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Physiology Flashcards

1
Q

What is static compliance?

A

It measures the lung at a fixed volume

Dynamic compliance measures the lung via rhythmic breathing

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2
Q

Anything that increases airway pressure will result in increased:

A

Transpulmonary pressure.

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3
Q

What is transpulmonary pressure?

A

The net distending pressure

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4
Q

Formula for airway compliance:what is the formula for elastance?

A

Change in volume/change in pressure.

Elastance is the reciprocal of compliance

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5
Q

What’s the difference in systolic upstroke at aorta vs radius? Why?

A

Lower upstroke at aorta, steeper upstroke at radial. Because it encounters increased vascular resistance in the arterioles.

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6
Q

Difference in dicrotic notch at aorta via radial?

A

Radial-smoother diacritic notch and later in cardiac cycle.

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7
Q

What about MAP for more distal sites?

A

It will be decreased at further sites . MAP is calculated via algorithm-area beneath the curve divided by beat period and averaged over consecutive heartbeats

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8
Q

Why does SUX dose have to be increased in myasthenia gravis? what about NMDB?

A

Because, in MG there are decreased Functional ach receptors, and Sux is basically two Ach molecules that bind to the receptors. Decreased doses of non-depolrozing

Lambert Eaton-decreased doses of sux, and decreased doses of NDNMB

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9
Q

Blood products cause which derangements?

A

Hypocalcemia, hypomagnesemia, and can cause hyperkalemia if infused too quickly

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10
Q

How does hyperbaric oxygen therapy work?

A

HBOT works by increasing PAO2 and subsequently PaO2, whichbincreases the amount of oxygen dissolved in blood.

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11
Q

What is closing capacity and when does it rise above FRC, and in what position? What increases and decreases closing capacity?

A

Volume in which small airways begin to close. Rises above FRC after age 40. Closing capacity increases with age and body position. Obesity and pregnancy don’t have any effect on closing capacity

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12
Q

What breaks down Remi? What breaks down esmolol? Cisatricurium?

A

Remi: RBC and tissue esterases
Esmolol: RBC esterases
Cisatricurium: Hoffman elimination

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13
Q

When is paeudocholinesterase affected? Where does BCHE break down sux? Heroin and cocaine and BCHE?

A

Liver disease, genetic mutation, or inhibited (ecthiophate, neostigmine). BCHe breaks down sux in the blood NOT at the NMJ. Those drugs are broken down by BCHE

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14
Q

Why is decreased cardiac output a thing in anterior pituitary tumors?

A

Because decrease in ACTH AND TSH can lead to decreased plasma volume, cardiac contractility, and heart rate.

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15
Q

Is ARDS shunt or dead space? What does that mean for FiO2 supplementation?

A

SHUNT, which means increasing the FiO2 isn’t very likely to help anything because gas exchange is severely impaired.

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16
Q

What is the goal of treatment in ARDS? What can that be done with?

A

To recruit alveoli for gas exchange. This can be done with PEEP, nitric oxide(Doesn’t reverse HPV), ecmo, and inverse ratio ventilation-favors more time spent in inspiration.

Of note-nitric oxide increases blood flow only to areas that are already ventilated.

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17
Q

Acromegaly and lung volumes: , and do patients with this have soft tissue overgrowth? Most sensitive test for acromegaly? Specific test?

A

They are actually increased causing v/q mismatch. Yes they have soft tissue overgrowth.
Sensitive-IGF1 l.
Specific-lack of GH suppression following an oral glucose load.

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18
Q

T/F: sodium bicarbonate can raise calcium levels. How do pressors do in acidosis?
Sodium bicarbonate mixes with what to make what?
Can bicarbonate cause hypotension?
How can bicarbonate raise ICP?

A

False! They lower them, so do NOT give them to patients who are hyoocalcemic.
Vasopressors do NOT do well at low pH.
It mixes with H+ in blood to make carbonic acid which is converted to CO2 and H20.
Bicarbonate can cause hypotension
Can raise ICP by CO2 going to brain and vasodilating.

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19
Q

Control of ventilation can chemically be separated into:

A

PaO2 and PACO2
PaO2 or hypoxemic control is regulated by carotid body chemoreceptors in with minor contribution from aortic arch. When PaO2 is less than 100, then IX nerve signaling is increased, but increased ventilation is not seen until below 60-65. Volatile anesthetics, opioids and benzos can decrease this hypoxic respiratory drive. This is why we give O2 after surgery. B/l carotid endarterectomy can take away thisndeive as well as COPD, so use opioids cautiously with them.
PaCO2-central receptors-LITTLE Contribution to hypoxic drive. In medulla, sensitive to H+. H+ increases respiratory rate and tidal volume.
Metabolic acidosis won’t do this because H+ can’t cross the BBB. Opioids and benzos and volatile can also impair response to PACO2.
In patients with chronic CO2 retention, CSF pH is normalized by crossing if HCO3- into CSF in arachnoid villi, and therefore more PACO2 is required to stimulate an increase in ventilation.

