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213 Cards in this Set
- Front
- Back
Loss of isotonic fluid
(urine, hemorrhage, diarrhea/vomiting) |
Loss of ECV
|
|
Loss of hypotonic fluid
(sweating, Diabetes insipidus) |
Loss of ECV and ICV
(RBCs shrink) |
|
Gain of hypotonic fluid
(drinking water) |
Gain of ICV and ECV
(RBCs swell) |
|
Infusion of hypotonic fluid
|
Gain of ICV and ECV
(RBCs swell) |
|
Infusion of isotonic saline
|
Gain of ECV only
(no effect on RBCs size, used to increase BP) |
|
Infusion of hypertonic saline
|
Loss of ICV, Gain of ECV
(RBCs shrink) |
|
Loss of sodium
(Hypertonic loss) |
Loss of ECV, Gain of ICV
(RBCs grow) |
|
The SA and AV node are supply but what artery?
|
Right coronary Artery (RCA)
|
|
Most common site of coronary occlusion
|
Left anterior descending artery (LAD)
|
|
Coronary artery that supplies posterior left ventricle
|
circumflex artery (CFX)
|
|
Coronary artery that supplies apex and anterior interventricular septum
|
Left anterior descending artery (LAD)
|
|
Coronary artery that supplies posterior septum
|
Posterior descending/interventricular artery (PD)
|
|
Coronary artery that supplies right ventricle
|
acute marginal artery
|
|
The most posterior chamber of the heart
|
Left atrium
|
|
The most anterior chamber of the heart
|
Right ventricle
|
|
Cardiac output formula
|
rate of O2 consumption/
(arterial O2 content - venous O2 content) |
|
Mean arterial pressure (MAP) formula
|
cardiac output x TPR
(2/3 diastolic pressure + 1/3 systolic) |
|
Stroke volume affected by what?
|
Preload, Afterload, contractility
|
|
Contractility (and Stoke Volume) increases with what?
|
- catecholamines
- Digitalis |
|
Contractility (and Stroke Volume) decreases with what?
|
- Beta1-blockers
- Ca+ channel blockers - Acidosis - Hypoxia/Hypercapnia(CO2) |
|
Venodilators (ie. NO) decrease what?
|
decreases preload
|
|
Vasodilators (ie Hydralazine) decrease what?
|
decrease afterload
|
|
Examples of Right-to-left shunts that causes (early cyanosis "blue babies")
|
- Tetralogy of Fallot
- Transposition of great vessels - Truncus arteriosus - Tricuspid atresia - Total anomalous pulmonary trunk and aorta (TAPVR) |
|
Examples of Left-to-right shunts that causes (late cyanosis "blue kids
|
- VSD
- ASD - PDA |
|
Uncorrected VSD, ASD, or PDA can lead to?
|
Eisenmenger's syndrome
-reversal of L->R to R->L |
|
Clinical finds of Tetralogy of Fallot
|
PROVe
1- Pulmonary stenosis 2- Right Ventricular hypertrophy 3- Overriding aorta 4- VSD (Pt will have boot shape heart; cyanotic spells) |
|
Clinical finds of D-transposition of great vessels
|
- aorta leaves right ventricle (anterior)
-pulmory trunks leaves left ventricle (posterior) -Pt must have: VSD, PDA, or patent ovale for life |
|
Coarctation of the aorta type?
- associate w/Turner's - proximal to insertion of ductus arteriosus |
Infantile type
|
|
Coarctation of the aorta type?
