Abstracts and Test 2• Earning up to 5 points for Test # 2 based

on topics of Frog Heart Lab:– Regulation of pacemaker cells by

temperature, hormones, neurotransmitters, antagonists

– Heart block: 1st, 2nd, and 3rd degree– The conducting system– Strategies for prolonging survival of in vitro

organs

Cardiac Cycle Animation

1QQ #24 for 10:30Write each letter and circle the letter of correct statements.

a) Heart murmurs are caused by the closure of heart valves.

b) The first heart sound is produced by the closure of the atrioventricular valves.

c) Blood is about 65% plasma.

d) Pacemaker cells produce action potentials that last about 200-300 milliseconds.

e) Chordae tendonae and papillary muscles prevent eversion of the semilunar valves.

1QQ #24 for 11:30Write each letter and circle the letter of correct statements.

a) The buffy coat is thicker in a person with an infection.

b) The first heart sound is produced by the closure of the atrioventricular valves.

c) Blood is about 45% plasma.

d) Pacemaker cells produce action potentials that last about 200-300 milliseconds.

e) The tricuspid valve is situated between the right ventricle and the pulmonary artery.

F=Q=ΔP/RFlow = Pressure gradient/Resistance

from Ohm’s Law (V=IR)

R = 8Lη/πr4

Q= ΔP πr4

8LηPoiseulle’s equation

S 8

Double radius … 16x flow

Half radius….1/16th flow

R = 8Lη/πr4

Cardiac Output = Heart Rate X Stroke Volume

What regulatesheart rate?

CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat

The Cardiac Cycle animation

S 1

What regulatesStroke Volume?

Figure 12.11

SA node cells do not have stable resting membrane potential, spontaneously produce AP, are Pacemaker cells

S 5

S 4

Figure 12.22Intrinsic Rate = 100 beat/min

S 15

2 effects of Parasymp:hyperpolarization &slower depolarization

Effect of “Beta blockers”

NE EPI ACh

mAChR

Effect of atropine

Beta-adrenergic receptors

S 6

Recall: CO = HR x SV

Fibrous connective tissue between atria and ventricles prevents the conduction of action potential. Only route is via AV node, bundle of His, bundle branches, Purkinje fibers, and to ventriclular myofibers.

What prevents the AP from being conducted from ventricles to atria?

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1st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole

2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole

S 8 “Sis-toe-lee”

“die-ass-toe-lee”

Figure 12.20Systolic

Diastolic

Ejection Fraction = SV/EDV

Atrial Fibrillation

Ventricular Fibrillation & Defibrillation

Stroke Volume

Animation

S 9

Events are same for Cardiac Cycle for Right Side of Heart; only difference is lower systolic pressures in right atrium and right ventricle.

S 10

CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat

S 1

So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate.

+ sympathetic- parasympathetic

2

1

3

The Cardiac Cycle animation

Figure 12.20

Stroke Volume

Animation

S 2

Frank-Starling Law of the Heart

FS LoH = SV is proportional to EDV

Ventricular Function Curve

Does not depend on hormones or nerves

Assures that the heart adjusts its output based on VENOUS RETURN

Ways to enhance Venous Return:1) muscle contractions2) “respiratory pump”3) venoconstriction

S 3

↑VR→ ↑EDV → ↑SV

Respiratory pump

Muscle pump

Mechanical pump for bedridden patients

Fig. 09.21

Low EDV

High EDV

Length-tension “curve” for Cardiac muscle

Overinflation of ventricles leads to less effective pumping

S 4

Overinflation of ventricles results in reduction in stroke volume

S 5

Treatments?…..diuretics

Contractility

NE from Symp postganglionics & EPI from Adrenal medulla

Note: cardiac myofibers NOT innervated by parasympathetic division

Increase Ejection Fraction

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3 Effects of SympatheticStimulation

1: Increase rate of contraction2: Increase peak tension3: Decrease twitch duration

S 7

Why should the contraction be shorter?

Summary: Control of Stroke Volume

• End diastolic volume (preload)

• Contractility (strength of ventricular contraction due to adrenergic stimulation)

• Pressure in arteries that must be overcome = Afterload

FS LoH

S 8

Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.)

High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart

S 9

Hypertrophic cardiomyopathy

CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat

S 11 Factors that control Cardiac Output by changing heart rate and stroke volume.

+ sympathetic- parasympathetic

VR and EDV (FSLoH)

Contractility (catecholamines)

Afterload (MAP)