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CardioResp > Week 6 > Flashcards

Week 6 Flashcards

1
Q

What occurs in heart valve dysfuncton histologically?

A
  • Heart valve histology
    • Thick fibrous layer
    • Thin endothelial layer
    • No arteries or veins
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2
Q

What can occur to the aortic valve pathologically and what is it usually caused by?

A
  • Aortic Valve – stenosis and insufficiency caused by calcifications
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3
Q

What are congenital conditions associated with the aortic valve?

A
  • Congenital
    • Congenital bicuspid aortic valve
    • Unicuspid aortic valve
    • Quadricuspid aortic valve
    • Subvalvular aortic stenosis – membrane obstructs flow through the valve
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4
Q

What are the 4 acquired vavular pathologies for the aortic valve and how do they occur. Be very specific. What complications or diseases for each one?

A
  • Acquired
    • Calcific aortic stenosis – thickening of the valve leaflets in old age
      • Complications: LVH, endocarditis, angina, syncope, HF
    • Post-inflammatory aortic disease – occurs 10 days to 6 weeks after pharyngitis due to Group A, beta-hemolytic streptococcus
      • Rheumatic fever: develops when antibodies formed against the Group A, beta-hemolytic streptococcus attack heart, joints, etc.
    • Aortic regurgitation – dilation of the annulus or valvular ring leads to stretched out leaflets which will not be able to close in diastole
      • Older age patients
      • Marfan’s syndrome
    • Endocarditis
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5
Q

What are the three acquired conditions that can cause a pathological mitral valve. What occurs in each one? Symptomatic?

A
  • Acquired
    • Mitral valve prolapse – leaflets bulge into the left atrium during systole
      • Mostly asymptomatic
      • Histology: thinning of fibrosa layer and expansion of spongiosa layer
      • Possible complications: regurgitation
    • Mitral annular calcification – usually asymptomatic
    • Mitral regurgitation – patient with MI can have ruptured papillary muscles and may lead to death
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6
Q

What are three congenital conditions associated with the mitral valve?

A
  • Congenital
    • Atrioventricular canal defect
    • Hypoplastic left heart
    • Transposition of great vessels
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7
Q

What is the main congenital condition associated with the tricuspid valve?

A
  • Ebstein’s anaomaly – leaflets of the tricuspid valve are attached low within the right ventricle
    • Closure of valve is impaired resulting in regurgitation
    • Increase in right atrial pressure creates atrial septal defect and shunts blood from RA to LA, causing cyanosis
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8
Q

What occurs in rheumatic fever?

A

Rheumatic fever: develops when antibodies formed against the Group A, beta-hemolytic streptococcus attack heart, joints, kidneys, skin, CNS, etc.

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9
Q

What are the major manifestations in rheumatic heart disease?

A
  • Major manifestations
    • Polyarthritis of the large joints
    • Endocarditis, myocarditis, pericarditis
    • Chorea
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10
Q

What is this condition?

A

Rheumatic heart disease affecting the valves

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11
Q

What are the microscopic conditions associated with the myocardium in rheumatic heart disease?

A
  • Microscopic
    • Aschoff body – focal interstitial inflammation within the myocardium
    • Fibrinoid necrosis with granulomatous type inflammation with lymphocytes (healing process is through fibrosis)
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12
Q

What are the gross appearances and complications associated with rheumatic heart disease?

A
  • Gross
    • Thickened, deformed leaflets
    • Thick chordae tendinae
  • Complications
    • Atrial fibrillation
    • RVH – decrease flow from LA to LV (due to mitral valve stenosis) → increase in pressure in the pulmonary system à RV has to contract more to overcome afterload
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13
Q

Define infective endocarditis. What are the complications? What two conditions are associated with noninfectious endocarditis?

A
  • Infective endocarditis – colonization and invasion of the valves, mural endocardium, and chords
    • Complications:
      • Perforation of cusps
      • Rupture of chords
    • Noninfectious endocarditis
      • Nonbacterial thrombotic (marantic) endocarditis
      • Endocarditis of SLE
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14
Q

What is this condition?

A

Infective endocarditis with vegetations.

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15
Q

Understand what populations get valve disease and which type of valve disease is most common.