- associated w/notching of the ribs - distal to insertion of ductus arteriosus |
Adult type
|
|
Closes PDA
|
Indomethacin
|
|
Keeps PDA open
|
Misoprostol
|
|
Cogenital cardiac defect association
- Defect: Tetralogy of Fallot; truncus arteriosus - Disorder: ? |
DiGeorge's (22q11)
|
|
Cogenital cardiac defect association
- Defect: ASD, VSD, AV septal defect (endocardial cushion defects) - Disorder: ? |
Down Syndrome
|
|
Cogenital cardiac defect association
- Defect: PDA - Disorder: ? |
Congenital rubella
|
|
Cogenital cardiac defect association
- Defect: Coarctation of aorta - Disorder: ? |
Turner's
|
|
Cogenital cardiac defect association
- Defect: Aortic insufficiency; Dissection of Aorta - Disorder: ? |
Marfan's Syndrome
|
|
Cogenital cardiac defect association
- Defect: Transposition of great vessels - Disorder: ? |
Infant of a diabetic mother
|
|
Primary HTN (90%) is related to?
|
increase Cardiac output or increase TPR
|
|
Secondary HTN (10%) is related to?
|
renal disease
|
|
Arteriosclerosis
- calcification of the media (especially radial or ulnar) - benign; "pipestem" - do not obstruct flow |
Monckeberg
|
|
Arteriosclerosis
- Hyaline thickening - seen in HTN and diabetes - Hyperplastic- "onion skinning" in malignant HTN |
ArteriOlOsclerosis
|
|
Arteriosclerosis
- Fibrous plaques and atheromas from in the intima of arteries |
ATHERosclerosis
|
|
Ischemic heart disease
- ST depression in ECG - pain on exertion - relieved by nitrate |
Stable Angina
|
|
Ischemic heart disease
- occurs at rest 2nd to coronary artery spasm - ST elevation on ECG |
Prinzmetal's variant angina
|
|
Ischemic heart disease
- thrombosis but no necrosis - ST depression on ECG - nitrates don't work - pain without exertion |
Unstable Angina
|
|
Ischemic heart disease
- acute thrombosis due to atherosclerosis - results in myocyte necrosis - LDA most common site; increase troponin |
myocardial infarction (MI)
|
|
Ischemic heart disease
- death within 1 hour of onset - commonly due to a lethal arrhythmia |
Sudden cardiac death
|
|
Ischemic heart disease
- progressive onset of CHF over many years - due to myocardial damage |
Chronic ischemic heart disease
|
|
Chest pain that worsens by sitting up or leaning forward
|
Pericarditis
|
|
Evolution of MI- time frame?
- contraction bands - earl coagulative necrosis - neutrophil emigration |
First Day
|
|
Evolution of MI- risk?
- First Day |
- contraction bands
- earl coagulative necrosis - neutrophil emigration |
|
Evolution of MI- time frame?
- tissue surrounding infarct shows acute inflammation - increased neutrophil emigration - dilated vessels (hyperemia) - muscle show extensive coagulative necrosis |
2-4 days
|
|
Evolution of MI- risk?
- 2-4 days |
- tissue surrounding infarct shows acute inflammation
- increased neutrophil emigration - dilated vessels (hyperemia) - muscle show extensive coagulative necrosis |
|
Evolution of MI- time frame?
- risk for free wall rupture - tamponade - papillary muscle rupture - interventricular septal rupture - dues to macrophages degrading structural components |
5-10 days
|
|
Evolution of MI- risk?
- 5-10 days |
- risk for free wall rupture
- tamponade - papillary muscle rupture - interventricular septal rupture - dues to macrophages degrading structural components |
|
Evolution of MI- time frame?
- Risk for ventricular aneurysm - contraction scar complete |
7 weeks
|
|
Evolution of MI- risk?
