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CVPR > cvpr physiology 2 > Flashcards

cvpr physiology 2 Flashcards

1
Q

What is the primary defect in perfusion limited O2 (normal health) CO2 N2O gas equilibrates early along the length of the capillary

A

Diffusion can be ↑ only if blood flow ↑

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2
Q

What is the primary defect in diffusion-limited O2

A

Gas does not equilibrate by the time blood reaches the end of the capillary

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3
Q

A consequence of pulmonary hypertension is cor pulmonale and subsequent right ventricular failure

A

Diffusion Vgas = A x D x (P1-P2)/T where A = area Dk= diffusion coefficient of gas P1-P2 = pressure difference

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4
Q

Manipulations of the diffusion equation in emphysema

A

A↓ in emphysema

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5
Q

Manipulations of the diffusion equation in pulmonary fibrosis

A

↑T in pulmonary fibrosis

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6
Q

What is DLCO

A

Diffusing capacity of the lungs for carbon monoxide (DLCO) is a medical test that determines how much oxygen travels from the alveoli of the lungs to the blood stream.

DLCO a good measure of lung disease severity

The extent to which CO, a surrogate for O2 passes from air sacs of lung into blood Pg 650

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7
Q

Equation for Pulmonary vascular resistance

A

PVR = (P pulm artery - PL atrium) / Cardiac output

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8
Q

What is hypoxemia

A

(↓PaO2)

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9
Q

Alveolar gas equation

A

PaO2 = PIO2 - PaCO2/R PAO2 = alveolar PO2 (mmHg)

PIO2 = PO2 in inspired air (mmHg) PaCO2 arterial PCO2 (mmHg)

R = respiratory quotient = CO2 produced/O2 consumed A-a gradient = PAO2 - PaO2

Normal range = 10-15 mmHg

↑ A-a gradient may occur in hypoxemia

Causes of ↑ A-a gradient

Shunting, V/Q mismatch, Fibrosis (impairs diffusion)

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10
Q

What is hypoxia?

A

(↓O2 delivery to tissue)

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11
Q

Causes of hypoxia

4 listed

A
  • ↓ cardiac output
  • Hypoxemia
  • Anemia
  • CO poisoning
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12
Q

What causes hypoxemia?

A

Normal A-a gradient

High altitude

Hypoventilation (eg opioid use)

↑ A-a gradient

V/Q mismatch

Diffusion limitation

Right-to-left shunt

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13
Q

What is Ischemia?

A

(Loss of blood flow)

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14
Q

Causes of ischemia

2 listed

A

Impeded arterial flow or ↓ venous drainage

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15
Q

Ventilation/perfusion mismatch

A

Ideally ventilation is matched to perfusion (ie V/Q = 1) for adequate gas exchange

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16
Q

Lung zones and V/Q properties

A

V/Q at apex of lung = 3 (wasted ventilation)

V/Q at base of lung = 0.6 (wasted perfusion)

Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung

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17
Q

Effects of exercise on V/Q matching

A

With exercise (↑ Cardiac output) there is vasodilation of apical capillaries → V/Q ratio approaches 1

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18
Q

Organisms in the lung

A

Some organisms that thrive in high O2 (eg TB) flourish in the apex

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19
Q

V/Q = 0 = 0

A

“oirway” obstruction (shunt), In shunt, 100%, O2 does not improve PaO2 (eg foreign body aspiration)

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20
Q

V/Q = ∞

A

Blood flow obstruction (physiologic dead space) Assuming <100% dead space, 100% O2 improves PaO2 (eg pulmonary embolus)

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21
Q

Methods of CO2 transport 3 listed

A

HCO3- (70%)

Carbaminohemoglobin or HbCO2 (21-25%)

CO2 bound to Hb at N-terminus of globin (not heme)

CO2 favors deoxygenated form (O2 unloaded)

Dissolved CO2 (5-9%)

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22
Q

In lungs oxygenation of Hb promotes dissociation of H+ from Hb

A

This shifts equilibrium toward CO2 formation Therefore CO2 is released from RBCs (Haldane effect)

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23
Q

Describe the Bohr effect

A

In peripheral tissue ↑H+ from tissue metabolism shifts curve to the right unloading O2 (Bohr effect)

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24
Q

The majority of CO2 is transported as?

A

HCO3- in the plasma

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25
Q

CO2 transport diagram

A

652

26
Q

Describe the response to high altitude

A

↓ atmospheric O2 (PO2) → ↓PaO2 → ↑ventilation → ↓PaCO2 → respiratory alkalosis → altitude sickness

Chronic ↑ in ventilation ↑EPO → ↑Hct and Hb (due to chronic hypoxia)

↑ 2, 3-BPG (binds to Hb causing left shift so that Hb releases more O2)

Cellular changes (↑ mitochondria)

↑renal excretion of HCO3- to compensate for respiratory alkalosis (can augment with acetazolamide)

Chronic hypoxic pulmonary vasoconstriction results in pulmonary HTN and RVH

27
Q

Describe the response to exercise

A

↑CO2 production ↑O2 consumption ↑ventilation rate to meet O2 demand V/Q ratio from apex to base becomes more uniform ↑pulmonary blood flow due to ↑ cardiac output ↓pH during strenuous exercise (2° to lactic acidosis) No change in PaO2 and PaCO2, but ↑ in venous O2 content

28
Q

What is Rhinosinusitis?