A
  • Old people get valve disease
  • Mitral regurgitation is most common
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16
Q

Define sclerosis and stenosis

A
  • Sclerosis is hardening
  • Stenosis is narrowing
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17
Q
  • How does concentric hypertrophy occur?
  • How does ventricular dilation occur?
    • Which conditions are associated with each?
A
  • Concentric hypertrophy – increase in pressure/afterload requires more muscle/wall thickening to overcome increased resistance
    • Hypertension, aortic stenosis
  • Ventricular dilation (eccentric hypertrophy) – increase in volume/preload leads to stretching/chamber enlargement of ventricle
    • Regurgitation and ASD (RV) and VSD (LV)
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18
Q

What are the causes of aortic stenosis (3)?

A
  • Causes – calcification of the leaflets, bicuspid/congenital, prosthetic, post-rheumatic fever inflammation
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19
Q

What are the 5 clinical manifestations associated with aortic stenosis?

A
  • Manifestations
    • LVH
    • Syncope
    • HF
    • Angina
    • Dyspnea
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20
Q

What are the clinical signs associated with aortic stenosis and what is a treatment?

A
  • Signs
    • Systolic ejection murmur
    • S4 can develop with LVH
  • Management
    • Surgery
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21
Q

What are the three big causes of aortic insuffiency?

A
  • Causes – leaflet damage, aortic root dilation, valvular ring dilation
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22
Q

What are the manifestations associated with aortic insufficiency?

A
  • Manifestations
    • Dyspnea
    • Concentric LV hypertrophy and left ventricular dilation due to increase in pressure AND volume
    • Bounding pulse – do not have continuous flow due to regurgitation
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23
Q

What are the clinical signs and treatment associated with aortic insufficiency?

A
  • Signs
    • Diastolic murmur
    • Displaced PMI
  • Management
    • Surgery
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24
Q

What is the disc betweent the endoderm and ectoderm called?

A

trilaminar disc

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25
Q

Where do the cells that form the mesoderm come from?

A

Primitive streak of ectoderm during gastrulation

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26
Q

Out of the three mesoderm sections, which one differentiates into cardiac cells? What does that mesoderm differentiate into? What do they form?

A
  • The lateral mesoderms differentiate into the somatic mesoderm (on the ectoderm side) and the splanchnic mesoderm (on the endoderm side)
    • The splanchnic mesoderm forms the heart forming fields (endo-, myo-, epi-cardium, visceral pericardium, + coronary vessels)
    • The somatic mesoderm forms the parietal serous pericardium
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27
Q

What are the three sections of the primitive heart tube and what do they turn into later?

A
  • Formed primitive heart tube has three sections
    • Venous pole (inflow tract)
      • Sinus venosus – turns into the atria later
    • Arterial pole (outflow tract)
      • Bulbus cordis – turns into the RV later
    • Primitive ventricle (hollow space)
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28
Q

What occurs in ventricular looping? What occurs in atrial expansion?

A
  • Ventricular looping – tube bends ventrally and to the right
    • If goes to the left, dextrocardia
  • Atrial expansion – inferior venous pole expands dorsally and cranially
    • As the atria expands, it absorbs the primary pulmonary vein into its wall
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29
Q

What occurs in the formation of the endocardial cushions?

A
  • Formation of endocardial cushions
    • Endocardial tissue reverts back to mesenchymal tissue and proliferates to separate ventricles and atria
    • Valves form from apoptosis of endocardial cushions
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30
Q
  • What occurs in atrial spetation and what are the two main septums that form here? Where is the foramen ovale?
  • What are the defects?
A
  • Atrial septation
    • Septum primum – crescent shaped formation descends from roof of atrium towards endocardial cushions; once the points of the crescent reach end point, the hole left is called the foramen primum
    • Septum secundum – also grows from the roof of atrium to the right of the septum primum
    • The space between these two septum growths is the foramen ovale
      • When a baby takes its first breath, the flap from the septum primum closes shut, blocking the shunt pathway
    • Defects
      • Patent foramen ovale – hole does not close
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31
Q

What occurs in ventricular septation? What defect can occur?

