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CDL301 - Cardiovascular Pharmacology: Personalising Medicine > 3. Cardiac Function > Flashcards

3. Cardiac Function Flashcards

1
Q

Define cardiac output (CO).

What is the equation for CO?

A
  • The amount of blood delivered to the circulation every minute
  • CO (L/min) = Heart Rate (bpm) x Stroke Volume (ml)
  • 4.9L/min = 70bpm x 70ml
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2
Q

Define stroke volume (SV).

What is the residual volume?

A
  • The amount of blood delivered to the circulation with each beat
  • Each time the heart contracts, about 60% of blood in ventricles is ejected at rest
  • Residual volume is the volume of blood remaining in the ventricles
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3
Q

What does having a residual volume allow?

A

Allows the SV to be increased instantly upon exertion

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4
Q

Define the ejection fraction.

How does this differ to SV?

A
  • The % volume of blood ejected with each beat
  • If two people have the same ejection fraction (e.g. 60%) but if one person has a larger heart (increased volume) then their SV will be different
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5
Q

What factors affect heart rate?

A
  • Sympathetic stimulation (increases HR)
  • Parasympathetic stimulation (decreases HR)
  • Circulating catecholamines (increases HR)
  • Drugs
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6
Q

What factors affect strove volume?

A

Intrinsic contractility:

  • Intracellular Ca2+ availability
  • Oxygen, Free Fatty Acid and ATP availability

External factors:

  • Preload (filling pressure)
  • Afterload (resistance to ejection)
  • Sympathetic stimulation (if preload and afterload are constant, sympathetic stimulation will increase SV)
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7
Q

Define preload and afterload.

A
  • Preload is the volume/pressure of blood in the ventricles prior to contraction (increase in blood volume increases preload)
  • Afterload is the pressure in the arteries ebyond the heart which must be overcome to eject blood into the circulation (afterload determined by vasoconstriction/dilation)
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8
Q

Describe the events that lead to a large increase in intracellular Ca2+ during contraction.

A
  1. During plateau phase of AP, Ca2+ enters the cell but levels are insufficient to initiate contraction
  2. Ca2+ binds to Ryanodine receptors on the sarcoplasmic reticulum (Ca2+ store) leading to release of Ca2+ into cytoplasm
  3. Ca2+ binds to more Ryanodine receptors resulting in a large increase in [Ca2+]i
  4. Ca2+ initiates contraction in an ATP-dependent process
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9
Q

Describe the ATP-dependent process that causes contraction of cardiac muscle.

A
  1. At rest, tropomyosin blocks myosin binding site on actin filament
  2. Ca2+ binds to troponin which causes a conformational change, pulling tropomyosin away to reveal myonsin binding site on actin filament
  3. ATP is hydrolysed when myosin head is unattached
  4. Myosin head binds to actin filament with ADP+Pi bound
  5. Release of ADP+Pi causes myosin head to change position and actin filaments slide along
  6. Binding of ATP to myosin head causes it return to resting position
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10
Q

What is the structure of cardiac muscle?

What does this help to ensure?

A
  • Cardiac muscle is highly branched with cells connected side-by-side
  • This ensures that wave of depolarisation is conducted rapidly and so all cells depolarise and contract at same time
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11
Q

Describe the Frank-Starling mechanism.

A
  • Increased preload (filling pressure) during diastole causes increased LV EDP
  • Increased LV EDP causes increased myocardial fibre stretching, which causes increased force of contraction
  • This leads to increased SV and CO
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12
Q

Explain how changes in venous return affect CO.

A
  • Increased venous return (fluid intake or postural change) gives an increased preload and therefore increased LV EDP resulting in increased SV and CO
  • Decreased venous return (blood loss) gives a decreased preload and therefore decreased LV EDP resulting in decreased SV and CO
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13
Q

How does Frank-Starling mechanism control CO at rest?

A

Based on venous return (self-regulating)

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14
Q

Explain how changes in afterload and/or contractility affect CO.

A
  • Increased contractility and/or decreased afterload (vasodilation) shifts curve upwards and to the left - require a lower LV EDP to achieve the same CO
  • Decreased contractility and/or increased afterload (hypertension) shifts curve downwards and to the right - require a higher LV EDP to achieve the same CO
  • Position along the curve is still determined by preload
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15
Q

Explain how sympathetic stimulation affects CO.

A
  • Control - apply stimulation to isolated muscle strip to activate AP that causes Ca2+ influx and contraction
  • Sympathetic stimulation - apply stimulation to isolated muscle strip in presence of Isoprenaline (adrenaline analogue) gives increased Ca2+ influx and contraction
  • Vehicle - as volume of vehicle infused increases, preload increases giving increased LV EDP and SV
  • NA - if infuse same volume of NA, then curve shifts upwards and to the left
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16
Q

Describe the difference between the Frank-Starling mechanism between a non-failing and failing heart.

A
  • Non-failing - a small change in LV EDP gives a large change in CO
  • Failing - require a larger change in LV EDP for a small change in CO
17
Q

How does a failing heart attempt to maintain SV and CO?
Why is this an issue?
What can the patient be given to treat this?

A
  • Operates at higher LV EDP but there is not much difference in SV and CO compared to that at lower LV EDP
  • At higher LV EDP get symptoms (oedema and breathlessness)
  • Give patient diuretic to decrease blood volume and preload therefore decrease LV EDP
18
Q

What happens if CO drops below a certain level?

A

Get symptoms of low CO (fatigue, failure to maintain BP and poor exercise capacity)

19
Q

What happens if LV EDP increases beyond a certain level?

A

Get symptoms of high LV EDP:

  • Right side back pressure goes to venous system causing oedema
  • Left side back pressure goes to lungs causing breathlessness
20
Q

What treatments are given to heart failure patient to reduce LV EDP without decreasing CO?

A
  • Diuretic reduces blood volume and preload therefore decreases LV EDP without much change in SV and CO
  • ACE inhibitor (vasodilator) decreases afterload and shifts curve upwards and to the left
21
Q

Explain how Digoxin affects CO.

A

Apply stimulation to isolated muscle strip in presence of Digoxin gives increased Ca2+ influx and contraction

22
Q

Why is Digoxin’s use in heart failure unusual?

A

Increasing stimulation of the heart causes increased workload and O2 requirements so normally use vasodilators

23
Q

What are the features of Left Ventricular Dysfunction?

A
  • Left ventricular wall is thinner

- Heart is dilated due to operating at higher LV EDP to try to increase CO

CDL301 - Cardiovascular Pharmacology: Personalising Medicine (6 decks)

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