Cardiovascular 3 (Topic 16) Flashcards

1
Q

what is cardiac output (CO)

A

the volume of blood ejected by each ventricles per one minute

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2
Q

how do you calculate CO? (cardiac output)

A

HR (bpm/mins) x SV (ml/beat)

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3
Q

what is the stroke volume?

A

the volume of blood ejected by each ventricles per beat (ml/beat)

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4
Q

in a resting adult male, stroke volume averages about 70ml/beat, and the average HR is about 75 bpm/min. - 1. Calculate the total cardiac output pumped per ventricles
2. what is the Cardiac output ejected from right ventricle? left ventricle?

A

CO= 75 hr (Bpm/min) x 70 SV (ml/beat)
= 5250 mL/min pumped per ventricle

CO= 5.25L from right ventricles
CO = 5.25L from left ventricles

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5
Q

what is the total blood volume usually in the body?

A

5L (4-6L)

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6
Q

the total blood volume in the body is usually 5L or (4-6L) what does this mean?

A

the volume of blood in the body is 5L which means that the entire blood content in the body passes through the entire circulatory system (both systemic and pulmonary)

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7
Q

during exercise, explain what happens to the cardiac output.

A

CO may increase up to 5x or more during exercise

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8
Q

the basic heart rate is set by what portion of the conduction system?

A

the SA node

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9
Q

explain how modifiers, such as extrinsic and intrinsic factors, affect and modify the heart rate

A
  • any changes to the HR will not change the action potential because the SA node is an intrinsic factor - its built in- and its the natural pacemaker of the heart. But the heart rate will change if there is a change in the pacemaker potential
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10
Q

what are the 2 factors that contribute and or /affect Heart rate

A
  1. Autonomic nervous system:
    - SNS
    -PSNS
  2. Hormones
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11
Q

how does the sympathetic nervous system affect the heart rate

A
  • thru the thoracic nerves (cardiac accelerator nerves) extend to the SA and AV node and most of the myocardium
  • Na+ channels that make the pacemaker potential open wider which increases the Na+ permeability at the SA node
  • this results in an increased in the slope of the pacemaker potential which makes threshold reach faster and in turn increases the heart rate
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12
Q

explain how the PSNS affect the heart rate

A
  • thru the Vagus nerve which extends to the SA node, AV node, and the atrial myocardium (there’s less innervation to the ventricular myocardium)
  • keeps resting HR slower than the pace set by SA node
  • leads to an increased in K+ permeability at the SA node which makes the membrane potential more negative during repolarization
  • as a result, threshold is reach more slowly
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13
Q

what hormones increase heart rate

A
  1. epinephrine and norepinephrine
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14
Q

how do epinephrine and norepinephrine increase hHR

A

they both mimic the effect of SNS

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15
Q

explain how Thyroid hormone affects heart rate

A

it has a slow but direct effect on increasing HR which usually occur over days. It also increases the number of epinephrine receptors which in turn increases the sensitivity of cells to epinephrine

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16
Q

what are other factors that contribute to heart rate?

A

Ions
Fever
Age
Fitness

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17
Q

explain how Ions such as, K+, have an affect on heart rate

A

-High K+ in the ISF causes a membrane potential that’s higher than normal
- which causes the Na+ channels for the pacemaker potential to not open
- so repolarization is slow and heart rate decreases may occur = cardiac arrest

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18
Q

how does fever affect heart rate?

A

increased temp = increase HR due to the increased speed of AP firing from the SA node

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19
Q

How does age affect heart rate

A

newborns have a very high heart rate = higher than 120 bpm

20
Q

how does fitness affect heart rate

A

increased fitness leads to a decreased heart rate

21
Q

what is the average stroke volume?

A

70ml/beat

22
Q

what is END DIASTOLIC VOLUME? (EDV)

A

The volume of blood in each ventricle at the end of the ventricular diastole (right before contraction)

23
Q

EDV is also known as?

A

Preload

24
Q

what is the maximum ventricular volume in EDV

A

120 ml

25
Q

what is END SYSTOLIC VOLUME

A

the volume of blood in each ventricles at the end of ventricular systole
- what’s left after blood is removed (what’s left after contraction and ejection)

26
Q

ESV - end-systolic volume is usually how many mL?

A

50

27
Q

how do you calculate STROKE VOLUME?

A

SV= EDV-ESV

28
Q

what are 2 factors that contribute to controlling Stroke volume?

A
  1. intrinsic factors
  2. extrinsic factors
29
Q

how does the INTRINSIC CONTROL of the heart affect STROKE VOLUME

A

the heart has a built-in ability to change stroke volume

30
Q

INTRINSIC CONTROL:
- how does venous return affect SV

A

as venous return increases, the EDV increases

31
Q

INTRINSIC CONTROL:
an increase in EDV causes the heart muscle to?

A

stretch

32
Q

INTRINSIC CONTROL:
explain how an increase in EDV causes the heart muscle to stretch resulting in a stronger force of contraction

A
  • because when cardiac muscle fibres are at rest, they are not in their optimal length but when they stretch they approach their best length which means more cross bridges are attach and this results in a stronger force of contraction
33
Q

what is Frank Starling’s Law of the heart?

A
  • force of ejection is proportional to the length of ventricular contractile fibres - allows the heart to adjust to demands
34
Q

increased in venous returns occurs due to?

A
  1. exercise
  2. lower heart rate
35
Q

how does neural control like the, SNS, control Stroke volume?

A

activation via SNS: results in an increased force of contraction for a given EDV leads to increased SV

36
Q

EXTRINSIC CONTROL:
how does a force of contraction affect contractility of the heart

A
  • increased opening of Ca channels = more Ca2+ in the sarcoplasm= more cross bridges formed = greater force of contraction
37
Q

EXTRINSIC CONTROL:
Besides increasing the force of contraction, how else does the SNS affect SV

A
  • it also increases HR = heart have less time to fill = decreases EDV
38
Q

EXTRINSIC CONTROL:
explain how an increase in force of contraction and a lower ESV work to compensate a reduced EDV

A
  • an increase in force of contraction and a lower ESV (increase in SV) work together to compensate for a reduced EDV that happens cos of a high heart rate
39
Q

EXTRINSIC CONTROL:
by increasing both the force of contraction and the heart rate, how does this affect SV?

A

SV is usually increased due to the reduced ESV cos there’s less blood that stays in the ventricles cos its pumped out more, so this increases STROKE VOLUME

40
Q

what is the effect of PSNS on force of contraction

A
  • does not have an effect
  • few of it’s neuron go to the ventricular myocardium
41
Q

what is the general rule about SNS and PSNS regarding Cardiac output (CO)

A

SNS = increases CO
PSNS =decreases CO

42
Q

explain how hormones, such as epinephrine and norephinephrine affect SV

A

they have the same effect as SNS = increases force of contraction (increased SV)

43
Q

T or F: Thyroid hormone also increases force of contraction and epinpehrine receptors

A

TRUE

44
Q

what other factors INCREASES the force of contraction?

A
  1. Acidosis
  2. increased external potassium
  3. Drugs that block Calcium channels
45
Q

what other factors DECREASE the force of contraction?

A
  1. increasing the external calcium concentration-> more calcium moves into the cell during each action potential -> more cross bridge forms
  2. Digoxin drugs (digitalis) they act to increase the amount of Ca2+ into the sarcoplasm
46
Q

what is venous return?

A

the amount of blood returning to the right ventricle from veins