Exam 4 Flashcards
Cardiac and smooth muscle are similar how?
“Unitary” contract as a unit.
Where are intercalated disc located?
Convoluted borders (only found in the heart tissue)
How are the convoluted borders/intercalated disc beneficial to the heart tissue?
increase gap junctions (increased surface area)
What do cardiac muscle and skeletomuscular tissue have in common?
sarcomere & striated pattern (d/t actin and myosin alignment)
the different in cardiac muscle cell and skeletomuscular?
Only one cell nuclei
Fibroblast
cells that create scar tissue
Tx for CHF
ACEi and ARB - prevent growth factor causing too much scar tissue.
What component of RASS is the growth factor?
Angiotensin II
Syncytial connections
The majority of the heart cells are?
cardiac myocytes
What do conduction tissue lack?
Myofibrils, tissue specialized to generate APs
What kind of neuron can conduct AP faster?
large neuron more than a small neuron.
Endocardium
innermost layer of heart
Endocardium lining
one cell layer thick and composed of endothelial cells.
Myocardium
bulk of the muscle wall
Pericardium (4)
Epicardium, pericardial space, parietal pericardium, fibrous pericardium
what layer are the vessels in the heart?
Coronary art. and vein run along the epicardium
Epicardium also called
visceral layer
What cells and tissue in the epicardium
mesothelial cells and connective tissue
Pericardium space (cavity)
between the parietal and epicardium layer
Fluid found in the pericardial space
mucus and fluid
Parietal pericardium
can stretch (inner layer of sac)
fibrous pericardium
leather like material (like dura)
What can constrict the heart
Fluid accumulation in the fibrous pericardium
Where do MIs occur often?
Subendocardium
Cardiac sarcomeres at rest
not relaxed at an optimal degree (eliminating H band)
Frank-starling law and heart
preload is needed to increase the force of contraction
Ventricular Vrm
-80mV
Ventricular AP threshold
-70 mV
Purkinje Fiber Vrm
-90 mV
Purkinje fiber AP threshold
-70 mV
Intrinsic Purkinje fiber HR
20-40 bpm
Oculocardiac reflex
V & X stimulation = severe bradycardia
iCa, iNa, iK mean?
current crossing over resistance
duration of cardiac muscle AP
about 200 msec
normal HR
72 bpm
AP every sec for 72 bpm
0.83 sec
HR without nervous system influence
110 bpm
SA node + sympathetic (only)
120 bpm (10 bpm increase)
SA + vagal influence (only)
60 - 62 bpm
AV node instrinsic rate
40-60 bpm
Purkinje fibers instinct rate
15-30 bpm
Normal AP difference (magnitude)
100 mV
EKG (y-axis) Small box:
0.1 mv
EKG (Y axis) larger box:
0.5 mV
EKG (x-axis) small box:
0.04 sec
EKG (X-axis) big box:
0.2 sec
EKG (X Axis) 5 big boxes:
1 sec
Net magnitude of EKG
1.5 mV
P wave (boxes & deflection)
Positive deflection ( 2 boxes up and 2 boxes long)
Atrium repolarization
end of the S wave (buried in QRS)
QRS wave duration
0.06 sec
Tall QRS
misplacement of leads or heart tissue is enlarged. (hypertrophy of vent)
Prolonged QRS
dilated cardiomyopathy
j point
isoelectric point, point of reference for infarct.
unhealthy tissue and T wave
Chronic depolarization in post T wave, ischemic myocardium
QT interval
0.25-0.35 secs
R to R interval
usually 0.83 sec
HR Formula
60 sec/ R-R interval (sec)
Lusitropy
how fast repolarization of ventricles
SA nodal tissue threshold
-40 mV
SA nodal Vrm
-55mv
HCN Channel
hyperpolarization + cyclic nucleotide
HCN channel ion
Na+ primary / Ca++ secondary
cAMP
cyclic nucleotide
Beta agonist
increase HR by opening more HCN channels
hyperkalemia
increase HR by making Vrm more positive.
Hypercalcemia
decrease HR (make threshold more positive)
hypocalcemia
decrease threshold potential = faster HR
Diastolic depolarization
Phase 4 AP of nodal tissue
Phase 0 of Nodal tissue
lack VG Na+
Density of HCN channels
SA node (highest) AV node (less) Vent. (least)
sec for normal conduction of heart
0.22 sec
Interatrial bundle
Bachmann’s bundle
SA to AV node (sec)
0.03 sec
AV node to Bundle of His
0.12 sec
Bundle of His to bundle branches
0.01 sec
lead II placement
(-) R arm & (+) L ft
Lead I placement
(-) R arm & (+) L arm
lead III placement
(+) L ft & (-) L arm
Einthoven’s Triangle
aVR, aVL, aVF
Mean axis deviation
59 degrees
Right axis deviation
More than 59 degree
left axis deviation
less than 59 degrees
EKG diagnose WHAT
3 lead EKG
EKG diagnose WHERE
12 lead EKG
Einthoven’s Law
Lead I + Lead III = lead II
Einthoven’s law is based on what?
equilateral triangle
What does Einthoven’s law provide clinicals with?
help check the accuracy of ECG recordings and detect possible errors in lead placement.
When do you see the most positive deflection on the EKG?
when tissue is 50% depolarized and 50% at rest.
How do Ca++ channel blockers work?
Ca channel blockers inhibit “the calcium component” in phase 4 (diastolic depolarization) of nodal action potential, slowing the HR.
antagonizing the L type calcium channels, preventing CICR from SR.
Beta Agonist stimulation in heart tissue?
synthesis of cAMP
cAMP activated PK-A
PK-A phosphorylates:
- L type channels
- Troponin I
- Phospholamban
Phosphorlyated phospholamban
Loses its inhibitory effect on SERCA, which accelerates calcium reuptake into SR.
(+) chronotropic
Effect the lusitropy of the heart?
postive and negative?
- Phospholamban ( + chronotropy)
shorter ST segment
Negative lusitropy would be the unphosphrylation of phospholamban
Phosphorylation of Trop I
increase Ca++ sensitivity of contractile proteins
increasing cycling rate of cross bridge generation
(+) inotropic effect
Phosphorylation of L type Ca++ channels
increases sensitivity (chronotropic influence) of channel and easier to open.
This will increase the amount of calcium coming inside during an AP.
(+) inotropic and chronotropic
How does L type Ca++ channels contribute to EAD or DAD?
too much beta adrenergic activity = heart attacks by an increase in sensitivity by the phosphorylation of L type Ca channel .
too much sensitivity of L-type calcium channels is BADDDD : causing an MI
inhibition of PDe:
will increase the cAMP availability = increasing activity of PKA = phosphorylation of -lamban, Trop I, L CA++
