Exam 5 Mon 4.18 Heart Anatomy review PP Flashcards Preview

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Flashcards in Exam 5 Mon 4.18 Heart Anatomy review PP Deck (40)
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1

What type of circulation is the right side of the heart responsible for? 

Pulmonary circulation - Pumps blood through the lungs

2

What type of circulation is the left side of the heart responsible for? 

Systemic circulation - Pumps blood through the body

3

Deja vu review: long answer to Shappy's question on our first day of PT school 

  • Rt. Atrium
  • Rt. AV valve
  • Rt. ventricle 
  • Pulm SL valve
  • Pulm artery
  • Lung: arteries>arterioles>venules>veins
  • Pulm veins
  • Left atrium
  • Left AV valve
  • left ventricle 
  • aortic SL valve
  • aorta
  • Organs: arteries>arterioles>capillaries>venules>veins
  • vena cava

4

What is the mediastinum? 

area above diaphragm, between lungs

5

3 parts of the heart wall

  • Pericardium

  • Myocardium 

  • Endocardium 

6

A few things about the pericardium

  • a double-walled sac

  • †Parietal (outer layer) and visceral (inner)

  • Pericardial cavity and fluid separate them

7

What is the myocardium?

thickest layer, cardiac muscle

8

What is the Endocardium? 

internal lining, connective tissue and squamous cells

9

Info about the valves of the heart: 2 big categories, sub-categories, and a little extra

  • ˜Atrioventricular valves:
    1. Tricuspid valve – R AV, 3 cusps (flaps)
    2. Mitral valve – L AV, bicuspid
  • ˜Semilunar valves:
    1. Pulmonic semilunar valve – RV to pulmonary artery (trunk)
    2. Aortic semilunar valve – LV to aorta

10

What are the great vessels? (4ish) 

  • ˜Superior and inferior venae cavae
  • ˜Pulmonary artery (trunk)
    • Right and left pulmonary arteries
  • ˜Pulmonary veins
  • ˜Aorta

11

What's wrong with residual blood hanging out? (5) 

  • Can mean that there is a conduction issue
  • could be due to "flabby" heart walls
  • could be due to high volume of blood overwhelming heart
  • residual blood could cause coagulation
  • residual blood could cause infection

12

3 divisions of Right coronary artery

˜splits into:

  1. Conus
  2. Right marginal branch
  3. Posterior descending branch

13

2 divisions of left coronary artery

splits into:

  1. Left anterior descending artery
  2. Circumflex artery

14

List The Coronary Vessels, but you can omit coronary artery info b/c it's on another card (4 plus 3 subvessels) 

  1. ˜Collateral arteries
  2. ˜Coronary capillaries 
  3. Coronary veins: 
    • Coronary sinus
    • Great cardiac vein
    • Posterior vein of the left ventricle
  4. ˜Coronary lymphatic vessels 

15

Some basic info about Coronary lymphatic vessels 

  • drain with cardiac contractions into mediastinal lymph nodes
  • then into superior vena ca

16

Lub: what? where? how?

  • ˜Ventricular Contraction (Depolarization)

  • S1 = Tricuspid and Mitral Valve closing

17

Dub: what? where? how?

  • ˜Ventricular Filling (Repolarization)

  • S2 = Aortic and Pulmonic Valve closing

18

Things that control the heart electrically 

  • ˜Cardiac action potentials- electric impulses
  • ˜Conduction system
    • Sinoatrial node (SA) 
    • Atrioventricular node (AV) 
    • Bundle of His (AV bundle)
    • Right and left bundle branches
    • Purkinje fibers

19

SA node- location and electrical power 

  • in RA, just above tricuspid valve
  • Generates ~75 action potentials/minute

20

AV Node- location and electrical info

  • ˜also in RA, superior to tricuspid valve 

  • near autonomic parasympathetic ganglia – these slow the impulse conduction through the AV node

21

Heart conduction sequence

  • ˜Normal excitation originates in the sinoatrial (SA) node then propagates through both atria.
  • ˜The atrial depolarization spreads to the atrioventricular (AV) node, and passes through the bundle of His to the bundle branches/Purkinje fibers.
  • ˜Note that the intrinsic pacemaker rate is slower in structures further along the activation pathway. For example, the atrioventricular nodal rate is slower than the sinoatrial nodal rate.
  • ˜This prevents the atrioventricular node from generating a spontaneous rhythm under normal conditions, since it remains refractory at rates

22

Propagation of cardiac action potentials (4)

 

  • Resting membrane potential – voltage differential across the cell membrane
  • Depolarization – electrical activation of the cell - inside of cell is less negatively charged; important fact as drugs that alter ion movement can affect heart rate
  • Repolarization – electrical deactivation, reverse of above
  • Hyperpolarization – too much extracellular K+, resting potential more negative

23

What is Refractory period?

  • no new cardiac action potential can be initiated
  • gives time for channels that permit Na+ and Ca++ to re-enter cell
  • Abnormal refractory periods, due to heart disease, can cause dysrhythmias

 

24

What is Electrocardiogram?

sum of all cardiac action potentials

25

What is Automaticity?

˜generating spontaneous depolarization to threshold so that the SA and AV nodes generate cardiac action potentials without any stimulus

26

What is Rhythmicity?

SA sets the pace because it’s usually the fastest (60-100/min); AV (40-60/min) takes over if SA damaged; conduction cells in atria usually take over for the AV node; Purkinje fibers can also conduct (30-40/min)

 

27

˜6 parts of an EKG reading and what they are

  • P wave – atrial depolarization
  • PR interval – onset of atrial activation to ventricular activation
  • QRS – ventricular depolarization and atrial repolarization
  • ST interval – ventricular depolarization
  • QT interval – time between ventricles contracting and refilling
  • T – ventricular repolarization

 

28

Cardiac Innervation and ANS involvement (4)

  • ˜Autonomic system influences the rate of generation of action potentials, depolarization/repolarization, strength of contraction, diameter of coronary vessels. 
  • Sympathetic nerves – activation happens quickly, so that “fight or flight” response can be activated when needed
  • Parasympathetic nerves – through the vagus nerve (Cranial nerve X) to slow heart rate; acetylcholine decreases heart rate and slows conduction from AV node
  • ˜Adrenergic receptor function – increases contractile strength of the heart
    • Beta-adrenergic receptors
    • Norepinephrine or epinephrine

29

Why do we care about Calcium channels in myofibrils?

˜site of action for calcium blocker medications – work by:

  • blocking contraction 
  • dilating blood vessels
  • prescribed for hypertension and migraines

30

Points about Myocardial metabolism 

  • ˜like all muscles, ATP required
  • Myocardial oxygen consumption (MVO2) measures cardiac work, which is linked to cardiac energy requirements
  • MVO2 determined by:
    • Systolic blood pressure (amount of wall stress in systole)
    • Heart rate (duration of systolic wall tension)
    • Contractile state of the myocardium, for which no clinical measurement exists; is assumed in measurements
    • MVO2 can increase dramatically with exercise
  • O2 to myocardium is delivered by coronary arteries – 70-75% is used immediately, very little reserve; any increased energy need must be met by increasing blood flow