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20
Q

What is the sinus nerve of Herring?

A

Branch of glossopharyngeal that is in control of carotid baroreceptors (in the carotid sinus) NOT chemoreceptors

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21
Q

ECT and parasympathetics? Followed by what? Can bronchiapasm happen-if so, why?

A

Shortly after ECT there is an increase in PS-which could cause asystole, bradycardia, and increased secretions. PS is quickly followed by an increase in sympathetic- HTN, tachycardia, ST/T wave changes. Bronchospasm can happen due to instrumentation ofnthe airway, not autonomic nerve stuff.

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22
Q

How does the left handle up with coronary perfusion compared to the right?

A

LV is more sensitive than the right due to ischemia and imbalance of oxygen supply/demand to the myocardium m.

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23
Q

Equation for oxygen delivery:

A

DO2= CO x CaO2 (arterial oxygen content)

CaO2=(SaO2)(HB x 1.34) + 0.0031 x PaO2)

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24
Q

Soooo-tell me what each of these diseases are with regard to Depolarizing and non-depolarizing things
MG
LE
MS

A

Myasthenia gravis-sensitive to Non-depolarizing, resistant to depolarizong.
Lambert Eaton-sensitive to both
MS-sensitive to depolarizing

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25
Q

The single most effective method of augmenting CO in a patient with AF is

A

The single most effective method of augmenting CO in a patient with AF is the conversion to sinus rhythm. This may be achieved either through chemical or electrical cardioversion. Heart rate control is the next step if cardioversion is unsuccessful in order to promote increased LV filling during diastole.

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26
Q

What kind of anesthesia can MS patients have?

A

Patients with MS are susceptible to an exacerbation of their symptoms in the perioperative period caused by surgery and the use of general or spinal anesthesia. Succinylcholine should be used cautiously or avoided. Extended postoperative care may be required with emphasis on managing respiratory insufficiency

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27
Q

As far as temp, patients with MS can get too hot or cold

A

Hyperthermia

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28
Q

What is the winter formula and what does it tell you?

A

The expected amount of respiratory compensation for a given drop in pH due to a metabolic acidosis can be calculated using the Winter formula: PCO2 = (1.5 * [HCO3]) + 8 +/- 2.

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29
Q

Potassium in diarrhea:

A

lower (hypokalemia)

30
Q

Side effects of lumbar puncture in pseudotumor cerebri

A

In patients with pseudotumor cerebri, lumbar punctures can reduce ICP and potentially improve associated neurologic symptoms. Risks of the procedure include PDPH, back pain, bleeding, infection, and nerve damage.
No visual disturbances

31
Q

When you give neostigmine to a pregnant mom, what else should you give?

A

Atropine is a tertiary amine, which more easily crosses the placenta than does glycopyrrolate, a quaternary amine. Therefore atropine should be given in conjunction with neostigmine for reversal of pregnant patients to avoid fetal bradycardia.

32
Q

What does the A-a gradient tell you? What is a normal A-a gradient?

A

It tells you about ventilation/perfusion abnormalities. A normal A-a gradient is 5 - 10 mm Hg for a young adult nonsmoker.

33
Q

What does NOT cause an increase in the A-a gradient?

A

Hypoventilation and low FiO2.

KIM that hypoventilation has a lot of reasons-myopathies, myasthenia gravis, opioids, etc.

34
Q

R–>L shunt, examples, and what it does to the A-a gradient.

A

Increased A-a gradient- Atelectasis, pneumonia, VSD or ASD

35
Q

Dead space ventilation; examples and what it does to A-a gradient.

A

Increased Pulmonary embolism, venous air embolism

36
Q

Diffusion effect-examples and what it does to A-a gradient.

A

Increased Cystic fibrosis, interstitial lung disease

37
Q

Regarding cardiac transplantation, the heart rate is dependent on what:

A

Heart rate generation is dependent on the donor atrium

38
Q

How is a denervated heart dependent on preload? Explain. Is the Frank-Starling mechanism still present?

