cvpr physiology 2 Flashcards
What is the primary defect in perfusion limited O2 (normal health) CO2 N2O gas equilibrates early along the length of the capillary
Diffusion can be ↑ only if blood flow ↑
What is the primary defect in diffusion-limited O2
Gas does not equilibrate by the time blood reaches the end of the capillary
A consequence of pulmonary hypertension is cor pulmonale and subsequent right ventricular failure
Diffusion Vgas = A x D x (P1-P2)/T where A = area Dk= diffusion coefficient of gas P1-P2 = pressure difference
Manipulations of the diffusion equation in emphysema
A↓ in emphysema
Manipulations of the diffusion equation in pulmonary fibrosis
↑T in pulmonary fibrosis
What is DLCO
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
Equation for Pulmonary vascular resistance
PVR = (P pulm artery - PL atrium) / Cardiac output
What is hypoxemia
(↓PaO2)
Alveolar gas equation
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)
What is hypoxia?
(↓O2 delivery to tissue)
Causes of hypoxia
4 listed
- ↓ cardiac output
- Hypoxemia
- Anemia
- CO poisoning
What causes hypoxemia?
Normal A-a gradient
High altitude
Hypoventilation (eg opioid use)
↑ A-a gradient
V/Q mismatch
Diffusion limitation
Right-to-left shunt
What is Ischemia?
(Loss of blood flow)
Causes of ischemia
2 listed
Impeded arterial flow or ↓ venous drainage
Ventilation/perfusion mismatch
Ideally ventilation is matched to perfusion (ie V/Q = 1) for adequate gas exchange
Lung zones and V/Q properties
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
Effects of exercise on V/Q matching
With exercise (↑ Cardiac output) there is vasodilation of apical capillaries → V/Q ratio approaches 1
Organisms in the lung
Some organisms that thrive in high O2 (eg TB) flourish in the apex
V/Q = 0 = 0
“oirway” obstruction (shunt), In shunt, 100%, O2 does not improve PaO2 (eg foreign body aspiration)
V/Q = ∞
Blood flow obstruction (physiologic dead space) Assuming <100% dead space, 100% O2 improves PaO2 (eg pulmonary embolus)
Methods of CO2 transport 3 listed
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%)
In lungs oxygenation of Hb promotes dissociation of H+ from Hb
This shifts equilibrium toward CO2 formation Therefore CO2 is released from RBCs (Haldane effect)
Describe the Bohr effect
In peripheral tissue ↑H+ from tissue metabolism shifts curve to the right unloading O2 (Bohr effect)
The majority of CO2 is transported as?
HCO3- in the plasma
CO2 transport diagram
652
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
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
What is Rhinosinusitis?
Obstruction of sinus drainage into nasal cavity → inflammation and pain over affected area
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
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)
Complications of Rhinosinusitis
Infections in sphenoid or ethmoid sinuses may extend to cavernous sinus and cause complications (eg cavernous sinus syndrome)
What is epistaxis?
Nose bleed
Most common location of epistaxis?
Anterior segment of nostril (Kiesselbach plexus)
Complications of epistaxis
Life-threatening hemorrhages occur in posterior segment (Sphenopalatine artery, a branch of maxillary artery)
Common causes of epistaxis
- Foreign bodies
- Trauma
- Allergic rhinitis
- Nasal angiofibromas (common in adolescent males)
Epistaxis Mnemonic
Kiesselbach drives his Lexus with his LEGS: Superior Labial artery, anterior and posterior Ethmoidal arteries, Greater palatine artery, Sphenopalatine artery
Most common types of head and neck cancer
Mostly squamous cell carcinoma
Risk factors of head and neck cancer
tobacco
alcohol
HPV-16 (oropharyngeal)
EBV (nasopharyngeal)
What is field cancerization?
Carcinogen damages wide mucosal area → multiple tumors that develop independently after exposure
Presentation of Deep vein thrombosis
Blood lot within a deep vein → Swelling Redness Warmth Pain
Risks for deep vein thromboses
Predisposed by Virchow triad (SHE)
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)
Tests for pulmonary embolism
D-dimer has high sensitivity but low specificity and is used to clinically rule out DVT
Most pulmonary emboli arise from?
Proximal deep veins of lower extremity
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)
Imaging test of choice for deep venous thrombosus
Compression ultrasound with doppler
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
Pulmonary emboli histological features
Lines of Zahn are interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death
Types of emboli in pulmonary embolism
An embolus moves like a FAT BAT
- Fat
- Air
- Thrombus
- Bacteria
- Amniotic fluid
- Tumor
Describe fat emboli
Associated with long bone fractures and liposuction
Symptoms of fat embolus
Classic triad of
- hypoxemia
- Neurologic abnormalities
- Petechial rash
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)
Treatment of air emboli
Hyperbaric O2
Concerns of amniotic fluid emboli
Can lead to DIC especially postpartum
Test of choice for pulmonary emboli
CT pulmonary angiography (look for filling defects
Common causes of diffusion-limited O2 exchange
emphysema, fibrosis exercise CO
Common causes of perfusion-limited O2 exchange
Pulmonary embolism V/Q mismatch with low Q
Causes of ↑ A-a gradient
- Shunting
- V/Q mismatch
- Fibrosis (impairs diffusion)
What is enoxaparin?
low molecular weight heparan
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