A
  • Ventricular septation
    • As ventricles grow outward and inferiorly, the muscular part of the interventricular septum grows (from the bottom of the ventricles)
    • The membranous part of the interventricular septum (the superior portion) is formed by the endocardial cushion
    • Defects
      • Ventricular septal defect – most common in the membranous portion of the interventricular septum, shunting blood form left to right
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32
Q
  • How is the outlfow tract formed? What are the two big vessels that make it up?
  • What is a big thing that arises out of this?
A
  • Outflow tract
    • Endocardial cushion spirals upwards to form pulmonary artery and aorta
    • Ductus arteriosus – arises out of the left sixth pharyngeal arch artery and closes after birth
      • Conduit between aortic arch and pulmonary trunk
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33
Q

Defects in the outflow tract (2).

A
  • Patent ductus arteriosus – the ductus arteriosus should gradually close after birth to become the ligamentum arteriosum
    • A larger patent ductus arteriosus that did not close could overwork the lungs and heart
    • A smaller PDA that did not close will not have much affect and may close on its own
  • Tetralolgy of Fallot
    • Pulmonary stenosis – endocardial cushion dysfunction
    • Ventricular septal defect – endocardial cushion dysfunction
    • Dextroposition of the aorta – folding dysfunction
    • Right ventricular hypertrophy – progressive development due to increase in pressure from LV shunt and pulmonary stenosis
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34
Q

What is the process of vasculogenesis? 5 steps.

A

Vasculogenesis – process is happening all over the mesodermal layer

  • Mesenchymal cells differentiate into angioblasts (vessel forming cells)
  • Angioblasts aggregate to form blood islands
  • Cavities appear within blood islands
  • Angioblasts flatten and differentiate into endothelial cells
  • Endothelial cavities fuse together into endocardial tubes (multiple lumens become one)
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35
Q

Sketch the fetal blood flow.

A
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36
Q

Diagram the fetal circulation.

A
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37
Q

What is the anatomy of an AV valve? What are some diseases that can occur with each anatomy?

A
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38
Q

What are some causes of mitral regurgitation (5)?

A
  • Causes – infective endocarditis, ruptured papillary muscle, mitral stenosis, rheumatic disease, mitral prolapse
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39
Q

How is mitral valve regurgitation diagnosed?

A
  • Diagnostic evaluation – atrial fibrillation (dilation of atrium causes stretching out of conduction pathway), pulmonary rales, holosystolic murmur, S3
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40
Q

What are the clinical manifestations and treatment associated with mitral regurgiation?

A
  • Clinical manifestations – exertional dyspnea, pulmonary hypertension, right heart failure, LV dilation
  • Treatment – repair rather than replace
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41
Q

what are the causes associated with mitral stenosis?

A
  • Causes – rheumatic heart disease, senile calcification, bronchial carcinoid (releases chemical leading to calcification)
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42
Q

How is mitral stenosis evaluated?

A
  • Diagnostic evaluation – diastolic murmur, pulmonary rales, RV dilation and hypertrophy (RV lift), atrial fibrillation
43
Q

What are the clinical manifestations and treatment associated with mitral stenosis?

A
  • Clinical manifestations – thrombus in LA, pulmonary congestion, atrial hypertrophy and dilation cause displacement of PMI
  • Treatment – typically asymptomatic; intervene for symptoms
44
Q

How common is tricuspid and pulmonic valve disease?

A
  • Rare, degenerative causes but can be congenital
45
Q

What are the 6 types of valve procedures used for valve issues? What is the procedure for each one?

A
  • Valvotomy – cutting the valve to open better; often recalcify
  • Repair – preferred for AV valves because it is less risky
  • Homograft (human), heterografts (mammal), autografts (self)
  • Bioprosthesis – no anticoagulation
  • Mechanical prostheses – highly durable but requires life long anticoagulation
  • Interventional approaches
46
Q

innocent vs. pathologic murmurs

A
  • Innocent: grades I-III, asymptomatic, not a diastolic murmur, no murmur in the back, and normal S2
  • Pathologic: symptomatic, diastolic murmur, cyanosis, abnormal pulses, single S2
47
Q

prevalence

acyanotic vs. cyanotic

A
  • Prevalence: 1%
  • Acyanotic: 65% of congenital heart disease
  • Cyanotic: 35% of congenital heart disease
48
Q

Patent ductus arteriosus

presentation? Hemodynamis? Tx?