- 7 weeks |
- Risk for ventricular aneurysm
- contraction scar complete |
|
Diagnosis of MI
- Gold standard in the first 6 hours |
ECG
|
|
Diagnosis of MI
- rises after 4 hour and is elevated for 7-10 days - most specific protein marker |
Troponin I
|
|
Diagnosis of MI
- predominantly found in myocardium but is also release in skeletal muscle - useful in diagnosing reinfarction on top of acute MI - seen for 3 days |
CK-MB
|
|
Diagnosis of MI
- nonspecific - can be found in cardiac, liver, and skeletal muscle - if cardiac no ALT will be seen |
AST
|
|
ECG diagnosis of MI
Leads: V1-V4 Location: ? |
Anterior wall
|
|
ECG diagnosis of MI
Leads: V1-V2 Location: ? |
Anteroseptal
|
|
ECG diagnosis of MI
Leads: V4-V6 Location: ? |
Anterolateral
|
|
ECG diagnosis of MI
Leads: I & aVL Location: ? |
Lateral wall
|
|
ECG diagnosis of MI
Leads: II, III, & aVF Location: ? |
Inferior wall
|
|
MI complication
- important cause of death before reaching the hospital - common in first 3 days |
Cardiac arrhythmia
|
|
MI complication
- autoimmune phenomenon - results in fibrinous pericarditis - several weeks post-MI |
Dressler syndrome
|
|
Cardiomyopathy
-Dilated (congestive) "Systolic Heart failure" Cause: ? |
- Alcohol abuse
- wet Beriberi - Coxsackie B - Cocaine - Chagas' - Doxorubicin - Hemochromatosis |
|
Cardiomyopathy
-Findings: S3 Myopathy: ? |
Dilated (congestive) "Systolic Heart failure"
|
|
Cardiomyopathy
-Hypertrophic "Diastolic Heart failure" Cause: ? |
- IV septum too close to mitral valve
- familial; autosomal dominant - friedreich's ataxia - sudden death in athletes |
|
Cardiomyopathy
-Findings: S4, apical impulses, systolic murmur Myopathy: ? |
Hypertrophic "Diastolic Heart failure"
|
|
Treatment for Hypertrophic "Diastolic Heart failure"
|
beta-blockers & Ca+ channel blockers
|
|
Cardiomyopathy
-Restrictive/obliterative "Diastolic Heart failure" Cause: ? |
- sarcoidosis
- amyloidosis - fibrosis - seen w/ rheumatoid arthritis - Loffler's syndrome |
|
Presence of hemosiderin-laden macrophages are known as
|
Heart failure cell (in the lung)
|
|
Round white spots on the retina surrounded by hemorrhage
|
Roth's spots
|
|
Roth spots are a sign of
|
Endocarditis
|
|
Tender raised lesion on finger or toe pads are know as
|
Osler's nodes
|
|
Osler's nodes are a sign of
|
Endocarditis
|
|
Small erythematous lesion on palm or sole is
|
Janeway lesion
|
|
Janeway lesions is a sign of
|
Endocarditis
|
|
The main signs of Endocarditis
|
- Fever
- new murmur - Janeway lesions - splinter hemorrhages |
|
Bacterial endocarditis
- large vegetations on previously normal valves - rapid on set - high virulence |
Acute- S. aureus
|
|
Bacterial endocarditis
- smaller vegetation on conenitally abnormal or disease valves - after dental procedure - slow on set - low virulence |
Subacute- Strep. viridans
|
|
Bacterial endocarditis
- present in Pts w/colon cancer |
S. bovis
|
|
Bacterial endocarditis
- present on prosthetic valves |
S. epidermidis
|
|
Bacterial endocarditis
- most common valve involved |
Mitral
|
|
Bacterial endocarditis
- valve associated with IV drug absue |
Tricuspid
|
|
- Verrucous (wart-like)
- Sterile vegetations located on both side of the valve - associated with mitral regurgitation |
Libman-Sacks
|
|
Cause of Libman-Sacks
|
SLE (lupus)
|
|
Organism that causes Rheumatic heart disease
|
beta-hemolytic strep. "Group A"
(S pyogenes) |
|
Underlying pathology of Rheumatic heart disease
|
Antibodies to M-protein
(type II hypersensitivity) |
|
Elevated in Rheumatic heart disease
|
ASO titers
|
|
Granuloma with giant cells seen in Rheumatic heart disease
|
Aschoff bodies
|
|
Activated histiocytes seen in Rheumatic heart disease
|
Anitschkow cells
|
|
-Exaggerated decrease amplitude of pulse during inspiration
- seen in cardiac tamponade, asthma, sleep apnea, pericarditis, and croup |
Pulsus paradoxus
|
|
- calcification of the aortic root and ascending aortic arch
- tree bark appearance - dilation of the aorta and valve ring |
Syphilitic heart disease
(tertiary) |
|
Most common site of a Myxoma
|
Left atrium
|
|
- associated with multiple syncopal episodes
- "ball-valve" obstruction - in left atrium |
Myxoma
|
|
Most frequent cardiac tumor in children
|
Rhabdomyomas
|
|
Rhabdomyomas are frequently associated with?
