Cardiopulmonary Physiology Flashcards

1
Q

Equation defining blood pressure

A

MAP = CO x SVR

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2
Q

Equation for Pulse Pressure

A

SBP - DBP

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3
Q

The compliance of _ is responsible for the difference of the DBP and SBP (pulse pressure)

A

The aorta is responsible for most of this compliance.

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4
Q

What is the most common cause of an increase pulse pressure? (not as compliant = inc. P)

A

Poor aortic compliance that accompanies aging.

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5
Q

Equation for SVR?

A

80 [(MAP - CVP)/CO]

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6
Q

What is the purpose of the factor 80?

A

converts units into dyne/sec/cm5 from mmHg (MAP) and L/min (CO)

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7
Q

How do causes of hypotension and hypertension differ generally?

A

Hypotension diverse range of causes (rate, rhythm, contractility, preload, afterload).

Hypertension nearly always excessive vasoconstriction.

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8
Q

What is the relationship between resistance and radius?

A

Resistance is inversely proportional to the 4th power of the radius.

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9
Q

T or F: Capillaries contribute most to SVR.

A

F.

Individually, small vessels = inc. resistance.
However, when arranged in PARALLEL = SVR decreased.

Most resistance originates in arterioles.

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10
Q

What is the definition of CO?

vs. equation

A

The amount of blood (L/min) pumped by the heart

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11
Q

What is the equation for CO?

A

CO = HR x SV

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12
Q

List 2 methods by which you can actually measure CO?

A

Pulmonary Artery Catheter

TEE

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13
Q

Definition and equation for Cardiac Index

A

Relates CO to BSA, hence relating heart performance to the size of the individual

CI = CO/BSA

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14
Q

What 4 factors influence HR?

A
  1. Intrinsic rate: natural rate of discharge of cardiac tissue
  2. SNS activity
  3. PNS activity
  4. Pharmacologic
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15
Q

What is the definition and equation of EF?

A

EF = % of ventricular blood volume pumped by the heart in a single contraction.

SV / EDV

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16
Q

T or F: EF is dependent on BSA.

A

F.

EF does not differ on the basis of body size unlike CI.

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17
Q

What range of EF is considered normal?

A

60-70%

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18
Q

Definition of preload

A

Amount of cardiac muscle that is “stretched” before contraction.

EDV of the heart

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19
Q

What is a method of measuring EDV?

A

TEE

Other parameters like LA, PCWP, PAD can also be used to assess preload.

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20
Q

Since the same goes in and out of the heart, can you use CVP on the R side of the heart to guesstimate preload on the L side of the heart?

A

Yes. CP correlates with filling pressures on the L side of the heart in the absence of pulmonary disease and when cardiac function is normal.

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21
Q

Definition of the Frank-Starling mechanism

A

Physiologic description of increased contractility with increased filling.

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22
Q

List 4 categories of causes of low preload.

A
  1. Hypovolemia
  2. Venodilation (GA and neuraxial anesthesia)
  3. Obstruction (Tension PTX, tamponade)
  4. R-sided HTN (PE, pulmonary HTN)
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23
Q

Definition of contractility?

A

Inotropic state of the heart

Measure of the force of contraction independent of loading conditions (preload or afterload)

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24
Q

What is the definition of afterload?

A

Resistance to the ejection of blood from the LV with each contraction.

Largely determined by SVR.

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25
Q

What happens when SVR is increased?

A

Increased cardiac filling pressures –> heart doesn’t empty completely –> dec. SV, EF, and CO

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26
Q

What are some conditions associated with decreased myocardial contractility?

A

MI/ Previous MI
Anesthetic drugs
Cardiomyopathy
Valvular Heart Disease

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27
Q

Describe the relationship between the CV and CNS.

A

The CV system in the brainstem integrates the signal and provides a response through the ANS.

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28
Q

Describe the innervation of the SA and AV nodes.

A

The SNS and PNS efferents innervate the SA and AV nodes.

The SNS ↑HR via stimulation of b-receptors.

The PNS ↓JR via stimulation of muscarinic acetylcholine receptors

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29
Q

What is the location of baroreceptors and what do they respond to?

A

Carotid sinus
Aortic arch
Activated by increased SBP = stimulates stretch receptors to send signals through the vagus and GP nerves to CNS

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30
Q

What cranial nerves transmit baroreceptor signals to the CNS?

A

Vagus

Glossopharyngeal

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31
Q

What affects the sensitivity of the baroreceptors?

A

The sensitivity of the baroreceptors to pressure changes varies

Altered by long-standing essential HTN.

