Cardiac Output Flashcards

1
Q

What is bradycardia and what would its ECG look like?

A

Impulses originate at SAN at slower rate

A sinus rhythm of less than 60/min

May be a consequence of increased vagal or parasympathetic tone

ECG: All complexes normal, evenly spaced out BUT rate of <60/min

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2
Q

What is Sinus Tachycardia and what would its ECG look like?

A

Impulses orginate at SAN at a rapid rate.

All complexes normal, evenly spaced. Rate >100/min

Higher than 100/min is classed as sinus tachycardia

It occurs most often as a physiological response to:

Physical exercise or physical stress

May also result from congestive heart failure

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3
Q

What does first degree heart block cause?

A

AV block, first degree= Atrioventricular conduction lengthened. Increased delay of the AVN node.

Abnormal slow conduction in the AVN can result in incomplete heart block- causes an extended PR interval

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4
Q

What does second degree heart block cause?

(Wenckebach)

A

Sudden dropped QRS-complex (missing QRS complex). Because the conduction is delayed for a very long time the QRS complex is missed out.

Heart block occurs when a fraction of impulses from atria are conducted

If the PQ-interval is longer than normal and the QRS complex sometimes does not follow the P wave, the atrioventricular block is second degree.

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5
Q

What is third degree heart block?

A

When the atria and ventricles are depolarising indepedently.

This can suddenly lead to cardiac death.

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6
Q

What are the two stages in the cardiac cycle?

A

Diastole:Ventricles are relaxed and not contracting

Systole: Ventricles contract and eject blood into the aorta and pulmonary artery

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7
Q

How do you calculate the normal cardiac output using the end diastolic and systolic volumes?

A

CO= HR x (EDV-ESV) ( end-diastolic volume- End-systolic volume)

In normal 70kg - CO ~ 5L/min

CO= 70 x (120-50)

= 70/min x 70mL

~ 5 L/ min

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8
Q

What are the 7 phases in the cardiac cycle?

A

Phase 1: Atrial contraction

Phase 2: Isovolumetric contraction

Phase 3: Rapid ejection

Phase 4: Reduced ejection

Phase 5: Isovolumetric relaxation

Phase 6: Rapid filling

Phase 7:Reduced filling

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9
Q

What rate can your cardiac output increase to whilst excercising

A

Exercise can increase output to 25L/min

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10
Q

If activity in the parasympathetic system increase, how does this effect heart rate?

A

Heart rate decreases.

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11
Q

If activity in the sympathetic system increase, how does this effect heart rate?

A

Heart rate increases.

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12
Q

What are chronotopic agents?

A

Influences the currents which then alter the slope of the pacemaker and thus the Heart rate.

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13
Q

Give 2 examples of chronotropic agents?

A

Noradrenaline: Increases HR

Acetylcholine: Decreases HR

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14
Q

What are inotropic agents?

A

These alters the force or energy of muscular contractions.

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15
Q

Give 2 examples of inotropic agents.

A

Positive inotropic agent (increase contractility) e.g, digoxin.

Negative inotropic agent (decrease contractility e.g, beta-blockers (propranolol)

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16
Q

What is End-diastolic volume?

A

Filled volume of ventricle prior to contraction(~120ml)

17
Q

What is End-systolic volume?

A

Volume of blood remaining in the ventricals after ejection(~50ml)

18
Q

How do you calculate SV using EDV and ESV?

A

SV= EDV-ESV

19
Q

What is preload?

A

Volume of blood entering ventricles.

20
Q

What is afterload?

A

Resistance in the ateries as blood leaves th eleft ventricle

21
Q

What 2 factors influence SV?

A

Increased preload during hypervolemia

Increased afterload during hpertesnion vasoconstriction

22
Q

What is hypervolemia?

A

When there is too much fluid in the blood due to increase sodium content.

23
Q

What is the Frank Starling Mechanism?

A

It describes the relationship between EDV and SV.

The effect is due to the heart msucle firbres responding to stretch by contracting more forcefully.

This is not due to elastic effect but due to an increased expenditure of ATP energy.

24
Q

How woudl you go about increasing SV?

A

Increase EDV.

25
Q

Where would the line shift in a patient when they are excercising?

A

Shift left and upwards

26
Q

Where would the line shift when a patient has heart failure?

A

Right and down

27
Q

What cardiac drugs are used to alter cardiac output and to treat hypertension

A
28
Q

What is the difference between 2nd degree heart block type 1 and 2?

A

Type 1:Has a wenckebach pattern- prolongonged PQ until QRS goes missing

Type 2: No pattern, QRS is missing throughout

29
Q

Describe atrial contraction?

A
  • It initiates the P wave on the ECG
  • Represents the electrical depolarisation of the atria
30
Q

Describe isovolumetric contraction?

A
  • Begins with at the start of the QRS complex
  • Represents ventricle depolarisation
  • This triggers excitation-contraction coupling, myocyte contraction and a rapid increase in intraventricular pressure.
31
Q

Describe Rapid ejection.

A
  • Ejection begins when the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, which causes the aortic and pulmonic valves to open.
32
Q

Describe rapid ejection

A
  • After the QRS and the beginning of ventricular contraction, ventricular repolarization occurs as shown by the T-wave.
33
Q

Decribe Isovolumetric Relaxation.

A
  • When the intraventricular pressures fall sufficiently at the end of phase 4, the aortic and pulmonic valves abruptly close (aortic precedes pulmonic) causing the second heart sound (S2) and the beginning of isovolumetric relaxation.
34
Q

Describe Rapid filling.

A
  • As the ventricles continue to relax at the end of phase 5, the intraventricular pressures will at some point fall below their respective atrial pressures. When this occurs, the AV valves rapidly open and passive ventricular filling begins. Despite the inflow of blood from the atria, intraventricular pressure continues to briefly fall because the ventricles are still undergoing relaxation.
35
Q

Describe reduced filling.

A

As the ventricles continue to fill with blood and expand, they become less compliant and the intraventricular pressures rise. The increase in intraventricular pressure reduces the pressure gradient across the AV valves so that the rate of filling falls late in diastole.