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Advanced A&P II > Exam I - Cardiac II > Flashcards

Exam I - Cardiac II Flashcards

1
Q

What factor changes the slope on a venous return curve?

A

Resistance to Venous Return (RVR)

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2
Q

What is the body’s primary mechanism to increase cardiac output?

A

Constriction of the veins
Just a small increase in venous constriction increases Psf and dramatically increases venous return

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3
Q

What drug increases venous return?
How does it work?

A
  • Phenylephrine
  • Constricts veins more than arteries increasing Psf and therefore venous return
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4
Q

Why is maximal sympathetic stimulation alone not enough to raise CO significantly?

A

Because when the heart is working very hard, RAP decreases which causes veins to collapse and max out CO around 6 L/min
Without an increase in venous return, sympathetic stimulation is not very effective

Green dot represents max SNS with no change in venous return

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5
Q

What pressure changes in the right heart would you expect in patients with cardiac dysfunction?

A
  • ↑ RAP, ↑ CVP, ↑ Psf
  • This occurs because the body compensates for the low CO by greatly increasing volume/pressure in order to maintain a normal CO.

Psf increased to +20 and RAP increased to +13 to keep normal CO

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6
Q

Describe the compensation differences between acute and chronic cardiac dysfunction?

A
  • Acute: catecholamines increase to quickly bring up venous return and CO
  • Chronic: catecholamines cause fluid retention by the kidneys which expands circulating volume to increase CO, allowing catecholamine levels to be reduced

Squeeze replaced by volume

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7
Q

What do we need to be cautious of in patients with heart failure who undergo GETA?

A

GETA relaxes the veins and drops Psf
Because HF patients are reliant on high filling pressures to maintain their CO, undergoing anesthesia can drop their CO dramatically

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8
Q

What drug increases tissue metabolism?

A

Dinitrophenol

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9
Q

What determines our cardiac output?

A

Metabolic demand of tissues
↑ Metabolic demand = ↑ CO
↓ Metabolic demand = ↓ CO

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10
Q

What happens to the arteries and veins under increased and decreased metabolic demands?

A

↑ Metabolic demands = Arteries dilate, veins constrict
↓ Metabolic demands = Arteries constrict, veins dilate

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11
Q

What is the relationship between CO and peripheral vascular resistance (SVR)?

A

The higher the SVR, the lower the CO (inversely related)
Increased SVR (constriction of arterioles) decreases blood flow to tissues - requiring a lower CO
Decreased SVR (dilation of arterioles) increases blood flow to tissues - requiring an increased CO

Can also be thought of as dilation of arterioles decreases arterial pressure so CO increases to maintain normal MAP

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12
Q

What conditions decrease metabolism and therefore cardiac output?

A
  • Hypothyroidsim
  • Loss of limbs
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13
Q

What conditions cause hypermetabolic states?

A
  • Berberi; vitamin B1 (thiamine) defiecency causing cells to be less energy efficent
  • Hyperthyroidsim
  • AV shunt - adds an additional pathway for blood to take which reduces PVR and increases CO
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14
Q

What would occur if metabolic rate increased dramatically, but the nervous system was not functioning?

A

Arterioles would dilate, but the veins would be unable to constrict causing minimal increases in CO and a large drop in arterial pressure

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15
Q

How is cardiac index calculated?

A

CO (L/min)/ surface area (m2)

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16
Q

What is a normal surface area for a 70kg patient?
Cardiac index?

A

1.7 m2
5 L/min ÷ 1.7 m2 = 2.94 L/min/m2

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17
Q

How does gender effect CI?

A

Males have a higher CI except for women who are late in pregnancy

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18
Q

At what age does our CI reach its peak?
How does CI trend with age?

A
  • 10 years old
  • Increases rapidly until age 10 and then steadily declines due to decreased metabolic demands
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19
Q

Why are left heart filling pressures greater than right heart filling pressures?

A

Right heart: has lower filling pressures because the pulmonary circuit is low resistance which requires lower pressures
Left heart: has higher filling pressures because it has to pump against a higher resistance and has an increased workload

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20
Q

How does CVP change based upon where it is measured?

A

If measured directly outside of the RA then it should closely match RAP.
The further from the RA that CVP is measured, the higher it is.
Pressure has to be higher the further you move from the RA in order for there to be a gradient for blood to move from the veins into the heart.