A
  • Hemodynamic effects: continuous “machinery” murmur that is heard from the back
  • Presentation: impacted ability to grow as infants because overworked lungs increases caloric needs
  • Treatment: coil placement to induce thrombosis
49
Q

what happens when septal defect is left unrepaired ?

A

If left unrepaired, large septal defect (Eisenmenger Syndrome) causes buildup of pulmonary hypertension due to increased fluid causes RVH, leading blood to be shunted from RV to LV

Child becomes cyanotic

50
Q

atrial septal defect

Types? Hemodynamis? Tx?

A
  • Types
    • Primum ASD – endocardial cushion failure
    • Secundum ASD
    • Sinus venosus defect
  • Hemodynamic effects: widely split and fixed S2
  • Treatment: patch closure
51
Q

Ventricular septal defect

Types? Hemodynamis? Tx?

A
  • Types
    • Perimembranous
    • Muscular
  • Hemodynamic effects: harsh systolic murmur that may be holosystolic
    • Early large septal defects shunt blood from left to right
      • Child is acyanotic
  • Treatment: patch closure
52
Q

Five t’s?

A
  • Transposition of the Great Vessels
  • Tetralogy of Fallot
  • Tricuspid Valve Atresia, Truncus Arteriosus, Total Anomalous Pulmonary Venous Return
53
Q

Tetralogy of Fallot

presentation, hemodynamic, tx?

A
  • Presentation: ventricular septal defect, right ventricular outflow tract obstruction (protects the pulmonary system from HTN), aortic valve override, right ventricular hypertrophy
  • Hemodynamic effects: RVH from pressure increase from LV, deoxy and oxy blood mix, causing cyanosis
  • Treatment: surgery
54
Q

Tetralogy of Fallot

symptoms, sign?

A
  • Aortic coarctation: narrowing of the isthmus due to lack of blood flow through aorta and instead through the ductus arteriosus
  • Symptoms:
    • Decreased ABI
    • Decreased femoral pulses
  • Signs:
    • Rib notches due to expansion of posterior intercostal arteries from hypertension
55
Q

Fick’s Law of Diffusion

A
57
Q

The amount of gas transferred in the alveoli is:

A
  • Directly proportional to: diffusion coefficient (D), surface area (A), and the partial pressure gradient across the barrier (P1-P2)
  • Indirectly proportional to: thickness of the barrier (T)
58
Q

Conditions that decrease diffusion capacity

A
  • Thickening of the barrier: interstitial or alveolar edema, interstitial or alveolar fibrosis, sarcoidosis, scleroderma
  • Ventilation-perfusion mismatch
  • Decreased surface area: emphysema, tumors, low CO, low pulmonary capillary blood volume
  • Decreased uptake by erythrocytes: anemia, low pulmonary capillary blood volume
59
Q

Diffusion-limited

use CO as an example in explantion

A
  • Gas transfer is limited by the ability of a gas to move across a barrier (diffusion)
  • CO has a hard time moving across the alveolar wall (less soluble) despite a continuously high partial pressure gradient (due to it immediately binding Hb), resulting in a blood saturation that is never reached
60
Q

Mixed-limited

use O2 as an example in explantion

A
  • Can be diffusion-limited or perfusion-limited
  • O2 is more soluble than CO, but has less binding affinity to Hb
    • In healthy individuals, O2 is considered perfusion-limited because it reaches blood saturation
61
Q

Explian Co2 diffusion

A
  • CO2 has a very small partial pressure gradient (45 mmHg in capillaries to 40 mmHg in the lungs), but has 20x diffusivity (D) of O2
    • Equilibrium is reached at the same time oxygen reaches blood saturation
62
Q

why the pulmonary vasculature has low resistance

A
  • Pulmonary vessels are shorter than systemic vessels
  • Pulmonary vessels are thinner walled than systemic vessels
63
Q

Explain how altitude effects diffusion or pefusion limitations?

effects of altitude and exercise ?

A
  • The PAO2 is already lower at higher altitudes (using PAO2 = F(Patm – PH2O)), therefore lowering the threshold for blood saturation
  • Lower atmospheric pressure decreases the partial pressure difference; therefore, O2 moves across the barrier more slowly and takes more distance along the capillary bed to reach blood saturation
  • Severe exercise at high altitude is one of the few times that O2 becomes diffusion-limited (because flow is high and diffusion is low)
64
Q

Explain how exercise effects diffusion or pefusion limitations?