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32
Q

Describe how the carotid sinus reflex acts as an effective treatment for supraventricular tachycardia.

A

Carotid massage –> baroreceptor reflex –> CNX/IX –> CNS –> PNS /vagal stimulation –> ↓HR and address supraventricular tachycardia.

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33
Q

What is the Bainbridge reflex?

A

Atrial stretch that can ↑HR which may help CO to venous return.

34
Q

What is the oculocardiac reflex?

A

Bradycardia with ocular pressure

35
Q

What is the Cushing reflex?

A

Bradycardia in response to increased intracranial pressure.

36
Q

What is the general effect of anesthetics on cardiac reflexes?

A

Blunt cardiac reflexes in a dose-dependent fashion.

SNS responses to hypotension are reduced.

37
Q

What organ extracts the largest % of O2?

Why is this significant?

A

Coronary circulation to the heart (60-70%)

The heart cannot use increased O2 extraction as a reserve mechanism.

38
Q

Since the heart cannot use increased O2 extraction as a reserve mechanism, what compensatory method is used instead?

A

Vasodilation to increase blood flow to the heart is the primary compensatory mechanism of the heart in threatened O2 supply.

39
Q

What is coronary reserve?

A

The ability of the coronary circulation to increase flow over the baseline state.

40
Q

What endogenous substances influence coronary blood flow?

A

Adenosine
Nitric oxide
Adrenergic stimulation

41
Q

In CAD, at what % blockage does coronary reserve begin to become exhausted?

A

90%

42
Q

What is perfusion pressure?

A

The perfusion pressure of a vascular bed is usually calculated as the difference between MAP and venous pressure.

43
Q

T or F: The myocardial wall tension developed during systole can completely stop blood flow in the subendocardium.

A

T.

This is why the LV is perfused predominantly during diastole.

44
Q

What comprises the pulmonary circulation?

A
RV
Pulmonary arteries 
Pulmonary capillary bed 
Pulmonary veins 
LA
45
Q

What is the function of bronchial circulation?

A

Supplies nutrients to lung tissue and empties into the pulmonary veins and LA.

46
Q

How is the pulmonary circulation unique from the systemic circulation?

A

Difference in pressures and response to drugs.

Resistance thought to occur in larger vessels, small arteries, capillary bed.

Changes in pulmonary circulation is the “distention” of capillaries and the “recruitment” of new capillaries.

47
Q

T or F: Pulmonary Artery Pressure (PAP) is higher than systemic pressure

A

F:
PAP is much lower than systemic pressure because of low pulmonary vascular resistance.
It must accept the entire CO and must adapt its resistance to meet different conditions

48
Q

What is the effect of ↑PAP on the distention and recruitment of capillaries?

A

↑PAP = ↑distention + recruitment –> ↑cross-sectional area + ↓PVR

49
Q

What is the effect of SNS stimulation on pulmonary vasculature?

A

SNS stimulation causes pulmonary vasoconstriction.

50
Q

What is Hypoxic Pulmonary Vasoconstriction (HPV)?

A

The pulmonary vascular response to low PAO2 (partial pressure of O2 in alveolar blood)

51
Q

How does HPV improve gas exchange?

A

Diverts blood away from poorly ventilated areas decreasing the shunt fraction.

52
Q

What is West’s Zones of the Heart?

A

Concept of how gravity determines the way pressures change in the vascular system relative to the measurement at the level of the heart.

53
Q

Every _cm of change in height produces a _mmHg pressure difference.

A

Every 20 cm of change in height produces a 15 mmHg pressure difference.

This can create significant positional differences in PAP that affects blood flow in the lung in various positions.

54
Q

Hydrostatic pulmonary edema is expected with high _ ventricular filling pressures, and patients become at risk of pulmonary edema as PCWP exceeds _ mmHg

A

↑L ventricular filling pressures = pulm edema

> 20mmHg PCWP –> pulm edema

55
Q

What is arterial hypoxemia?

Vs. hypoxia?

A

low PaO2 (low partial pressure of O2 in arterial blood)

PaO2 < 60 mmHg

(vs. hypoxia, a more general term including tissue hypoxia more reflective of circulatory factors)

56
Q

List 3 ways to measure arterial blood oxygen levels?

A
  1. PaO2
    (arterial partial P of O2)
  2. CaO2
    (arterial O2 content)
  3. SaO2 (oxyhemoglobin saturation)
57
Q

What is the relationship between PaO2 and SaO2

A

PaO2 and SaO2 are related through the oxyhemoglobin dissociation curve.

