Lab 4 - Heart function Flashcards

1
Q

How is the regulation of heart function demonstrated?

A

Trough the effect of epinephrine, propanolol, acetylcholine, atropine, verapamil and strophantine. Experiments carried out in situ heart preparation using a multimedia program.

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2
Q

In which ways are the pulse determined?

A

Palpating, el.recording (ECG, cardiac axis, base of vectorcardiography)

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3
Q

Which program examines the in situ heart function?

A

SimHeart multimedia program.

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4
Q

How are the changes in the intraventricular pressure for meauring the heart functions done?

A

Ox. isotonic sol. is perfused in the heart. Blood gets in via vv. cordis minimae, therefore both ventricles are filled w. fluid. A balloon catheter is inserted into the LV through LA and pulmonary veins to measure the changes.

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5
Q

Drug and effect on heart functions

  1. acetylcholine
  2. atropine
  3. epinephrine
  4. propranolol
  5. verapamil
  6. strophantine
A
  1. parasympathetic transmitter
  2. competitive antagonist of acetylcholine
  3. sympathetic hormone
  4. β receptor blocker
  5. calcium channel blocker
  6. Na+/K+ ATPase blocker
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6
Q

What can the change in the drug concentration (Q) in the nutrient solution (at a constant flow velocity of 10 ml/min) be calculated based on?

A

 Flow rate of drug administering (I, [μl/min]),

 Concentration of the drug solution used (C, [mol/litre]).

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7
Q

What is epinephrine and how does it effect the heart function?

A
  • Natural sympathetic hormone
  • From the adrenal medulla.
  • Pos. chronotropic effect: Incr. the heart rate
  • Pos. inotropic effect: both the velocity of contraction (vmax) and the maximal isometric tension (Sm) are incr.
  • Pos. bathmotropic effect: Lowers the threshold potential of the pacemaker cells
  • Pos. dromotropic effect: facilitates stimulus conduction
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8
Q

What is propranolol and how does it effect the heart function?

A
  • A sympathicolyticum

- inhibits type β1 and β2 adrenoceptors.

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9
Q

What is acetylcholine and how does it effect the heart function?

A
  • Natural parasympathetic neurotransmitter
  • From the synapses of the n. vagus.
  • Neg. chrono, bathmo, dromo and inotropic effect on the heart through type 2 muscarinic receptors.
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10
Q

What is atropine and how does it effect the heart function?

A
  • The competitive antagonist of acetylcholine.

- Binds to the muscarinic acetylcholine receptors without stimulating them.

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11
Q

What is verapamil and how does it effect the heart function?

A
  • Ca2+ channel blocker drug (prim. L type)
  • Leads to arrhytmias: delays the elicitation of spontaneous diastolic depolarization mainly in the AV node
  • Decr. power of the heart: blocks the power of the muscle fibres
  • Facilitates the nutrient supply of the heart: dilates the coronaries
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12
Q

What is strophantine and how does it effect the heart function?

A
  • Cardiac glycoside
  • Specific inhibitor of the cardiac Na+/K+-ATPase.
  • Pos. inotropic effect - incr. the heart power: Incr. the IC Na+ conc. and decr. the IC K+ conc. in the heart. Incr. of Na+ incr. the IC Ca2+ conc. as well.
  • Stimulates the sarcoplasmatic Ca2+-ATPase which is responsible for muscle relaxation.
  • Neg. dromotropic affect: delays stimulus conduction in AV node
  • Neg. chronotropic effect: frequency of V contractions will decr.
  • Accordingly, strophantine impede the spreading of atrial arrhythmias and protect the ventricles if atrial stimuli become too frequent.
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13
Q

How does strophantine effects the denervated Langendorff’s heart?

A

It decr. the atrial refractory period so the frequency of atrial contractions will incr.

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14
Q

What can overdosing strophantine lead to?

A

AV block, cardiac arrhythmias and heart failure.