A
  • Flow through the capillary is more rapid (because HR is increased)
  • Therefore, it takes O2 a longer distance along the capillary to reach blood saturation
65
Q

where is PVR (pulmonary vascular resistance) te lowest

A

Pulmonary vascular resistance (PVR) is at its lowest at functional reserve capacity (FRC)

66
Q

Explian resistance changes @ very high lung volumes…

A
  • Alveolar vessels: compressed alveolar vessels from decreased PTM, decreasing the radius, and thus increases resistance
  • Extra-alveolar vessels: inspiration makes chest pressure more negative (-PTM), increasing the radius of the vessels, and thus decreasing resistance
67
Q

Transmural pressure gradient of vessels: PTM

A

Transmural pressure gradient of vessels: PTM = (pressure inside a vessel) – (pressure outside the vessel)

68
Q

Distension versus Recruitment

A
  • Distension
    • At higher vascular pressures, widening of individual capillary segments occurs due to an increase in their PTM (more pressure inside than outside)
    • Increased diameter decreases resistance to blood flow
  • Recruitment
    • Under normal conditions, some capillaries are closed or are open but unperfused
69
Q

Describe Zone 1 the lung

A
  • Zone 1 (highest zone)
    • PA > Parterial > Pvenous, and PTM is always negative
    • Since the PA is 0, Pa or Pv would be less than 0 because there is no volume (due to gravity) in those vessels resulting in Zone 1 vessels being collapsed (alveolar dead space)
70
Q

describe zone 2

A
  • Zone 2 (middle zone)
    • Parterial > PA > Pvenous, PTM is positive in the arterioles
    • Increased volume in the middle zone causes the arterioles to open up and allow blood flow – example of recruitment
71
Q

describe zone 3

A
  • Zone 3 (lowest zone)
    • Parterial > Pvenous > PA, PTM is positive across all vessels
    • Since the most volume of blood is in the lowest part of the lung (due to gravity), pressure in the vessels is greater than PA
    • Since all vessels in this zone have all been recruited (due to high initial volume), an increase in flow will cause the vessels to be distended
72
Q

Alveolar pressure (PA)

A

pressure within the alveoli

73
Q

Intrapleural pressure (PIP)

A

pressure within the intrapleural space (between the lung and the chest wall)

74
Q

Explian the Pressure characteristics at rest

A
  • Negative PIP creates pressure gradients across the lungs and chest wall
    • At rest, PIP is -5 cm H2O (aka 5 cm less than atmospheric pressure)
    • Created by recoil forces of the lung and chest wall “pulling” on the space
75
Q

What determines lung volume

A
  • The interaction between the lung and the chest wall determines lung volume by balancing two forces:
    • Elastic recoil of the lungs pulling the lungs inward back to their original size
    • The chest wall has an elastic recoil that is exactly the opposite of the lungs, tending to pull the thoracic cage outward
76
Q

Compliance?

A
  • Compliance = change in Volume / change in Pressure
    • Ability for large change in volume with small change in pressure
77
Q

Elastance?

A
  • Elastance = change in Pressure / change in Volume
    • The inverse of compliance
    • The tendency to return to initial size after distension
78
Q

Explain how pulmonary fibrosis changes the lungs and its effect on FRC?

A
  • Restrictive disease: pulmonary fibrosis
    • Lungs are stiffened and thus less compliant, therefore significantly increasing lung elastic recoil
    • Increased lung elastic recoil causes lung to contract even more than normal
    • Decrease in FRC
79
Q

Explain how emphysema changes the lungs and its effect on FRC?

A
  • Obstructive disease: emphysema
    • Lungs become more compliant, therefore losing lung elastic recoil
    • Loss of lung elastic recoil prevents lungs from returning to original size after inspiration
    • Increase in FRC
80
Q

How is surfactant generated?

how does it reduce surface tension?