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21
Q

What would happen to CVP measurements in a supine patient?

A

CVP would be slightly increased because in the supine position the veins are located below the heart which causes them to have a small increase in pressure from gravity.

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22
Q

What is a normal intrapleural pressure?

A
  • 4 mmHg or -5 cm H2O
23
Q

What happens to our cardiac output during inspiration?

A

Initially CO drops from decreased preload. Then, CO increases and RAP decreases due to blood being sucked into the atria from the more negative intrathoracic pressure

Green dot is inspiration

24
Q

What happens to our cardiac output during sustained exhalation?
What might cause this?
Treatments?

A
  • CO decreases and RAP increases due to the increased pressures surrounding the heart
  • Positive pressure ventilation and open chest cavity
  • Increase volume or increase venous squeeze

Green dot

25
Q

What is occuring in the red line?
What would cause it?

A
  • The slope of the line has increased = Decreased SVR
  • Decreased SVR in the arterial system creates an increased flow of blood into the venous system (↑ venous volume and pressure). Because the venous system has more flow: RVR is decreased and venous return increases leading to increased RAP and CO.
    As seen in the graph overall pressures (Psf) remain unchanged because of the venous systems high compliance.
  • Can be caused by arterial vasodilators (ACEi/Hydralazine)
26
Q

How does nitroglycerin work to preserve heart function?

A

Nitro is a venous vasodilator that decreases preload (↓Psf)
This decrease in venous return reduces CO to lower cardiac workload

27
Q

What is occuring on the red line?
What would cause this?
What does this tell you about importance of systemic filling pressure?

A
  1. The slope of the line is higher = decreased SVR
    Caused by arterial vasodilation
  2. The Psf has decreased
    Caused by venous vasodilation

Normally a decreased SVR would increase CO via increase venous flow, but the graph shows a decreased CO. This implies that the effects of decreased Psf outweight a decreased SVR and is more important to CO.

28
Q

What drugs are mixed vasodilators?

A

Nitric oxide donors like nitroprusside

29
Q

What causes the changes seen in both red lines?

A

The slopes are the same so SVR is unchanged
The Psf has changed on both lines which is caused by an increase in volume/decrease in compliance (top line) or decreased volume/increased compliance (bottom line).

Decreased compliance = stiffer veins
Increased compliance = dilated veins

30
Q

Explain what is happening in the red lines?

A

The slope of the line has changed but the Psf is the same.
This means that the RVR/SVR has increased (bottom line) and decreased (top line).

This is what happens with arterial dilation and constriction

31
Q

What is occuring in the red line?

A

The slope of the line has decreased and the filling pressure has increased
This means an increased SVR (arterial vasoconstriction) and increased Psf (venous vasoconstriction)

32
Q

What is occuring in the indicated red line?

A

The slope has decreased indicating a higher SVR
The Psf has also increased indicating an increase in venous volume (chronic) or increase in venous constriction (acute) - both of which decrease venous compliance

33
Q

What causes an increase or decrease in venous compliance?

A

↑venous tone = ↓compliance (more stiff)
↓venous tone = ↑compliance (more relaxed)

34
Q

Explain what is occuring at point B?

A

Immediately following an MI, the CO drops which causes blood to back up into the atria, causing an increase in RAP
At this point there has been no compensatory mechanisms

35
Q

Explain what is occuring at point C?

A

The body is compensating now by increase SNS output which causes an ↑ venous tone (increases Psf) and ↑ cardiac activity

36
Q

Explain what is happening at point E?

A

The catecholamines released initially cause an increase in fluid retention, which decreases the need for the catecholamines (volume is replacing squeeze).
Also, now that there is adequate fluid returning to the heart aside from full SNS activity, the heart can return to normal sympathetic activity.

37
Q

What can happen if catecholamine levels remain high?

A

They can lead to a arrythmias from over-sensitivity of Ca+ channels

38
Q

What determines survivability of heart failure?

A

If CO is adequate enough to deliver oxygen to tissues

39
Q

Define preload?
Where is this found on a pressure volume loop?

A
  • The pressure available to fill the heart with blood
  • Pressure in the atria at the end of phase I (EDV)
40
Q

Define afterload?
What is normal?
What are effects on the heart of a high afterload?

