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Cardiovascular Summit3/5/16
How High Altitude Effects Us
2
What is High Alt i tude ?
5000 – 8000 Moderate Altitude 8000 - 12000 High Altitude 12000 – 18000 Very High Altitude 18000+ Extreme Altitude
High A l t i tude Popu lat ions• Most permanent high altitude dwellers show excellent adaption. >140 million people live above 2500 m (8200’).• Adaption to altitude appears to relate to duration and genetics. Ethiopia - oldest and most completely adapted 70000 years 2400 meters 5000 years >2500 meters Amhara (3000-3500 m) Himalayas – 5000 years Andes - 1000-2000 years Rocky Mountains - youngest and least adapted
Population of Summit Co
• 12000 yrs ago Indian Hunter Gatherers
• 4800 B.C. Ute Indians• 1859 (GOLD RUSH) ~10000• WW 1 ~1000• 1970 2665• 1980 8848
(232%)• 1990 12881
(45%)• 2000 23548
(83%)• 2010 29626
(26%)• 2020 *38788
(31%)• 2025 *43943
(13%)
*Summit County growth projections (www.co.summit.co.us/planning/demographics.html
D i ff e r e n c e s I n H y p o x i c Re s p o n s e s
Groves et al. JAP 1993)
High Altitude Cardiology Conditions
HYPOXIA(Sleep Apnea)
Systemic Hypertensio
nPulmonary Hypertension
ArrhythmiasCoagulation?
Coronary Spasm ?
Heart Failure-Diastolic
Dysfunction
Altitude Related Conditions
Acute Mountain Sickness (AMS) High-Altitude Pulmonary Edema (HAPE) High-Altitude Cerebral Edema (HACE) High-Altitude Pulmonary Hypertension(HAPH) High-Altitude Hypertension Arrhythmias may be induced Sleep Apnea Suicide (17.7 vs 5.7 per 100,000 pop.) Skin Cancer Increased longevity (81.3 vs 78 yrs: high vs sea level) Less obesity, heart dis, diabetes and cancer
HIF-1 alpha
Effects of Hypoxia on Pulmonary & Systemic Physiology
Bärtsch P , and Gibbs J S R Circulation 2007;116:2191-2202
PAH: Hemodynamic and Clinical Course
NORMAL
Time
PAP
PVR
CO
INYHA
Adventitia
Media
Intima
Adapted from Gaine S. JAMA. 2000;284:3160-3168.
NORMAL
Adventitia
Media
Intima
REVERSIBLE DISEASE
Time
PAP
PVR
CO
I II III
BNP
NYHA
PAH: Hemodynamic and Clinical Course
Smooth Muscle Hypertrophy
Early Intimal Thickening
Adapted from Gaine S. JAMA. 2000;284:3160-3168.
NORMAL
Adventitia
Media
Intima
Smooth Muscle Hypertrophy
Early Intimal Thickening
REVERSIBLE DISEASE
IRREVERSIBLE DISEASE
Plexiform Lesions
Thrombosis
Adventitial, Intimal Proliferation
Smooth Muscle Hypertrophy
Time
PAP
PVR
CO
I II III IV
BNP
NYHA
PAH: Hemodynamic and Clinical Course
Adapted from Gaine S. JAMA. 2000;284:3160-3168.
Mechanisms of Action of Therapies for PH
Humbert M et al. N Engl J Med. 2004;351:1425-1436.