A
  • Generated by type II epithelial cells in the lungs
    • Consists of phospholipids that reduce surface tension
81
Q

Explian surface tension in small alveoli w surfactant

A
  • With surfactant, surface tension is proportional to surface area
    • Because smaller alveoli have less surface area, they have a lower surface tension and thus an equal inflation pressure with larger alveoli
    • This would allow all alveoli to be inflated during inspiration
82
Q

Explian surface tension in small alveoli w/o surfactant

A
  • Without surfactant, surface tension would not be proportional to surface area
    • Smaller alveoli would have much greater inflation pressure than larger alveoli
    • This higher pressure would create a pressure gradient between small and larger, thus collapsing the smaller alveoli
83
Q

Breathing cycle: End of Expiration

What happens?

A
  • Expiration
    • Air flows out of the alveoli until alveolar pressure re-equilibrates with atmospheric pressure
84
Q

Breathing cycle: Before inspiration

What happens?

A
  • Before inspiration begins, PIP = -5cm H2O and PA = 0cm H2O
    • PTP = PA – PIP = 0 – (-5) = +5cm H2O
85
Q

Breathing cycle: inspiration

What happens?

A
  • Inspiration
    • Active process
    • Inspiratory muscles contract, the chest wall expands
    • Lungs are pulled outwards and alveoli distend,
      • As alveolar pressure increases, alveolar volume falls below atmospheric pressure (due to Boyle’s Law: P1V1 = P2V2), allowing air to flow into the lungs
    • Elastic recoil of the chest increases, causing PIP to become more negative
86
Q

Define these terms?

VT, ERV, IRV, RV, TLC, FRC, IC, VC

A

Tidal volume (VT) – the amount of air entering and leaving the lungs with each breath (~500mL)

Expiratory reserve volume (ERV): after a quiet expiration, the amount of air one can expire with maximal effort (~1000mL)

Inspiratory reserve volume (IRV): at the end of a quiet expiration, the additional volume a subject could inhale with maximum effort (~3300mL)

Residual volume (RV) – air that remains behind after a maximal expiratory effort (~1200mL)

Prevents collapse of alveoli

Allows for continuous gas exchange

Total lung capacity (TLC) – the sum of all four volumes

Functional residual capacity (FRC) – ERV + RV; the amount of air remaining inside the respiratory system after a quiet expiration

Inspiratory capacity (IC) – IRV + VT; after a quiet expiration, the maximum amount of air one can still inspire

Vital capacity (VC) – IRV + VT + ERV; the maximal achievable tidal volume; often monitored to follow progress of pulmonary diseases

87
Q

Breathing cycle: end of inspiration

What happens?

A
  • End of Inspiration
    • Inspiratory muscles are still contracted and pulling lungs outward
    • Lung elastic recoil potential is very large
    • Air flows into the alveoli until alveolar pressure equilibrates with atmospheric pressure, and PA = Patm again
    • PIP is at its most negative, meaning its volume has to be at its largest due to strong recoil forces pulling in opposite directions
89
Q

How to calculate PIO2?

A
  • PIO2 = FO2 * (Patm - PH2O)
    • FO2 = 0.21
    • Patm = 760 mmHg – this decreases with altitude
    • PH2O = 47 mmHg
90
Q

Describe the Hb-02 disscociation curve

A
91
Q

What are the partial pressures for arterial and venous O2 and Co2

A
  • Alveolar and arterial PO2 = 100 mmHg
  • Alveolar and arterial PCO2 = 40 mmHg
  • Venous PO2 = 40 mmHg
  • Venous PCO2 = 45 mmHg
92
Q

anatomic versus alveolar versus physiologic dead space

A
  • Anatomic dead space – air in the conducting pathways that is unable to diffuse due to thickness of walls
  • Alveolar dead space – the volume of gas that enters unperfused alveoli; these alveoli are ventilated but not perfused, therefore no gas exchange occurs
  • Physiologic dead space = anatomic dead space + alveolar dead space
    • In healthy people, physiologic dead space = anatomic dead space
94
Q

CO versus O2 binding affinity

A

CO has a 200x binding affinity for hemoglobin than O2

95
Q

Compare loading of oxygen in lungs and unloading at tissues.

