Exam 2 - Lecture 1 Flashcards

1
Q

What is lost first during shock, cardiac output or arterial pressure?

A

Cardiac output

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2
Q

what needs to be high to deliver blood around the body where it is needed?

A

pressure, no shit..

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3
Q

Instantaneous reflex when someone stands up? What structures communicate to the reflex?

A

SNS reflexes, receiving information from carotid sinus and aortic baroreceptors

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4
Q

Where are carotid sinus located? What nerve are they branched off of?

A

bifurcation of carotid artery; glossopharyngeal nerve

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5
Q

Where are aortic baroreceptors located? what nerve are they branched off of?

A

Aortic arch; Vagus

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6
Q

Which pressor is the main pressor of the CV?

A

norepinephrine, maintains SVR, contractility

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7
Q

How does norepi/epi get into blood stream?

A

Nerves or adrenal gland

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8
Q

Protected vascular beds per lecture

A

Coronary circulation, brain, somewhat kidneys..

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9
Q

Instantaneous reflex when someone stands up? What structures communicate to this reflex?

A

RAAS (renin-angiotensin-aldosterone-system)

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9
Q

Vasopressin is part of what reflex and how much does it get involved?

A

CV reflex system…?

Not much, changes osmolarity, and if there is an emergency, the nervous system will dump this to increase SVR and support norepi/epi

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10
Q

If a patient is taking ________, norepi/epi will be affected negatively

A

beta-blocker

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11
Q

In the low pressure parts of the large veins/heart (atria), there are what kind of receptors?

A

Low pressure stretch sensors

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12
Q

If there is increased stretch in the atria, it will

A

cause an increase in output by the kidneys

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13
Q

How does atrial stretch increase output by kidneys? (The actual action on the kidneys, not communication)

A

by decreasing SYMPATHETIC TONE

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14
Q

The more blood volume you have, the lower _____. Why is this bad?

A

blood circulation rate

e.g. if you have 5L/min of blood, and total blood volume of 5L, it all gets cycled per minute.

but if you have 5L/min of blood, with total blood volume of 8L, it sits longer than it should/lower velocity. more likely to clot.

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15
Q

How are the low pressure strech sensors connected to kidney?

A

DIRECT neural connection, and also hormones

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16
Q

ANF/ANP

A

Atria-natriuretic peptides

protiens formed pre-dominantly in right atria (but does happen in both), and ANP is released when atria is stretched, increasing urine output

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17
Q

What does the natriuretic part mean?

A

Get rid of sodium (natriu?)

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18
Q

BNP

A

Brain-natriuretic peptide

formed in VENTRICLES, and when they get stretched, more BNP, and does same thing at kidney.

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19
Q

BNP levels are used to measure the

A

progression of heart failure.

If levels are going down, then pt is responding appropriately to treatment.

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20
Q

ANP and BNP effects last how long?

A

about a week to be a natriuretic

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21
Q

Why is it called BNP instead of VNP?

A

discovered in the brain first, until they realized it was formed in ventricles.

22
Q

Diuretics are increasing or decreasing the effects of BNP/ANP?

A

INCREASING. BNP/ANP are trying to rid the body of excess fluid.

23
Q

Blood totals

A

5L total, 3L plasma and 2L Hct

24
Q

Total ECF

A

14L total

1/4 - 1/5 makes up plasma
Rest in interstitium (3/4 - 4/5)

25
Q

Whats a normal % of HCT?

26
Q

Normal PIEcap and what proteins are they made up of?

A

28mmHg

Albumin, fibrinogen, immunoglobulin (antibodies/coag factors)

27
Q

If we lost 1L of blood, how much is plasma and how much is HCT?

A

600mL/400mL

28
Q

What should happen with the fluid after we lose 1L of blood?

A

will redistribute itself between compartments

ICF will shift into ECF (CV system) to make up for it, the ratios will try to stay relatively constant.

29
Q

If we lose 1L of blood, what does that specifically do to the proteins?

A

We lose proteins, lowering the oncotic pressure, which causes fluid to leak out of the CV system.

Even though ICF will redistribute to the CV system, the less colloid pressure will cause it to leak back out.