A

Obstruction of sinus drainage into nasal cavity → inflammation and pain over affected area

29
Q

Most common site of Rhinosinusitis?

A

Typically affects maxillary sinuses, which drain against gravity due to ostia located superomedially (red arrow points to fluid-filled right maxillary sinus in diagram pg 653

30
Q

Common causes of Rhinosinusitis

A

Most common acute cause is viral URI May lead to superimposed bacterial infection (most commonly S pneumoniae, H influenzae, M catarrhalis)

31
Q

Complications of Rhinosinusitis

A

Infections in sphenoid or ethmoid sinuses may extend to cavernous sinus and cause complications (eg cavernous sinus syndrome)

32
Q

What is epistaxis?

A

Nose bleed

33
Q

Most common location of epistaxis?

A

Anterior segment of nostril (Kiesselbach plexus)

34
Q

Complications of epistaxis

A

Life-threatening hemorrhages occur in posterior segment (Sphenopalatine artery, a branch of maxillary artery)

35
Q

Common causes of epistaxis

A
  • Foreign bodies
  • Trauma
  • Allergic rhinitis
  • Nasal angiofibromas (common in adolescent males)
36
Q

Epistaxis Mnemonic

A

Kiesselbach drives his Lexus with his LEGS: Superior Labial artery, anterior and posterior Ethmoidal arteries, Greater palatine artery, Sphenopalatine artery

37
Q

Most common types of head and neck cancer

A

Mostly squamous cell carcinoma

38
Q

Risk factors of head and neck cancer

A

tobacco

alcohol

HPV-16 (oropharyngeal)

EBV (nasopharyngeal)

39
Q

What is field cancerization?

A

Carcinogen damages wide mucosal area → multiple tumors that develop independently after exposure

40
Q

Presentation of Deep vein thrombosis

A

Blood lot within a deep vein → Swelling Redness Warmth Pain

41
Q

Risks for deep vein thromboses

A

Predisposed by Virchow triad (SHE)

42
Q

What is Virchow triad

A

Stasis (post-op, long drive/flight)

Hypercoagulability (eg defect in coagulation cascade proteins such as factor V Leiden, oral contraceptive use)

Endothelial damage (exposed collagen triggers clotting cascade)

43
Q

Tests for pulmonary embolism

A

D-dimer has high sensitivity but low specificity and is used to clinically rule out DVT

44
Q

Most pulmonary emboli arise from?

A

Proximal deep veins of lower extremity

45
Q

Treatment of deep venous thrombosus

A

Unfractionated heparin or low-molecular-weight heparins (eg enoxaparin) for prophylaxis and acute management

Use oral anti-coagulants (eg warfarin, rivaroxaban) for treatment and (long-term prevention)

46
Q

Imaging test of choice for deep venous thrombosus

A

Compression ultrasound with doppler

47
Q

Presentation of Pulmonary emboli

8 listed

A
  • V/Q mismatch
  • Hypoxemia
  • Respiratory alkalosis
  • Sudden-onset dyspnea
  • Pleuritic chest pain
  • Tachypnea
  • Tachycardia w/ large emboli or saddle emboli
  • May cause sudden death due to electromechanical dissociation
48
Q

Pulmonary emboli histological features

A

Lines of Zahn are interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death

49
Q

Types of emboli in pulmonary embolism

A

An embolus moves like a FAT BAT

  • Fat
  • Air
  • Thrombus
  • Bacteria
  • Amniotic fluid
  • Tumor
50
Q

Describe fat emboli

A

Associated with long bone fractures and liposuction

51
Q

Symptoms of fat embolus

A

Classic triad of

  • hypoxemia
  • Neurologic abnormalities
  • Petechial rash
52
Q

Common causes of Air emboli

A

Nitrogen bubbles precipitate in ascending divers (Caisson disease/decompression sickness)

Can be iatrogenic 2° to invasive procedures (eg central line placement)

53
Q

Treatment of air emboli

A

Hyperbaric O2

54
Q

Concerns of amniotic fluid emboli

A

Can lead to DIC especially postpartum

55
Q

Test of choice for pulmonary emboli

A

CT pulmonary angiography (look for filling defects

56
Q

Common causes of diffusion-limited O2 exchange

A

emphysema, fibrosis exercise CO

57
Q

Common causes of perfusion-limited O2 exchange

A

Pulmonary embolism V/Q mismatch with low Q

58
Q

Causes of ↑ A-a gradient

A
  • Shunting
  • V/Q mismatch
  • Fibrosis (impairs diffusion)
59
Q

What is enoxaparin?

A

low molecular weight heparan

60
Q

Rivaroxaban MOA and clinical use

A

Mechanism of action. Rivaroxaban inhibits both free Factor Xa and Factor Xa bound in the prothrombinase complex. It is a highly selective direct Factor Xa inhibitor with a rapid onset of action.

Treat and prevent DVT and Pulmonary embolism

CVPR (93 decks)

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