Cardiac Anatomy Flashcards

0
Q

What’s the largest venous channel

A

Coronary sinus

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1
Q

Parietal portion…

A

Adheres to fibrous pericardium

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2
Q

What is left atrium responsible for

A

20-30% LVEDV via the atrial kick

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3
Q

Characteristics of myocardium and types

A

Skeletal and smooth muscle

  • epicardium - outer
  • myocardium - middle
  • endocardium- inner
  • subendocardium - the greatest risk for MI
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4
Q

When is each ventricle supplied?

A

LV - diastole

RV - both systole and diastole

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5
Q

ventricular cells

Phase 0

A

Na influx,
Depolarization
Gates open at -70 to -65 mV

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6
Q

Ventricular cells

Phase 1

A
Initial repolarization
K efflux
Na closed
Ca slowly in
Overshoot 20 to 30
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7
Q

Ventricular cells

Phase 2

A

Plateau

Ca channels are open

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8
Q

Ventricular cells

Phase 3

A

Rapid repolarization
K efflux
Ca inactivated

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9
Q

Ventricular cells

Phase 4

A

Resting potential

Na/K pump restored

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10
Q

Absolute refractory

A

No stimulation can cause another AP

First part of the refractory period

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11
Q

How does relaxation occurs in phase 4

A

Ca is actively pumped back into the sarcoplasmic reticulum by Ca, Mg, ATPase

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12
Q

Relative refractory period

A

Possible to cause another AP, but the intensity of the cantor action will be relative to the time in this period

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13
Q

Refractory period

A

Minimal interval between two depolarizing impulses that are propagated

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14
Q

Characteristics of Atrial and Ventricular APs

A

Fast
RMP -80 to -90 mV. Resting membrane potential
Bigger upstroke, faster conduction
Occurs: atria, ventricles, purkinje

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15
Q

SA & AV node AP

A

Slow
RMP -55 to -60 mV due to slow leak of Ca++
Th ESA & AV nodes are pacemaker cells
No plateau, just phases 4, 0, 3 since NO rapid depolarization
Slow phase 4 depolarization

16
Q

What is compliance of ventricle

A

Relationship between LVEDV & LVEDP

Volume & pressure

17
Q

What will increase inotropy

A
PNS inhibition
SNS activation
Circulating catecholamines 
HR -- Bowditch effect
Afterload -- Anrep Effect
18
Q

Cardiac innervation

A

SNS: greater effect on contractility
T1-T4, cardiac plexus, SA node, muscle, Inc HR

PSN: predominates, Vagus X
Originate in the Medulla, dec HR/contractility
R Vagus innervates SA node
L Vagus innervates AV node

19
Q

Cardiac reflexes

A
  1. Afferent n sense a change— sends info to brain
  2. Brain processes & implamants appropriate response
  3. Efferent n. activity is altered, homeostatic response
20
Q

Where are Baroreceptors

A

Afferent
Carotid sinuses: dominant: travel via n. Herring branch of CN IX
Aortic arch: secondary. T ravel by aortic n.

21
Q

Marey’s law

Baroreceptor reflex

A

Inc BP - inc stretching - HR reflex dec

Response to local stretch

22
Q

Bainbridge reflex

A

True reflex rather than a response to local stretch
Incr in preload directly stretches the SA-incr SA node automaticity/HR

Inc filling will incr HR, except if HR was high

23
Q

Respiratory reflex

A

Receptors are in the medulla
Inspiration: inc HR,
expiration: decrease HR

24
Q

Determinants of myocardial O2 supply

A
Coronary artery anatomy
Diastolic pressure
Diastolic time
Arterial O2 content Hgb 
O2 extraction
25
Q

Determinants of myocardial O2 demand

A

HR
Myocardial contractility
Myocardial wall tension: preload, afterload

26
Q

What is EF

A

EF: fraction of the EDVV that is ejected
Way to evaluate the inotropoic state of the heart

EF= (SV/EDV) x 100%

27
Q

CPP=

A

CPP = Diastolic BP - PAWP

28
Q

SVR

A

SVR = (MAP-RAP) x 80/CO

29
Q

MAP

A

MAP = SBP + (DBP x 2)/ 3