A

In the normal innervated heart, the response to a sudden reduction in intravascular volume is an increase in heart rate and contractility. In a cardiac transplant recipient, the initial response is an increase in stroke volume dependent on an adequate preload and not an acute increase in heart rate or contractility. The increased contractility and heart rate is a secondary effect and is predominantly dependent on circulating catecholamine levels. Therefore, the transplanted heart is critically preload dependent
Yes, Frank is still around

39
Q

Heart rate and variability in the transplanted heart-does it have parasympathetic tone? What is the intrinsic heart rate?

A

The transplanted heart is void of parasympathetic tone and has a higher intrinsic rate (resting heart rate between 90-110 bpm) with less variability.

40
Q

How much CO does the uterus receive at term?

A

20%

41
Q

what type of blood do umbilical arteries carry?

A

The paired umbilical arteries carry deoxygenated blood from the fetus to the placenta. Oxygenated blood returns to the fetus via a single umbilical vein.

42
Q

Blood supply to uterus

A

Uterine arteries supply about 85% of blood flow and ovarian arteries up to 15%. Approximately 70% to 90% of uterine blood flow passes through the intervillous space in the placenta to undergo metabolic exchange with fetal terminal villi.

43
Q

T/F: Uterine arterial bed is autoregulated

A

FALSE

44
Q

What 3 things affect SSEPs?

A

Anemia, PaO2, and hypothermia affect SSEPs.

45
Q

Inhibitors of hypoxic pulmonary vasoconstriction:

A

Direct inhibitors of HPV include, but are not limited to: hypocarbia, infection, vasodilators (e.g., nitroglycerin, nicardipine, sodium nitroprusside, etc.) and metabolic alkalosis. Volatile agents generally preserve HPV up to 1 MAC but inhibit it at higher concentrations

46
Q

T/F: LEMS and MG are both autoimmune

A

TRUE

47
Q

Can stroids be used in LEMS and MG?

Deep tendon reflexes in LEMS and MG?

A

Yes. and they can be helpful. Second line for LEMS Deep tendon reflexes are reduced or absent with LEMS but typically normal in MG

48
Q

Does LV systolic pressure affect myocardial oxygen supply?

A

No, but it does affect myocardial oxygen demand.

49
Q

Myocardial oxygen supply is affected by:

A

Myocardial oxygen supply is affected by AoDP, LVEDP, heart rate, Hgb, and CVR (coronary vascular resistance)

50
Q

What helps prevent evaporative heat loss in neonates? Is it the room temp?

A

Maintenance of a neutral thermal environment does not decrease heat loss through evaporation. Drying off the neonate and/or covering with plastic barriers will help in this loss.

51
Q

How does a neutral thermal environment protect a neonate against hypoglycemia?

A

When neonates are hypothermic, nonshivering thermogenesis is the primary means to generate heat (oxidation of brown fat). This increases glucose consumption and increases the risk of hypoglycemia. Maintenance of a neutral thermal environment will help decrease the risk of hypothermia and thus decrease the risk of hypoglycemia.

52
Q

Why is it that phentolamine can really, really raise BP?

A

Unlike the alpha1 selective blockers, phentolamine also inhibits the alpha2 receptors. This can result in increased norepinephrine release due to blockade of the alpha2 negative feedback loop, which can potentially cause a drastic increase in heart rate.

53
Q

Quick overview of the RAAS system:

A

The renin-angiotensin-aldosterone system is vital in maintaining blood volume and vascular smooth muscle tone. Renin is released from the kidneys when low flow is sensed. Renin converts angiotensinogen to angiotensin I which travels to the lungs and is converted to angiotensin II by angiotensin-converting enzyme. Angiotensin II has many effects including direct activation of alpha-adrenergic receptors on vascular smooth muscle and direct effects on the endothelium. Furthermore, angiotensin II causes release of aldosterone, which alters blood volume.

54
Q

which vasodilating agents act directly on the vascular smooth muscle?

A

The prototypical vasodilating agents which act directly on the vascular smooth muscle are nitroglycerin and nitroprusside.

55
Q

How does sodium nitroprusside work? which type of vascular smooth muscle does it prefer? how quick is the onset of action? what can happen over time? What happens to SVR? How does that affect heart rate?

A

Sodium nitroprusside is a non-selective vasodilator, which causes relaxation of arterial and venous smooth muscle. It works by dissociating into nitric oxide which vasodilates the vascular smooth muscle. Onset of action is almost immediate and using the lowest possible infusion rate for the shortest amount of time can help decrease the risk of cyanide toxicity. Tachyphylaxis may develop over time to nitroprusside and usually heralds potential toxicity.The venous and arterial dilation will cause a decrease in systemic vascular resistance. Tachycardia can develop as a side effect of a decreased cardiac output (as a compensatory mechanism). It is possible that an increase in myocardial ischemia can occur if coronary steal occurs from arteriolar vasodilation.

