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Anatomy > Cardiovascular > Flashcards

Flashcards in Cardiovascular Deck (33):
1

Location of heart

Within thorax between lungs, anterior and inferior to the left. In the mediastinum.

2

Mediastinum

Surrounds great vessels, heart, pericardium

3

Percardium

3 layers, unique to heart.
Fibrous pericardium: dense irregular CT anchors pericardium to thorax. At the base, it turns back on itself and become parietal layer of the pericardium.
Parietal layer of the serous pericardium. SSE secrete serous fluid.
Visceral layer of the serous pericardium. SSE

4

Names of sulci

Coronary, anterior inter ventricular
, posterior intervetricular

5

Layers of the heart

Epicardium: SSE aka visceral layer of the pericardium. Plus underlying adipose tissue
Myocardium: nodal cells plus myocardiocytes. Intercalated discs= desmosomes physical junctions, gap junctions chemical junction, allow for synchronization of contracting and relaxing cells.
Endocardium: SSE lines heart chambers. Continuous with endothelium of blood vessels

6

Muscles on the atria

Pectinate muscles

7

Muscles of the ventricles

Trabecular carnae, papillary muscles hold onto chordae tendonae.

8

AV valves

Tricuspid, bicuspid, mitral, atrioventricular

9

SL valve

Pulmonary semilunar or aortic semilunar valves

10

Right coronary artery splits to

(In coronary sulcus) branches to rt marginal artery and posterior interventricular artery.

11

Coronary veins

Great cardiac vein, (in anterior interventricular sulcus)
Middle cardiac vein( in posterior interventricular sulcus)
Small cardiac vein ( near right marginal artery)

All drain into coronary sulcus,

12

Parts of the heart conduction system

SA node: sinoatrial node sets heartbeat pace.
AV node: atrioventricular node
AV bundle = bundle of His
R and L bundle branches
Purkinje fibers: conduct impulses from apex to base. Cause contraction of ventricular myocardium

13

Electrical events in nodal cells

1. Slow VGNC open (triggered by repolarization from previous cycle.) reaching threshold -60 to -40 mV.
2 depolarization occurs when fast VGCC open. Inflow of Ca changes membrane potential to 0 mV.
3.repolarization occurs when fast VGCC close and VGKC open. Membrane potential returns to -60 and k channels close.

14

Electrical events in cardiac cells

1. Depolarization: AP transmitted through conduction system triggers opening of fast VGNC. -70 to +30
2. Slow VGCC opens with depolarization and Ca trickles in. This opens VGCC in sarcoplasmic reticulum and creates plateau with VGKC
3. Repolarization VGCC close but VGKC remain open, so k moves out of the cardiac cells allowing repolarization

15

Diastole

Muscle relaxation

16

Systole

Cardiac Muscle contraction

17

Ventricular filling

Slow: late ventricular diastole. Blood passively flows through AV valves. 4 chambers relaxed, semilunar valves closed.

Rapid: atrial systole: atria squeeze remaining blood into ventricles.

18

Isovolumetric contraction

Early ventricular systole. Ventricles contract, atria relax. Av valves close. First sound!

19

Ventricular ejection

Late ventricular systole increasing ventricular pressure forces blood through SL valves.

20

Isovolumetric relaxation

Early ventricular diastole. Ventricles begin to relax, blood in great arteries flows back and close SL valves. 4 chambers relaxed, 4 valves closed, 2nd sound

21

Cardiac output

Amount of blood pumped through one ventricle per minute,

hR x SV (stroke volume)

Each Ventricle pump same amount of blood.

22

Changing heart rate

Chronotropic agents

Positive increase heart rate, ie, sns releases NE and E hit SA node and AV node, increase intracellular Ca so depolarize faster

Negative decrease heart rate, ie pns activation dumps Ach on SA AND aV node which opens K channels. Repolarization or hyperpolarize

23

Changing stroke volume

Venous return, after load, inotropic agents

24

Venous Return

Volume of blood returned to heart per unit. Increased venous return->increases stretch of heart wall, which results in greater overlap of thick and thin filaments within the sarcomeres of the myocardium --> additional cross bridges form, and ventricles contract with greater force. --> stroke volume increases

25

Inotropic agents

Substances that act on the myocardium to alter contractility. Positive inotropic agents --> increased Ca levels in the sarcoplasm results in greater binding of Ca to trponin of thin filaments within sarcomeres of the myocardium --> Additional cross bridges form and ventricles contact with greater force.

26

Afterload

resistance in arteries to ejection of blood. Athleroclerosis,--> arteries become more narrow i diameter--> increases the resistance to pump blood into the arteries-->stoke volume decreases.

27

P wave

Atrial depolarization.

28

T-P

Late ventricular diastole, ventricular slow filling.

29

P-R

Atrial systole. Rapid ventricular filling

30

R to just after S

Early ventricular systole. Isovolumetric contraction

31

After S to T

Late ventricular systole: ventricular ejection

32

T wave

Ventricular repolarization

33

After T

Early ventricular diastole. Isovolumetric relaxation.