cGMP
cAMP
Vasoconstriction and proliferation
Endothelinreceptor A
Exogenous nitric oxide
Endothelin-receptor
antagonists
Endothelinreceptor B
Phosphodiesterase type 5 inhibitor
Vasodilatationand antiproliferation
Phosphodiesterase type 5
Vasodilatationand antiproliferation
Prostacyclin derivatives
Nitric Oxide
Endothelin-1
Pre-proendothelin
L-arginine
Prostaglandin I2
L-citrulline
Nitric OxidePathway
EndothelinPathway
ProstacyclinPathway
Endothelial cells
Proendothelin
Endothelial cells
Arachidonic acid
Smooth muscle cells
Prostacyclin (prostaglandin I2)
Smooth muscle cells
RIGHT HEART CATHETERIZATION HEMODYNAMICS
Date 2/14/2012Patient/DOB #5/45 yrsHeight 62"/157 cmWeight 180lbs/82kgBSA 1.83Hgb 16.3
Baseline Rest w/O2 Bike rest Bike Rm Air Bike Rm Air Bike Rm Air Bike O2/res t Bike O2 Bike O2 Bike O2HR 76 60 82 103 139 160 94 104 131 155BP 127/76 119/80 142/93 150/80 166/110 180/110 140/96 170/94 182/94 210/120BP mean 85 93 109 103 129 133 111 119 123 150Watts 0 25 75 100 0 25 75 100Sx/RPE 2 4 7 4 6Minutes 10 3 3 3 3 5 3 3 3FIO2% Rm Air 100% Rm Air Rm Air Rm Air Rm Air 100%NRB 100%NRB 100%NRB 100%NRBArt O2 sat 96 100 92 88 91 87 100 100 100 98RA O2 sat 56RA mmHg 16/10RA mean 13 12 4 11 8 5 3 6 3 3PA O2 sat 61 76 45 35 26 25 46 38 54PA mmhg 51/24 38/19 30/13 67/36 95/50 97/50 39/18 43/20 51/24 61/29PA mean 36 25 21 49 67 67 27 30 35 40PAW mmHg 18/12 21/15 12/5 15/9 26/10 10/4 16/9 20/11 25/5PAW mean 14 19 9 11 17 13 6 12 17 12CO 4.9 4 5.2 14.6 7 8.1 14.6 16.2CI 2.7 2.2 2.8 3.8 3.8 4.4 8.0 8.9PVR Woods 4.5 1.5 2.3 3.7 3.0 2.2 1.2 1.7PVR dynes 359 120 185 296 240 178 99 138SVR Woods 14.7 20.3 20.2 8.8 15.4 14.0 8.2 9.1SVR dynes 1176 1620 1615 701 1234 1116 658 726
Right Heart Cath PAH
Baseline 25w 75w 100w 150w0
20
40
60
80
100
120
mPAP '12mPAW '12O2 Sat '12mPAW '13mPAP '13O2 Sat'13
O2 sat ’12 &’13
mPAW ‘13
mPAP ‘13
mPAW ‘12
mPAP‘12
R i g h t H ea r t C a t h - E xe rc i seRoo m a i r a n d 1 0 0 % O 2
Rest Rm Air Rest 100% O2
Ex Rm Air Ex 100% O20
1020304050607080
mPAP
PVR
4.5
1.5
3.7
1.7
PVR 3 Woods
36
67
40mPAP
25
Maximum Work Load Decreases With Altitude
300' 3300' 5000' 6600' 9900'
-35
-30
-25
-20
-15
-10
-5
0
NormalMild HFSevere HF
Per
cent
cha
nge
Agostoni. Am J Med 2000;109:450-455:
T h a n k s f o r Yo u r At t e n t i o n
Mechanisms of Action of Therapies for PH
Humbert M et al. N Engl J Med. 2004;351:1425-1436.
cGMP
cAMP
Vasoconstriction and proliferation
Endothelinreceptor A
Exogenous nitric oxide
Endothelin-receptor
antagonists
Endothelinreceptor B
Phosphodiesterase type 5 inhibitor
Vasodilatationand antiproliferation
Phosphodiesterase type 5
Vasodilatationand antiproliferation
Prostacyclin derivatives
Nitric Oxide
Endothelin-1
Pre-proendothelin
L-arginine
Prostaglandin I2
L-citrulline
Nitric OxidePathway
EndothelinPathway
ProstacyclinPathway
Endothelial cells
Proendothelin
Endothelial cells
Arachidonic acid
Smooth muscle cells
Prostacyclin (prostaglandin I2)
Smooth muscle cells
PULMONARY HYPERTENSION CLASSIFICATION
I Idiopathic PH/Hereditary PH(BMPR2) 70%+ Drugs & toxins, connective tissue disease, HIV,
cong. heart disease, persistent PH of the new born, and a few others.
II PH assoc with left heart disease.III PH assoc with hypoxemia (lung disease, sleep
apnea, HAPH)IV Thromboembolic PH (acute and chronic) V Unclear multifactorial mechanisms (hematologic,
systemic[sarcoid, histicytosis, vasculitis] thyroid, dialysis, fibrosing mediastinitis, tumors
*JACC Vol. 54, No.1, Suppl S, 2009 6/30/2009,555-66
Pu lmonary Hyper tens ion Preva lence - USA
• IPAH 5.9/million• PE 3-5 %• Scleroderma 21-26%• Heart Failure• Lung Disease• High Altitude ??%
Non-Acclimated Response To High Altitude At Rest
• Increased ventilation• Increased heart rate• Increased cardiac output• Increased blood pressure• Increased pulmonary pressure
Acute Mountain Sickness Symptoms
• Headache• Nausea / Vomiting• Fatigue or Weakness• Dizziness or Lightheadedness• Difficulty Sleeping
Acute Mountain Sickness• Caused by rapid ascent• Symptoms occur around 3000 m (9842 ft)• Develop 4-12 hours after ascent• Resolve in 3-7 days
• People with known disease and/or arrhythmias, increased age, acute altitude exposure, and exercise should use caution and acclimate for several days. Limit stimulants and alcohol, hydrate.
• People with high risks (family history, hypertension, diabetes, abnormal lipids, known disease, elderly) should have a cardiovascular evaluation.
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