56
Q

How does NTG work? Veno or arterial dilator? First line therapy in myocardial ischemia-why?

A

Nitroglycerin is a smooth muscle relaxant, which works because it is converted to nitric oxide, which stimulates cGMP production. Nitroglycerin is a venodilator because it preferentially works on the venous system. It is the first line therapy during myocardial ischemia because it also causes dilation of the epicardial coronary arteries.

57
Q

How does hydralazine work? What happens with heart rate?

A

Hydralazine is a potent vasodilator, which is arterioselective. It stimulates cyclic guanosine monophosphate (cGMP) and inhibits the vascular smooth muscle myosin light chain kinases. Onset of action is between 5 and 15 minutes after administration and duration of action is 6 to 12 hours. It causes a widespread dilation that may not be uniform. An increase in heart rate may be seen to compensate for a decreased cardiac output.

58
Q

Phenoxybenzamine MOA:

A

Phenoxybenzamine is usually administered orally and it has a non-selective, non-competitive blockade of alpha-1 and alpha-2 receptors.

59
Q

Labetalol MOA:

A

Labetalol is a competitive antagonist at the alpha-1 and beta receptors (beta effects dominate with a ratio of alpha/beta blockade of 1:4-7). It is administered intravenously with an onset of action within 10 minutes and duration of action of 2 to 6 hours. A decrease in systemic blood pressure and cardiac output occur secondary to negative inotropy and arterial/venous vasodilation.

60
Q

Prazosin MOA:

A

Prazosin is administered orally and it is relatively alpha-1 receptor selective

61
Q

Clonidine MOA:

A

Clonidine is a centrally acting alpha-2 receptor agonist which reduces sympathetic outflow from the central nervous system. It also has centrally acting analgesic properties which make it an excellent choice in perioperative period if vasodilation is required. It also acts on the peripheral alpha-2 receptors to cause a postjunctional decrease in norepinephrine release.

62
Q

How can sodium nitroprusside possibly cause cerebral ischemia even though it increases CBF?

A

Sodium nitroprusside is a cerebral vasodilator that can lead to increases in cerebral blood flow and blood volume. Rapid and profound reductions in mean arterial pressure may exceed the autoregulatory capacity of the brain to maintain adequate cerebral blood flow resulting in cerebral ischemia.

63
Q

If you’re trying to slow the heart rate in a denervated heart, how do you feel about esmolol?

A

Esmolol is a selective beta1 receptor blocker and can be used to slow and terminate supraventricular tachycardia. However, its response may be limited in a denervated heart unless the tachycardia is from norepinephrine or epinephrine that is secreted into the bloodstream from the adrenal medulla. This is not likely to be as efficacious as cardioversion.

64
Q

Carotid sinus stimulation in a denervated heart:

A

Carotid sinus stimulation (A) normally results in vagus nerve firing with resultant slowing of the AV node of the heart. This is typically used to terminate stable supraventricular tachycardia prior to pharmacologic intervention. However, because the heart is denervated the signal from the vagus nerve is never transmitted and thus carotid sinus stimulation is ineffective.

65
Q

What would you expect phenylephrine to do in a DENERVATED HEART?

A

Phenylephrine (C) would increase blood pressure but is unlikely to stop the tachycardia. The arterial baroreceptor reflex, triggered in the carotid sinus, is blunted in patients with transplanted heart

66
Q

Don’t forget-synchronized cardioversion is best for UNstable supraventicular tachycardia

A

Okay

67
Q

Why would lateral wall MI decrease SvO2?

SvO2 is inversely proportionate to:

A

Because it will decrease CO

Inversely proportionate to VO2

68
Q

what does PPV do to ADH secretion?

A

increase it-apparently this is a minor thing.

69
Q

PPV and sympathetics and how it affects renal function

A

Positive pressure ventilation also results in an increase in sympathetic nervous system output which secondarily results in an increase in renin release through beta-1 receptor stimulation with resultant release of angiotensin-2 and aldosterone. This results in vasoconstriction with salt and water retention which can decrease urine output. There is also an increase in the release of ADH (also seen with surgical stress) which increases free water reabsorption and decreases urine output, however this is a minor component. Lastly, there is a decrease in atrial natriuretic peptide which decreases natriuresis and vasodilation.

70
Q

What can large tidal volumes do to lung and renal function?

A

Large tidal volumes have shown to cause both lung and renal injury compared with lung protective ventilation.

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