Exam 4 Flashcards by Leonardo Fajardo III

Cardiac and smooth muscle are similar how?

“Unitary” contract as a unit.

How well did you know this?

Not at all

Perfectly

Where are intercalated disc located?

Convoluted borders (only found in the heart tissue)

How well did you know this?

Not at all

Perfectly

How are the convoluted borders/intercalated disc beneficial to the heart tissue?

increase gap junctions (increased surface area)

How well did you know this?

Not at all

Perfectly

What do cardiac muscle and skeletomuscular tissue have in common?

sarcomere & striated pattern (d/t actin and myosin alignment)

How well did you know this?

Not at all

Perfectly

the different in cardiac muscle cell and skeletomuscular?

Only one cell nuclei

How well did you know this?

Not at all

Perfectly

Fibroblast

cells that create scar tissue

How well did you know this?

Not at all

Perfectly

Tx for CHF

ACEi and ARB - prevent growth factor causing too much scar tissue.

How well did you know this?

Not at all

Perfectly

What component of RASS is the growth factor?

Angiotensin II

How well did you know this?

Not at all

Perfectly

Syncytial connections

How well did you know this?

Not at all

Perfectly

The majority of the heart cells are?

cardiac myocytes

How well did you know this?

Not at all

Perfectly

What do conduction tissue lack?

Myofibrils, tissue specialized to generate APs

How well did you know this?

Not at all

Perfectly

What kind of neuron can conduct AP faster?

large neuron more than a small neuron.

How well did you know this?

Not at all

Perfectly

Endocardium

innermost layer of heart

How well did you know this?

Not at all

Perfectly

Endocardium lining

one cell layer thick and composed of endothelial cells.

How well did you know this?

Not at all

Perfectly

Myocardium

bulk of the muscle wall

How well did you know this?

Not at all

Perfectly

Pericardium (4)

Epicardium, pericardial space, parietal pericardium, fibrous pericardium

How well did you know this?

Not at all

Perfectly

what layer are the vessels in the heart?

Coronary art. and vein run along the epicardium

How well did you know this?

Not at all

Perfectly

Epicardium also called

visceral layer

How well did you know this?

Not at all

Perfectly

What cells and tissue in the epicardium

mesothelial cells and connective tissue

How well did you know this?

Not at all

Perfectly

Pericardium space (cavity)

between the parietal and epicardium layer

How well did you know this?

Not at all

Perfectly

Fluid found in the pericardial space

mucus and fluid

How well did you know this?

Not at all

Perfectly

Parietal pericardium

can stretch (inner layer of sac)

How well did you know this?

Not at all

Perfectly

fibrous pericardium

leather like material (like dura)

How well did you know this?

Not at all

Perfectly

What can constrict the heart

Fluid accumulation in the fibrous pericardium

How well did you know this?

Not at all

Perfectly

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++

Exam 4 Flashcards

(98 cards)