30
Q

What happens if you give NS during hemorrhage? How much stays in CV system?

A

Normal saline doesnt have colloids in it, so if you give that, only 1/4 - 1/5 will actually stay in the CV system.

A little bit is helpful, but alot will be harmful. It will mess up the ISF, especially in the lungs, affecting gas exchange.

31
Q

What is better than NS for hemorrhage?

A

Synthetic colloids such as dextran or hetastarch

Large sugar molecules that breakdown over time, but initially they are large enough to increase oncotic pressure and keep fluid in CV system.

32
Q

When you give a bolus, regardless of fluid, but especially NS/LR, what happens?

A

Increase in pressure initially, but then will drop back down.

20-25% stays in CV, rest goes into interstitium.

33
Q

Other than leaking into interstitium, what causes the drop in pressure after initial rise of pressure with a bolus?

A

Stretch-relaxation

Large veins become distended/tight, and the reaction is relaxation from the SMOOTH MUSCLE, reducing venous pressure.

34
Q

If we have a hemorrhage, what reflex is REVERSED?

A

Reverse stretch-relaxation

Autonomic nervous system overrides veins, causing them to constrict and tighten up the walls of the veins.

35
Q

what are the benefits for stretch-relaxation?

A

Papa-Docta Schmidt is not sure… theres probably stuff out there, but none that he can relate.

36
Q

CNS Ischemic response

A

happens when someone has had low brain stem perfusion for a few minutes, for example during an MI..

The brain will enact every single response it can from the SNS
SNS reflex, epi/norepi, vaso, SVR, contractility, HR, RAAS, ANP/ANF REDUCTION

37
Q

Tissue that doesnt get adequate perfusion during shock, what will happen?

A

Cell necrosis, and everything inside cells is released into environment

e.g. Potassium leaks out, causing hyperkalemia

38
Q

Which is usually the first organ to fail during shock?

A

Liver

super sensitive to under-perfusion.

39
Q

Cardiac output measured using blood gas samples equation (FICK EQUATION)

A

CO L/min = O2 absorbed per minute by lungs (mL/min) divided by Arteriovenous O2 difference (mL/L of blood)

e.g. 250mL/min divided by (200mL/O2/L left heart - 150mL/O2/L Right heart) 50mL/min

= 5L/min (mL cross eachother out, leaving just L/min)

40
Q

Arterial mL of O2 per dL of blood?

A

20mL/O2/dL (oxygen content numbers, and it includes both dissolved + bound oxygen)

41
Q

Venous mL of O2 per dL of blood?

A

15mL/O2/dL (oxygen content numbers, and it includes both dissolved + bound oxygen)

42
Q

Normal oxygen consumption for average healthy adult

A

250mL/O2/min

43
Q

Another equation to calculate CO:

If arterial is 20mL/O2/dL and venous is 15mL/O2/dL, whats cardiac output?

A

well we know we use 250mL/O2/min.. and we get 5mL/O2 per deciliter of blood (100mL) USED UP

(250mL/O2/min (what we need) divided by 5mL/O2) X 100mL (how much blood is needed for 5mL/O2 to be delivered) = 5000mL/min

44
Q

Digoxin is what?

A

Na/K pump inhibitor

45
Q

Cardiac reserve

A

maximum amount of CO you can get above baseline, measured in %

e.g. If normal is 5L/min, and we got 25L/min, then we have a 400% reserve.
10L is 100%, 15L is 200%, and so forth…

46
Q

Athlete cardiac reserve (%)

A

600%, 40L/min

47
Q

What happens to cardiac reserve as we age?

48
Q

what are things that reduce cardiac reserve?

A

Coronary artery disease, coronary thrombosis, valvular disease

49
Q

What is worse for cardiac reserve: moderate coronary disease or mild valvular disease?

50
Q

What conditions don’t have any cardiac reserve at all?

A

Severe valvular disease and severe coronary thrombosis

51
Q

Most common heart valve problem is

A

aortic stenosis

52
Q

What % of population has a congenital aortic valve?

A

1-2%, only has 2 cusps instead of 3

53
Q

Who had a congenital aortic valve that was famous and what did it develop into?

A

Bono, singer for U2, developed into aortic aneurysm