Heart Week 2A

Question 1

What is a vEnodilator?

Answer 1

NitroglycErin.

dereases prEload.

Question 2

What is a vAsoldilator?

Answer 2

hydrAlAzine.

decreases AfterloAd.

Question 3

What do ACE inhibitors and ARBs do to preload and afterload?

Answer 3

they both decrease preload and afterload.

ACE is given first, then ARBs if ACE is not well-tolerated.

Question 4

What artery usually supplies the SA and AV nodes?

Answer 4

RCA

Question 5

What are S1, S2, S3 and S4?

Answer 5

S1: mitral and tricuspid closing

S2: aortic and pulmonary valves closing

S3: early diastole, during rapid ventricular filling, associated with increased filling pressures (eg- regurgitation)

S4: “atrial kick”, late diastole, associated with ventricular hypertrophy, atrium must push against stiff LV wall.

Question 6

What do the three elements do in the Renin-Angiotensin-Aldosterone axis?

Answer 6

Renin: decreased renal blood flow releases Renin, which begets…

Angiotensin: increases peripheral vascular resistance

Aldosterone: increases intravascular volume

Question 7

What is the normal size of the mitral valve orifice?

Answer 7

4-6cm^2

Question 8

What is the size of the mitral orifice for mild, moderate and severe disease?

Answer 8

(size of mitral orifice in cm^2)

mild: < 2
moderate: 1.0 - 1.5
severe: < 1

Question 9

What is the normal size of the aortic orifice?

Answer 9

3-4 cm^2

Question 10

What is the size of the orifice for moderate and severe aortic stenosis?

Answer 10

moderate: 1 - 1.5 cm^2
severe: <1 cm^2

Question 11

What does stretching muscle fibers and holding them at fixed end points make the contractions stronger? What type of contraction is this?

Answer 11

a. muscle becomes more sensitive to Ca++
b. optimizes overlap of actin and myosin, increasing total number of cross bridges

This is an isometric contraction.

Question 12

According to Frank-Starling, SV does what in relation to an increased preload?

Answer 12

SV increases.

Question 13

In an isotonic contraction, what is the load that the muscles are contracting against?

Answer 13

The afterload.

Question 14

In an isotonic contraction, what determines the final length of the muscle fiber?

Answer 14

The magnitude of the load it is contracting against. In cardiac muscle, this is the afterload.

Question 15

Exposure to norepi does what to a cardiac contraction? And are the muscle fibers shorter or longer at the end?

Answer 15

It increases the force per contraction, and the muslce fibers have a shorter final length.

Question 16

What are the three main components of CO?

Answer 16

a. contractility
b. preload
c. afterload

Question 17

What is LaPlace’s Law?

Answer 17

wall stress = Pr/(2h)

pressure)(ventricle radius)/(2 x wall thickness

Question 18

What can cause SV to rise?

Answer 18

a. up preload
b. down afterload
c. up contractility

Question 19

What causes heart failure with a reduced ejection fraction?

Answer 19

a. impaired contractility: destruction of myocytes, MI, fibrosis
b. increased afterload

Question 20

At what pressure will fluid leave pulmonary capillaries and enter the pulmonary interstitium?

Answer 20

> 20mmHg

Question 21

What does heart failure with preserved ejection fraction lead to? And what does that lead to?

Answer 21

At first, it leads to increased ventricular volume and pressure during diastole. And that can lead to increased pulmonary pressure which can lead to pulmonary congestion (if pressure > 20mmHg).

Question 22

When does heart failure with preserved ejection fraction occur? What are three things that can cause it?

Answer 22

It happens with impaired diastolic relaxation or increased ventricular stiffness. Can be cause by:

a. hypertrophy
b. cardiac tamponade
c. fibrosis

Question 23

What is the equation to define BP?

Answer 23

BP = TPR x CO

Question 24

What are three of the most important components of the neurohormonal reaction to heart failure?

Answer 24

a. adrenegic nervous system
b. renin-angiotensin-aldosterone
c. inreased production of antidiuretic hormones

Question 25

Are chronic effects of the neurohormonal system beneficial?

Answer 25

no.

Question 26

What are 3 immediate causes of stimulating the adrenergic system?

Answer 26

a. increase in heart rate b. augmentation of ventricular contractility c. vasoconstriction

Question 27

When would the adrenergic system be stimulated?

Answer 27

Hypotension. Fall in CO is sensed by the baroreceptors, this increases sympathetc tone, and decreases parasympathetic tone.

Question 28

What is the order of events of renin to angiotensin II?

Answer 28

a. decreased renal blood flow > release of renin b. renin cleaves circulation angiotensin (A) to make AI. c. angiotensin-converting enzyme cleave AI to make AII. d. AII is a potent vasoconstrictor.

Question 29

Where is aldosterone secreted from? How does it work?

Answer 29

It comes from the adrenal cortex. It increases Na reabsorption from distal convoluted tubules, thus increasing intravascular volume.

Question 30

What are the NY Heart Association classifications of heart failure?

Answer 30

1. no limits on activity 2. slight limit, eg- dyspnea running up stairs 3. marked limitation of activity, eg- dyspnea while walking slow up stairs 4. severe limitation of activity, eg- symptoms present even at rest.

Question 31

Why use diuretics with heart failure? When should they be used?

Answer 31

promotes excretion of Na and water, thus reducing venous return and reducing preload. This should only be used with evidence of edema, such as hearing rales.

Question 32

What are the vasodilating medicines?

Answer 32

a. ACEI b. ARBs c. Isosorbide Dinitrate (veins) d. Hydralazine (arteries) (*c and d can be used together when ACEIs and ARBs don't work or are counter-indicated)

Question 33

How do ACEIs work? Do they affect veins or arteries?

Answer 33

They inhibit the R-A-A system, specifically the aldosterone. They affect both veins and arteries. (*also augments brady-kinin which helps with vasodilation)

Question 34

What is the difference between concentric and eccentric hypertrophy?

Answer 34

Concentric: sarcomeres added in parallel, a result of chronic pressure overload, walls thicken. Eccentric: sarcomeres add in series, a result of chronic volume overload, walls stay same size, but ventricles get bigger.