|
Tuberous sclerosis
|
|
Metastasis to the heart is most common from?
|
Melanoma & lymphoma
|
|
Increase in jugular venous pressure on inspiration
|
Kussmaul's sign
|
|
Treatment for Raynaud's disease
|
Nifedipine (Ca+ channel blocker)
|
|
Causes of Raynaud's phenomenon
|
- SLE
- CREST - Scleroderma - Buerger's |
|
- Necrotizing vasculitis
- necrotizing granulomas in upper and lower respiratory - necrotizing glomerulonephritis |
Wegener's granulomatosis
|
|
Treatment for Wegener's granulomatosis
|
Cyclophosphamide and corticosteroids
|
|
Vasculitides that is ike Wegener's but p-ANCA
|
Microscopic polyangiitis
|
|
- Vasculitis limited to kidney
- pauci-immune= paucity of antibodies |
Primary pauci-immune crescentic glomerulonephritis
|
|
- granulomatous vasculitis with eosinophilia
- presents w/ asthma, sinusitis, skin lesions, and wrist/foot drop |
Churg-Strauss syndrome
|
|
- port-wine stain on face (nevus flammeus)
- leptomeningeal angiomatosis (intracerebral AVM) - seizures - early- onset glaucome |
Sturge-Weber disease
|
|
- rash on buttocks and legs (palpable purpura)
- arthralgia (joint pain) - intestinal hemorrhage, Abdominal pain - follows URIs and associated w/IgA nephropathy - Most common childhood systemic vasculitis |
Henoch-Schonlein
|
|
- intermittent claudication
- superficial nodular phlebitis - cold sensitivity (Raynauds) - seen in heavy smokers |
Buerger's
(Thromboangiitis obliterans) |
|
- strawberry tongue; lymphadenitis
- may develop coronary aneurysms - self-limiting necrotizing vasculitis in infants/child |
Kawasaki disease
|
|
- immune complex-mediated transmural vasculitis w/fibrinoid necrosis
- fever, weight loss, malaise - Multiple aneurysms; Hep B+ |
Polyarteritis nodosa
|
|
- granulomatous thickening of aortic arch
- associated w/ increase ESR - weak pulse "pulseless disease" |
Takayasu's arteritis
|
|
- vasculitis usually affecting carotid artery
- granulomatous inflammation - jaw claudication, unilateral headache, impaired vision - associated w/elderly females & increased ESR |
Temporal arteritis
(giant cell arteritis) |
|
Vascular tumor
- benign capillary hemangioma of infancy; - grows with child; than spontaneously regress |
Strawberry hemangioma
|
|
Vascular tumor
- benign capillary hemangioma of the elderly - does not regress |
Cherry hemangioma
|
|
Vascular tumor
- polypoid capillary hemangioma that can ulcerate and bleed - associated w/trauma and pregnancy |
Pyogenic granuloma
|
|
Vascular tumor
- Cavernous lymphangioma of the neck - associated w/Turner's |
Cystic hygroma
|
|
Vascular tumor
- Benign, painful, red-blue tumor under fingernails - arises from modified smooth muscle cells of glomus body |
Glomus tumor
|
|
Vascular tumor
- Benign capillary skin papules found in AIDS Pts - often mistake for Kaposi's |
Bacillary angiomatosis
|
|
Vascular tumor
- High lethal malignancy of the liver - associated w/vinyl chloride, arsenic, and ThO2 (thorotrast) |