PaO2 via ABG’s
SaO2 via SpO2 pulseox

58
Q

What is P50?

A

The pO2 at which Hb is 50% saturated with O2

A measurement of the position of the oxyhemoglobin dissociation curve.

59
Q

What is the normal P50 of adult Hb?

A

Normal P50 value of adult Hb = 26.8 mmHg

60
Q

What is a rightward shift on the OxyHb curve?

A

allows larger amounts of O2 to dissociate from Hb in the tissues

Improves tissue O2

61
Q

List events that shift the OxyHb curve to the R

A

P50 > 26.8 mmHg

“CADET, face Right!” for CO2, Acid, 2,3-DPG, Exercise and Temperature

62
Q

Equation for arterial oxygen content (CaO2)

“How much O2 is there?”
O2 (mL) per 100mL (1 dL) of blood.

A

CaO2 = SaO2(Hb x 1.39) + 0.003 (PaO2)

  1. 39 = capacity of Hb for O2 (1.39 mL of O2/g of Hb fully saturated)
  2. 003 mL O2/dL/mmHg = solubility of O2
63
Q

What does the alveolar gas equation describe?

A

Describes the transfer of O2 from the environment into the alveoli.

Describes the way in which inspired O2 and ventilation determine PaO2

Also describes how supplemental O2 improves oxygenation.

64
Q

What is the alveolar gas equation?

[Just review and think what its describing].

A

PAO2 = FiO2(PB-PH2O) - (PCO2/RQ)

PB = barometric pressure
PH2O = vapor pressure of water (47 mmHg at normal body T of 37C)
RQ = respiratory quotient (ratio of CO2 production to O2 consumption)
65
Q

What are some causes of incorrect delivery of hypoxic gas mixtures?

A

Errors in pipe connections
O2 tanks run dry
Failure to recognize accidental disconnection

66
Q

What is the normal O2 consumption?

A

300 mL/min

lower during anesthesia

67
Q

What happens physiologically during desaturation?

A

Begins when sufficient numbers of alveoli have collapsed and an intrapulmonary shunt develops, not simply when O2 stores have become exhausted.

68
Q

Normal A-a gradient

A

5-10 mmHg

69
Q

What is the most important cause of an increased A-a gradient and development of arterial hypoxemia?

A

Intrapulmonary shunt

70
Q

What is an intrapulmonary shunt?

A

Mixed venous blood is not exposed to alveolar gas and it continues through the lungs to mix with oxygenated blood from normal areas of the lung

The mixing lowers the PaO2.

Clinically, shunting happens when alveoli are not ventilated (atelectasis)

71
Q

T or F: V/Q mismatch and intrapulmonary shunt can be used synonymously

A

F:

V/Q mismatch is literally areas of high V/Q and areas of low V/Q

Intrapulmonary shunt is literally a shunting of deox blood to mix with ox blood.

Also, both respond differently to the administration of 100% O2

72
Q

How does administration of O2 affect V/Q mismatch vs. intrapulmonary shunt?

A

V/Q mismatch will respond to O2.

With intrapulm shunt only adds more dissolved O2 in already normal perfused alveoli and won’t respond - arterial hypoxemia despite 100% O2 = shunt

73
Q

In what forms does CO2 move around the body?

A

Dissolved gas
As bicarbonate
Small amt bound to Hb as carbaminohemoglobin.

74
Q

Describe the shape of the CO2 dissociation curve

A

linear

75
Q

At what level of PaCO2 would you see CO2 narcosis?

A

PaCO2 > 80 mmHg

Can lead to delayed awakening in the PACU

76
Q

What is the greatest concern of hypercapnia?

A

Indicate a risk of impending respiratory failure and apnea

sign of respiratory difficult or oversedation with opioids.

77
Q

What determines arterial CO2 partial pressure?

A

PaCO2 is a balance of production and removal.

  • Rebreathing
  • ↑CO2 prdxn
  • ↑dead space
  • Hypoventilation
78
Q

List some causes of ↑CO2 production

A
  • Malignant hyperthermia
  • Systemic absorption during laparoscopy procedures
  • Thyroid storm
  • Administration of bicarb which is converted to CO2
  • releasing of tourniquet
79
Q

What is dead space?

A

“Wasted ventilation” - areas receiving ventilation that don’t participate in gas exchange

80
Q

List three categories of dead space

A
  1. Anatomic
  2. Alveolar
  3. Physiologic
81
Q

What is anatomic dead space?

A

Areas of the tracheobronchial tree that are not involved in gas exchange

Includes equipment dead space (ETT, etc)