  • By decr. the ventricular refractory period and delaying intracardial stimulus conduction, strophantine enhances the secondary (latent) stimulus generation, which can lead to extrasystoles and consequently cardiac arrhythmia.
  • Decr. IC K+ conc. causes the resting potential of heart muscle cells to incr., which enhances spontaneous diastolic depolarization that in turn can result in extrasystoles.
  • Oversaturation of IC ca-stores and the fluctuation of free plasmatic ca-level enhance late post-depolarization, which may lead to extarsystoles as well.
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15
Q

How do we measure the pulse?

A

The volume of blood expelled by the heart into the aorta during systole dilates the aortic wall. During diastole the aorta contracts again and the blood proceeds in it further. This pressure fluctuation spreads in the arterial system in the form of a wave. In the periphery the pulse pressure is modified because of the appearance of reflection waves.

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16
Q

Which types of pulse do we have?

A
  • Pulse frequency: fast (pulsus frequenc) and slow (pulsus rarus)
  • Rhytmicity: uniform cycles of pulse pressure waves (pulsus regularis) and irregular - arrhythmic (pulsus irregularis)
  • Hardness: from power needed for compressing it, hard (pulsus darus) or soft (pulsus mollis)
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17
Q

Which features is used for evaluating the pulse?

A
  • Amplitude of the pulse waves: big / small (pulsus altus / pulsus parvus)
  • Equality – whether the amplitude of each pulse wave is the same: equal (pulsus equalis) / unequal (pulsus inequalis)
  • Length (duration) of the pulse waves: long / short Note that it is not equal to the pulse rate.
  • Slope of the pulse (alpha): fast ascending (pulsus celer) or slowly ascending (pulsus tardus)
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18
Q

Electrocardiography (ECG)

  1. Used for?
  2. Informs us about?
A
  1. To record electrical potential differences generated by the heart and conducted to the body surface.
  2. Position of the heart, the heart rate, the pacemaker rhythm and its origin, and the propagation of depolarization and repolarization.
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19
Q

ECG: Standard (bipolar) leads

A
  1. Lead I: potential diff. betw. the right and left arms
  2. Lead II: potential diff. betw. the right arm and left leg
  3. Lead III: potential diff. betw. the left arm and left leg
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20
Q

How is the ECG recorded?

A

Between an indifferent reference points and a different electrode.

  • Indifferent r.p.: formed by applying unipolar limb leads and connecting the electrodes on two limbs together through a strong resistor.
  • Different electrode: placed on another limb.
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21
Q

Name of the reference leads for the ECG?

A

Named after the place of the different electrode (right arm [VR], left arm [VL] and left leg [VF] leads).

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22
Q

Augmented (Goldberger’s) unipolar leads

A

The signals obtained by setting up special connections among the different points.

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23
Q

Parts of ECG trace

A
  • “Isoelectric line”: the physiological baseline (0 mV) of the ECG trace
  • Waves: deflections on the ECG trace. Waves above the isoelectric line are “positive” while those below it are “negative”.
  • Segment: A part of the ECG trace which falls between waves
  • Intervals/complexes: Larger parts which may contain one or more waves
24
Q

P wave

A

Positive wave indicating atrial depolarization. A bific P wave may occur in case of asynchronous activation of the atria.

25
Q

PQ segment

A

Propagation of the AP through the atrioventricular (AV) node (atrioventricular conduction). Isoelectric line.

26
Q

Q wave

A

Qssociated with the ventricular electrical actions. The first part, a small downward deflection that indicates the transmission of excitation from the His bundle to the ventricular muscle.

27
Q

R wave

A

The largest deflection, that indicates the depolarization of the major mass of the ventricles. Using standard leads it is a positive deflection, and its amplitude ranges to 1.5 mV.

28
Q

S wave

A

Small, negative wave occuring after the R wave. Originates from the depolarization in the RV spreading from the endocardium towards the epicardium.

29
Q

QRS complex

A

The result of the process of ventricular depolarization, a special pattern in the CG trace.

30
Q

ST segment

A

An isoelectric line, because the whole ventricle is depolarized.

31
Q

T wave

A

The pattern of ventricular repolarization.

