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Thompson Exam 4 and 5 > Exam 5 Mon 4.18 Heart Anatomy review PP > Flashcards

Exam 5 Mon 4.18 Heart Anatomy review PP Flashcards

1
Q

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

A

Pulmonary circulation - Pumps blood through the lungs

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2
Q

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

A

Systemic circulation - Pumps blood through the body

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3
Q

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

A
  • 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
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4
Q

What is the mediastinum?

A

area above diaphragm, between lungs

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5
Q

3 parts of the heart wall

A
  • Pericardium
  • Myocardium
  • Endocardium
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6
Q

A few things about the pericardium

A
  • a double-walled sac
  • †Parietal (outer layer) and visceral (inner)
  • Pericardial cavity and fluid separate them
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7
Q

What is the myocardium?

A

thickest layer, cardiac muscle

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8
Q

What is the Endocardium?

A

internal lining, connective tissue and squamous cells

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9
Q

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

A
  • ˜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
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10
Q

What are the great vessels? (4ish)

A
  • ˜Superior and inferior venae cavae
  • ˜Pulmonary artery (trunk)
    • Right and left pulmonary arteries
  • ˜Pulmonary veins
  • ˜Aorta
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11
Q

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

A
  • 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
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12
Q

3 divisions of Right coronary artery

A

˜splits into:

  1. Conus
  2. Right marginal branch
  3. Posterior descending branch
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13
Q

2 divisions of left coronary artery

A

splits into:

  1. Left anterior descending artery
  2. Circumflex artery
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14
Q

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

A
  1. ˜Collateral arteries
  2. ˜Coronary capillaries
  3. Coronary veins:
    • Coronary sinus
    • Great cardiac vein
    • Posterior vein of the left ventricle
  4. ˜Coronary lymphatic vessels
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15
Q

Some basic info about Coronary lymphatic vessels

A
  • drain with cardiac contractions into mediastinal lymph nodes
  • then into superior vena ca
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16
Q

Lub: what? where? how?

A
  • ˜Ventricular Contraction (Depolarization)
  • S1 = Tricuspid and Mitral Valve closing
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17
Q

Dub: what? where? how?

A
  • ˜Ventricular Filling (Repolarization)
  • S2 = Aortic and Pulmonic Valve closing
18
Q

Things that control the heart electrically

A
  • ˜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
Q

SA node- location and electrical power

A
  • in RA, just above tricuspid valve
  • Generates ~75 action potentials/minute
20
Q

AV Node- location and electrical info

A
  • ˜also in RA, superior to tricuspid valve
  • near autonomic parasympathetic ganglia – these slow the impulse conduction through the AV node
21
Q

Heart conduction sequence

A
  • ˜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
Q

Propagation of cardiac action potentials (4)

A
  • 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
Q

What is Refractory period?

A
  • 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
Q

What is Electrocardiogram?

A

sum of all cardiac action potentials

25
Q

What is Automaticity?

A

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

26
Q

What is Rhythmicity?

A

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
Q

˜6 parts of an EKG reading and what they are

A
  • 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
Q

Cardiac Innervation and ANS involvement (4)

A
  • ˜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
Q

Why do we care about Calcium channels in myofibrils?

A

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

  • blocking contraction
  • dilating blood vessels
  • prescribed for hypertension and migraines
30
Q

Points about Myocardial metabolism

A
  • ˜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
31
Q

What is Cardiac output?

A

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

32
Q

What is Ejection fraction? -and some additional info

A
  • ˜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)
33
Q

What is Preload?

A
  • volume and pressure in ventricle at end of diastole
  • Called left ventricular end-diastolic volume
34
Q

What is Laplace law?

A

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

35
Q

What is Frank-Starling law of the heart?

A

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

36
Q

What is Afterload?

A

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
37
Q

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

A

True

38
Q

Review of the components of the RAAS

A

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
39
Q

Norms for BP and numbers for the different stages of hypertension

A
  • ˜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
40
Q

˜The Two major categories of hypertension

A
  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

Thompson Exam 4 and 5 (9 decks)

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