Angiosarcoma
|
|
Organism that cause Bacillary angiomatosis
|
Bartonella henselae
|
|
Vascular tumor
- Lymphatic malignancy associated w/persistent lymphedema -post-radical mastectomy |
Lymphangiosarcoma
|
|
Vascular tumor
- Endothelial malignancy of the skin associated with HHV-8 and HIV - often mistaken as bacillary angiomatosis |
Kaposi's sarcoma
|
|
Accounts for most of the total peripheral resistance (TPR)
|
Arterioles
|
|
Cardiac Cycle (phase)
-period of highest O2 consumption -period between mitral valve closure and aortic valve opening |
Isovolumetric contaction
|
|
Cardiac Cycle (phase)
-period between aortic opening and closing |
Systolic ejection
|
|
Cardiac Cycle (phase)
- period between aortic valve closing and mitral valve opening |
Isovolumetric relaxation
|
|
Cardiac Cycle (phase)
-period just after mitral valve opens |
Rapid filling
|
|
Cardiac Cycle (phase)
-period just before mitral valve closes |
Reduced filling
|
|
Cardiac Cycle (sound)
- loudest at mitral area - mitral and tricuspid valve closure |
S1
|
|
Cardiac Cycle (sound)
- loudest at the left sternal border - aortic and pulmonary valve closure |
S2
|
|
Cardiac Cycle (sound)
- in early diastole during rapid ventricular filling phase - associated w.increase filling pressures - more common in dilated ventricles |
S3
|
|
S3 is normal when heard in
|
- Child
- pregnant women - post-MI |
|
Cardiac Cycle (sound)
- heard in late diastole - increased atrial pressure - left atrium must push against stiff LV wall - associated w/ventricular hypertrophy |
S4 (atrial kick)
|
|
S2 splitting
- wide splitting - Associated with: ? |
- Pulmonic stenosis
- Right bundle branch block |
|
S2 splitting
- Fixed splitting - Associated with: ? |
- ASD
|
|
S2 splitting
- Paradoxical splitting - Associated with: ? |
- Aortic stenosis
- Left bundle branch block |
|
Right-sided heart sounds increase with?
|
Inspiration
|
|
Left-sided heart sounds increase with?
|
Expiration and increased Carbon monoxide
|
|
Holosystolic (pansystolic), high-pitched "blowing murmur"
|
Mitral/tricuspid regurgitation
|
|
Heart murmur
- loudest at apex - radiates toward axilla |
Mitral regurgitation
|
|
What will enhance a mitral regurgitation?
|
maneuvers that increase TPR (squatting/hand grip)
|
|
Causes of mitral regurgitation?
|
- ischemic heart disease
- mitral valve prolapse - left ventricular dilaticulation |
|
Heart murmur
- radiates to the right sternal border - enhanced by (inspiration) maneuvers that increase RA return |
Tricuspid regurgitation
|
|
Causes of tricuspid regurgitation?
|
- RV dilation
- endocarditis "Rheumatic fever can cause both" |
|
Crescendo-decrescendo systolic ejection murmur following ejection click
|
Aortic stenosis
|
|
Heart murmur
- Radiates to carotids/apex - "pulsus parvus et tardus" weak pulse - leads to syncope |
Aortic stenosis
|
|
Cause of Aortic stenosis?