  • Varies between species. In humans and carnivores usually an upward deflection.
  • Background: that repolarization begins where cells were depolarized last.
32
Q

Integral vector

A

Result of adding up the potential differences measured at the same moment on the different leads.

33
Q

Vectorcardiogram

A

The total sum of the integral vector loops, formed by changes in size and direction of integral vectors.

34
Q

Cardiac axis

A

The definite direction. During normal heart function, on the summit of the R wave, the integral vector always points towards a definite direction. In practice cardiac axis refer to the size of the heart. Depends on the position and on the weight of the heart

35
Q

What is the normal direction of the cardiax axis?

A

From -30o to +110o.

36
Q

Cardiac axis deviation

A
  • Toward the left if it is less than - 30o.
  • Toward the right if it is more than 110o.
  • Mainly caused by a change in the spreading of the depolarization (cardiac dilatation, branch block etc.).
37
Q

The function of peripheral circulation

A

To ensure the material exchange between the intra- and extracellular space.

38
Q

Material transport

A

Mainly realized via diffusion. In the microcirculatory bed filtration and resorption also play a role.

39
Q

Flow types in the large vessels?

A
  • A quicker axial flow: RBCs

- A slower mural flow (plasmatic zone): WBCs

40
Q

The rate of diffusional exchange depends on?

A

The concentration gradient and transit time of the substance being exchanged, together with the permeability and diffusion surface area of the capillary wall.

41
Q

What is important for the formation and volume of ISF?

A

Filtration and resorption

42
Q

How is the volume of ISF determined?

A

By the ratio of filtration and resorption that depends on the blood pressure, on the hydrostatic pressure, on the oncotic pressure, and on the tissue turgor.

43
Q

What affects the formation of ISF?

A

Other factors such as the permeability of capillaries

44
Q

The effective filtration pressure (Peff)

A

The difference between the effective hydrostatic (Pheff) and effective oncotic (Poeff) pressures: Peff = Pheff - Poeff

45
Q

Types of blood pressure

A
  • Systolic: max. pressure
  • Diastolic: min. pressure
  • Mean arterial: average pressure
  • Pulse: diff. of systolic and diastolic pressure
46
Q

How can the mean arterial pressure me calculated?

A

Paverage=(Psystolic+2×Pdyastolic) / 3

47
Q

What is blood pressure a function of?

A

Cardiac output, the peripheral resistance, the total circulating blood volume in the arterial system, and the compliance of the vessels

48
Q

Indirect blood measuring

A

An artery (usually the brachial) is first compressed then released slowly. The values are determined by different sounds that originates from the turbulent blood flow and clapping of the walls of the artery.

  • Systole: appeareance of the tapping sound
  • Diastole: disappearance of the tapping sound
49
Q

Auscultatory method for blood pressure measuring

A

Use Riva-Rocci sphygmomanometer, consisting of an inflatable cuff, an inflating balloon with a bulb for pumping it up, and a mercury manometer.

50
Q

Heart rate (in resting state)

  1. horse
  2. cattle
  3. small ruminants
  4. swine
  5. dog large size
  6. dog new-born
  7. cat adult
  8. cat new-born
  9. rabbit
  10. poultry
A
  1. horse: 30-40/min
  2. cattle: 60-80/min
  3. Small Ru: 60-80/min
  4. swine: 60-80/min
  5. dog large size: 70-100/min
  6. dog new-born: 150-200/min
  7. cat adult: 120-160/min
  8. cat new-born: 200-250/min
  9. rabbit: 150-200/min
  10. poultry: 140-400/min
51
Q

List the main steps of determining the cardiac axis

A

Measure R-wave in each lead, construct vectors, direction of integral vector in c.a.

52
Q

Why does atropine inhibit the Accholine effect on the muscarine AcH-receptors?

A

It binds to receptors without stimulating it

53
Q

List the reg. waves in the ECG of dogs

A

P, Q, R, S and T

54
Q

Positive waves of ECG in humans?

A

P, R and T

55
Q

Neg. waves of the cardiac cycle?

A

Q, S and T (except in humans and car.)