicardipine, amlodipine, nifedipine)
Similarities between Diltiazem and Verapamil?
- both exert the most negative inotropic effects
- both possess local anesthetic activity (increased toxicity during regional anesthesia)
What adverse effects can Verapamil have on conduction?
- Augment conduction of cardiac impulse over accessory tract through reflex sympathetic activity
- resulting in increased ventricular response (WPW)
Which Ca++ channel blocker has the greatest degree of vasodilation?
-Nicardipine
coronary antispasmoditc/vasodilatory effects are GREATER than its systemic arterial vasodilatory effects
Adrenergic signaling
- beta-adrenergic stimulation enhances Ca++ fluxes
- NE binds to beta receptors
- STIMULATES adenylate cyclase production; increases force of contraction
Cholinergic signaling
- Ach from parasympathetic nerve terminals bind to M2 receptors
- INHIBITS adenylate cyclase; reduces HR
