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 ↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Manipulations of the diffusion equation in emphysema

A

A↓ in emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Manipulations of the diffusion equation in pulmonary fibrosis

A

↑T in pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Equation for Pulmonary vascular resistance

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is hypoxemia

A

(↓PaO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is hypoxia?

A

(↓O2 delivery to tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of hypoxia

4 listed

A
  • ↓ cardiac output
  • Hypoxemia
  • Anemia
  • CO poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Ischemia?

A

(Loss of blood flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of ischemia

2 listed

A

Impeded arterial flow or ↓ venous drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ventilation/perfusion mismatch

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Organisms in the lung

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

V/Q = 0 = 0

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

V/Q = ∞

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the Bohr effect

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

The majority of CO2 is transported as?

A

HCO3- in the plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
CO2 transport diagram
652
26
Describe the response to high altitude
↓ 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
Describe the response to exercise
↑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
What is Rhinosinusitis?
Obstruction of sinus drainage into nasal cavity → inflammation and pain over affected area
29
Most common site of Rhinosinusitis?
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
Common causes of Rhinosinusitis
Most common acute cause is viral URI May lead to superimposed bacterial infection (most commonly S pneumoniae, H influenzae, M catarrhalis)
31
Complications of Rhinosinusitis
Infections in sphenoid or ethmoid sinuses may extend to cavernous sinus and cause complications (eg cavernous sinus syndrome)
32
What is epistaxis?
Nose bleed
33
Most common location of epistaxis?
Anterior segment of nostril (Kiesselbach plexus)
34
Complications of epistaxis
Life-threatening hemorrhages occur in posterior segment (Sphenopalatine artery, a branch of maxillary artery)
35
Common causes of epistaxis
* Foreign bodies * Trauma * Allergic rhinitis * Nasal angiofibromas (common in adolescent males)
36
Epistaxis Mnemonic
Kiesselbach drives his Lexus with his LEGS: Superior Labial artery, anterior and posterior Ethmoidal arteries, Greater palatine artery, Sphenopalatine artery
37
Most common types of head and neck cancer
Mostly squamous cell carcinoma
38
Risk factors of head and neck cancer
tobacco alcohol HPV-16 (oropharyngeal) EBV (nasopharyngeal)
39
What is field cancerization?
Carcinogen damages wide mucosal area → multiple tumors that develop independently after exposure
40
Presentation of Deep vein thrombosis
Blood lot within a deep vein → Swelling Redness Warmth Pain
41
Risks for deep vein thromboses
Predisposed by Virchow triad (SHE)
42
What is Virchow triad
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
Tests for pulmonary embolism
D-dimer has high sensitivity but low specificity and is used to clinically rule out DVT
44
Most pulmonary emboli arise from?
Proximal deep veins of lower extremity
45
Treatment of deep venous thrombosus
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
Imaging test of choice for deep venous thrombosus
Compression ultrasound with doppler
47
Presentation of Pulmonary emboli 8 listed
* 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
Pulmonary emboli histological features
Lines of Zahn are interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death
49
Types of emboli in pulmonary embolism
An embolus moves like a FAT BAT * Fat * Air * Thrombus * Bacteria * Amniotic fluid * Tumor
50
Describe fat emboli
Associated with long bone fractures and liposuction
51
Symptoms of fat embolus
Classic triad of * hypoxemia * Neurologic abnormalities * Petechial rash
52
Common causes of Air emboli
Nitrogen bubbles precipitate in ascending divers (Caisson disease/decompression sickness) Can be iatrogenic 2° to invasive procedures (eg central line placement)
53
Treatment of air emboli
Hyperbaric O2
54
Concerns of amniotic fluid emboli
Can lead to DIC especially postpartum
55
Test of choice for pulmonary emboli
CT pulmonary angiography (look for filling defects
56
Common causes of diffusion-limited O2 exchange
emphysema, fibrosis exercise CO
57
Common causes of perfusion-limited O2 exchange
Pulmonary embolism V/Q mismatch with low Q
58
Causes of ↑ A-a gradient
* Shunting * V/Q mismatch * Fibrosis (impairs diffusion)
59
What is enoxaparin?
low molecular weight heparan
60
Rivaroxaban MOA and clinical use
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