A
  • The pressure directly outside of the aortic valve (blood pressure)
  • Normal is 80 mmHg or diastolic BP
  • ↑ afterload makes it take longer to open the aortic valve - makes it harder on the heart
41
Q

Define contractility?

A

The difference in stroke volume if preload and afterload remain constant

42
Q

What is happening in this pressure volume loop? (The red shape is the change)

A
  1. Preload has increased, shown by the increased pressure at the end of phase I (more pressure = more filling)
  2. Increased preload = Increased EDV
  3. An increased volume in the ventricle means more can be ejected = increasd SV

Contractility (black line) and after load (lower dashed line) remain unchanged

43
Q

Explain what is happening in this pressure volume loop?

A
  1. Pressure at the end of phase I is lower → decreased preload
  2. Decreased preload = Decreased EDV = Decreased SV = Decreased BP/CO
44
Q

Explain what is happening in this pressure volume loop?
Compensations?

A
  1. Increased afterload, top dashed line
  2. This causes a longer contraction to open the aortic valve = increased time in phase II
  3. More time in phase II takes away time for ejection in phase III = reduction in SV
    ~Can also be thought of as an increased P in the aorta causes the aortic valve to close prematurely
  4. The heart is filling normally but ejecting less = increased ESV
  5. Typically HR will increase in pt with high blood pressure to compensate for the low SV
45
Q

Explain what is happening in this pressure volume loop?
Compensations?

A
  • Decreased afterload - the aortic valve is opening sooner and clsoing later due to the decreased systemic pressure
  • This allows for more time spend in phase III which increases ejection time and therefore SV
  • The increased SV and ejection time reduces the ESV
  • If the SV is higher per beat, the HR can come down
46
Q

Explain what is happening in this pressure volume loop?

A
  • Increased contractility - shown by the red line with a steeper slope
  • This increases SV due to increased squeeze
  • Increasd SV causes a lower ESV

This causes an increased CO and increased BP

47
Q

Explain what is happening in this pressure volume loop?

A
  • Decreased contractility - shown by the red line that is less steep
  • ↓ contractility = ↓ stroke volume
  • ↓ stroke volume = ↑ ESV

This causes a decreased CO and BP

48
Q

Explain the mechanisms behind this pressure volume loop?

A
  • Aortic valve stenosis - the leaflets are not opening fully causing a higher resistance (↑afterload essentially)
  • ↑ time in phase II to overcome the increased aortic resistance = decreased time in phase III
  • ↓ time in phase III reduces stroke volume and increased ESV
  • Preload has increased d/t decreased CO in order to compensate
49
Q

Why would someone have a decreased blood and pulse pressure with aortic valve stenosis?

A

Because pressures are lower downstream from a high resistance (stenotic aortic valve)
Lower SBP creates a narrowed pulse pressure

50
Q

What are the mechanisms involved in this pressure volume loop?
Compensations?

A
  • Mitral stenosis - valve does not open fully preventing adequate filling = ↓ EDV
  • ↓ EDV = ↓ SV
  • Compensation for low SV is to increase HR and Psf/Atrial pressure → overtime can cause pulmonary edema
51
Q

Explain the mechanisms in the pressure volume loop?

A
  • Aortic valve insufficency - retrograde flow of blood from the aorta into the ventricle
  • The ventricle is filling from the aorta and the atria causing a ↑ EDV
  • Overtime this can cause ventricular dilatation and worsening valve regurgitation.
  • Phase III starts earlier becuase aortic pressure is low from leakage (lower diastolic pressure)
  • Systolic BP is high due to the ejection of a larger amount of blood
52
Q

When does aortic regurg happen?
When is it happening the most?

A
  • Occurs during phases 4 and 1 - slows as ventricle fills
  • Blood flows from the aorta to the ventricle most when aortic pressures are highest and ventricular pressures are lowest (end of phase IV/start of phase I)
53
Q

Explain the mechanisms involved in this pressure volume loop?

A
  • Mitral regurgitation
  • During ventricular contraction, blood moves backwards into the atria (phase II and phase IV)
  • EDV is increased because new blood entering the LA + blood that spilled into the atria during systole cause an increased ventricular volume
  • ESV is also reduced because even though the ventricle is relaxing, pressure in the ventricle > pressure in the atria causing loss of blood from the ventricle to the atria.
  • Remember, even though SV is increased, it is not all “forward” blood

Advanced A&P II (4 decks)

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