Exam 5 Mon 4.18 Heart Anatomy review PP

Question 1

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

Answer 1

Pulmonary circulation - Pumps blood through the lungs

Question 2

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

Answer 2

Systemic circulation - Pumps blood through the body

Question 3

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

Answer 3

• 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

Question 4

What is the mediastinum?

Answer 4

area above diaphragm, between lungs

Question 5

3 parts of the heart wall

Answer 5

• Pericardium
• Myocardium
• Endocardium

Question 6

A few things about the pericardium

Answer 6

• a double-walled sac
• †Parietal (outer layer) and visceral (inner)
• Pericardial cavity and fluid separate them

Question 7

What is the myocardium?

Answer 7

thickest layer, cardiac muscle

Question 8

What is the Endocardium?

Answer 8

internal lining, connective tissue and squamous cells

Question 9

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

Answer 9

• ˜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

Question 10

What are the great vessels? (4ish)

Answer 10

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

Question 11

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

Answer 11

• 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

Question 12

3 divisions of Right coronary artery

Answer 12

˜splits into:

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

Question 13

2 divisions of left coronary artery

Answer 13

splits into:

1. Left anterior descending artery
2. Circumflex artery

Question 14

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

Answer 14

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

Question 15

Some basic info about Coronary lymphatic vessels

Answer 15

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

Question 16

Lub: what? where? how?

Answer 16

• ˜Ventricular Contraction (Depolarization)
• S1 = Tricuspid and Mitral Valve closing

Question 17

Dub: what? where? how?

Answer 17

• ˜Ventricular Filling (Repolarization)
• S2 = Aortic and Pulmonic Valve closing

Question 18

Things that control the heart electrically

Answer 18

• ˜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

Question 19

SA node- location and electrical power

Answer 19

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

Question 20

AV Node- location and electrical info

Answer 20

• ˜also in RA, superior to tricuspid valve
• near autonomic parasympathetic ganglia – these slow the impulse conduction through the AV node

Question 21

Heart conduction sequence

Answer 21

• ˜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

Question 22

Propagation of cardiac action potentials (4)

Answer 22

• 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

Question 23

What is Refractory period?

Answer 23

• 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

Question 24

What is Electrocardiogram?

Answer 24

sum of all cardiac action potentials

Question 25

What is Automaticity?

Answer 25

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

Question 26

What is Rhythmicity?

Answer 26

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)

Question 27

˜6 parts of an EKG reading and what they are

Answer 27

* 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

Question 28

Cardiac Innervation and ANS involvement (4)

Answer 28

* ˜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

Question 29

Why do we care about Calcium channels in myofibrils?

Answer 29

˜site of action for calcium blocker medications – work by: * blocking contraction * dilating blood vessels * prescribed for hypertension and migraines

Question 30

Points about Myocardial metabolism

Answer 30

* ˜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

Question 31

What is Cardiac output?

Answer 31

˜amount of blood flowing through the systemic or pulmonary circuit/minute, usually 5 L/min at rest

Question 32

What is Ejection fraction? -and some additional info

Answer 32

* ˜amount of blood ejected in a beat. Can be estimated with echocardiography * Stroke volume – volume of blood ejected during systole * EF = Stroke volume/end-diastolic volume * Normal is around 50-75% * Decreased EF is sign of ventricular failure (36-49%, below normal; \<35%, severe)

Question 33

What is Preload?

Answer 33

* volume and pressure in ventricle at end of diastole * Called left ventricular end-diastolic volume

Question 34

What is Laplace law?

Answer 34

length/tension relationship – affects size of ventricle and the ability to produce a forceful contraction

Question 35

What is Frank-Starling law of the heart?

Answer 35

myocardial stretch determines the force of myocardial contraction. The greater the stretch, the stronger the contraction

Question 36

What is Afterload?

Answer 36

resistance to ejection of blood from the ventricle * Load muscle must move after it starts to contract * Determined by system vascular resistance in aorta, arteries, and arterioles

Question 37

True or False: Changes in preload, afterload, and contractility all interact to determine stroke volume and cardiac output

Answer 37

True

Question 38

Review of the components of the RAAS

Answer 38

Renin-Angiotensin-Aldosterone System * Renin- released by kidney due to decrease in blood pressure * Angiotensin I released systemically due to renin in circulation * Angiotensin I converted to Angiotensin II in lung by ACE * Angiotensin II causes vasoconstriction and decreased excretion of salt and water by the kidneys by increased release of aldosterone * Aldosterone- produces reabsorption of salt and water * If elevated BP (hypertension and potential long term CHF) * Drug: ACE inhibitor

Question 39

Norms for BP and numbers for the different stages of hypertension

Answer 39

* ˜Normal BP 120/80 (systolic BP and diastolic BP) * ˜Prehypertension - 120-139 mmHg and 80-89 mmHg * Stage 1 HTN 140-159 mmHg and 90-99 mmHg in stage 1 * Stage 2 160-179 mmHg and 100-109 mmHg * Stage 3 greater than 180 mmHg and greater than 110 mmHg

Question 40

˜The Two major categories of hypertension

Answer 40

1. _Essential hypertension (EH)_- unknown cause in 95% Genetics or stress hypothesized 2. _Secondary hypertension_- result of known cause kidney or bladder infection, Cushing’s syndrome, arterial disease