A
  • Lungs: higher partial pressure of oxygen means hemoglobin has a higher affinity for O2 and CO2 will dissociate
  • Tissues: lower partial pressure of oxygen means hemoglobin has a lower affinity for O2 and it will dissociate and pick up CO2
96
Q

name the 3 ways CO2 is carried in blood

A
  • Carried in the blood in three states
    • In physical solution
    • Chemically combined with amino acids in blood proteins (mostly Hb) – carbamino compounds; deoxy-Hb can bind more CO2 than oxy-Hb. As hb in the venous blood enters the lung and combines with O2, it releases CO2
    • As bicarbonate (Hb also binds up hydrogen ion)
97
Q

What is the bohr effect

A
  • Bohr effect – for any PO2, hemoglobin has a higher affinity for CO2 than O2, causing O2 unloading
    • Anything that shifts the Hb-O2 curve to the right
    • Takes place in the tissues
98
Q

what is the haldane effect?

A
  • Haldane Effect – for any PO2, hemoglobin has a higher affinity for O2 than CO2, causing CO2 unloading
    • Anything that shifts the Hb-O2 curve to the left
    • Takes place in the lungs
99
Q

Define the factors affecting alveolar PCO2

A
  • PACO2 ­~ VCO2 / VA
    • VA (alveolar ventilation)
      • Hyperventilation – elevation of VA causes PACO2 ­to be depressed (respiratory alkalosis)
      • Hypoventilation – depression of causes PACO2 ­to be elevated (respiratory acidosis)
    • VCO2 (metabolic rate) – for PACO2 ­to remain constant changes in CO2 output (i.e. exercise) must be matched with changes in alveolar ventilation
100
Q

Equation for PaO2

A
  • PAO2 ­= FO2 * (Patm - PH2O) – (PACO2 / R)
    • R = respiratory exchange ratio; normally 0.8
101
Q

Describe regional differences in V/Q ratios.

A
  • High V/Q: top of the lung because it is ventilated but not perfused
  • Low V/Q: bottom of the lung because blood flow exceeds ventilation (lower PO2 and higher PCO2)
102
Q

Define low V/Q

A
  • Low V/Q
    • Low ventilation or high blood flow
    • Alveolus at the base of the lung (perfusion exceeds ventilation)
    • PAO2 < 100mmHg, PACO2 > 40mmHg
103
Q

define high V/Q

A
  • High V/Q
    • High ventilation or low blood flow
    • Alveolus at the apex of the lung (ventilation exceeds perfusion)
    • PAO2 > 100mmHg, PACO2 < 40mmHg
    • Adds only small amount of O2 to the blood compared to normal
    • Note: this does not mean that ventilation is greater at the apex of the lung!
104
Q

when V/Q = infinity what clinically is going on?

what are the compensatory responses?

A
  • V/Q =
    • Blood flow is blocked by a pulmonary embolus
    • Alveolus is ventilated but not perfused
    • Becomes effectively alveolar dead space
    • Compensatory responses to alveolar dead space ventilation
      • Local PACO2 = 0 causes local respiratory alkalosis in the surrounding interstitial fluid
      • This alkalosis produces a compensatory bronchial constriction in the adjacent tissues
      • Airflow then diverts toward normal alveoli, which also have increased blood flow, and V/Q mismatch is corrected
105
Q

when V/Q = 0 what clinically is going on?

what are the compensatory responses?

A
  • V/Q = 0
    • Airway is completely occluded by a foreign body or tumor
    • Alveolus is perfused by not ventilated: air inside the alveolus will equilibrate with gas dissolved in the mixed venous blood
    • Acutely, right-to-left shunt occurs: deoxygenated venous blood from right side of heart goes through alveolus that does not participate in gas exchange and returns in deoxygenated state back to left side of the heart
    • Compensatory responses to shunt
      • Hypoxic pulmonary vasoconstriction – alveolar hypoxia (due to lack of O2 exchange from blockage), causes acidosis due to high CO2
      • This causes active vasoconstriction of the capillaries and blood is diverted away from poorly ventilated areas of the lung
106
Q

how to calculate A-a gradient?

what is a normal gradient?

A
  • P(A-a) * O2 = the alveolar – arterial O2 difference
  • PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure
  • PaO2 is always measured, on an arterial blood sample in a blood gas machine
  • Physiologic and normal anatomic shunts cause the normal A-a gradient to be 5 to 15 mmHg breathing room air
107
Q

what does a high A-a gradient indicate?

A

A higher than normal A-a gradient means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries

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