|
- age related calcification
- bicuspid of the valve |
|
Holosystolic (pansystolic), harsh-sounding murmur
Loudest at tricuspid area |
VSD
|
|
Late/Mid systolic crescendo murmur with midsystolic click
|
Mitral valve prolapse
|
|
Cause of midsystolic click in mitral valve prolapse
|
sudden tensing of chordae tendineae
|
|
Heart murmur
- Loudest at S2 - can predispose to endocarditis - most frequent valvular lesion |
Mitral valve prolapse
|
|
Cause of mitral valve prolapse
|
- myxomatous degeneration
- rheumatic fever - chordae rupture |
|
Immediate high-pitched "blowing" diastolic murmur
|
Aortic regurgitation
|
|
Heart murmur
- wide pulse pressure - presents w/head bobbing and bounding pulses |
Aortic regurgitation
|
|
Cause of Aortic regurgitation
|
- aortic root dilation
- bicuspid aortic valve - rheumatic fever |
|
Decreases intensity of Aortic regurgitation
|
Vasodilators
(nitrates) |
|
Heart murmur
- follows opening snap - LA>>LV pressure during diastole |
Mitral stenosis
|
|
Causes of Mitral stenosis
|
- rheumatic fever
- chronic MS |
|
Heart murmur
- loudest at S2 - continuous machine-like murmur |
PDA
|
|
Cardiac myocytes in contrast to skeletal muscle
|
1. action potential has a plateau (due to Ca+ influx)
2. nodal cells spontaneously depolarize during diastole 3. electrically couple by gap junctions |
|
Ventricular action potential: phase?
- rapid upstroke - voltage gated Na+ channels open |
Phase 0
|
|
Ventricular action potential: phase?
- initial repolarization - inactivation of voltage-gated Na+ channels - voltage-gated K+ channels begin to open |
Phase 1
|
|
Ventricular action potential: phase?
- plateau - Ca2+ influx through voltage-gated channels balances K+ efflux - Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum - myocyte contraction |
Phase 2
|
|
Ventricular action potential: phase?
- rapid repolarization - massive K+ efflux due to opening of voltage-gated slow K+ channels - closure of Ca2+ channels |
Phase 3
|
|
Ventricular action potential: phase?
- resting potential - high K+ permeability through K+ channels |
Phase 4
|
|
Pacemaker action potential: phase?
- upstroke - opening of voltage-gated Ca2+ channels (not fast) therefore no plateau |
Phase 0
|
|
Pacemaker action potential: phase?
- inactivation of Ca2+ channels - increase activation of K+ channels -> efflux |
Phase 3
|
|
Pacemaker action potential: phase?
- slow diastolic depolarization - membrane potential spontaneously depolarizes - accounts for automaticity of SA/AV node |
Phase 4
|
|
Electrocardiogram (ECG) read
- atrial depolarization |
P wave
|
|
Electrocardiogram (ECG) read
- conduction delay through AV node |
PR interval
|
|
Electrocardiogram (ECG) read
- ventricular depolarization |
QRS complex
|
|
Electrocardiogram (ECG) read
- mechanical contraction of the ventricles |
QT interval
|
|
Electrocardiogram (ECG) read
- ventricular repolarization |
T wave
|
|
Inverted T wave indicates
|
Recent MI
|
|
Electrocardiogram (ECG) read
- isoelectric, ventricles depolarized |
ST segment
|
|
Electrocardiogram (ECG) read
- hypokalemia, bradycardia |
U wave
|
|
Pt present with severe congenital sensorineural deafness
(Jervell and Lange-Nielsen) |
Torsades de pointes
(congenital long QT syndrome) |
|
Torsades de pointes (congenital long QT syndrome) can progress to?
|
V-fib
|
|
Torsades de pointes (congenital long QT syndrome) most due to?
|
Ca+ & K+ channel defects
|
|
- delta wave
- accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node - ventricular preexcitation |
Wolff-Parkinson-White syndrome
|
|
Electrocardiogram (ECG) Tracing
- chaotic and erratic baseline (irregularly irregular) - no discrete P waves - can result in stasis |
Atrial Fibrillation
|
|
Treatment of Atrial fibrillation
|
- beta blockers
- calcium blockers |
|
Electrocardiogram (ECG) Tracing
- rapid succession of identical, back-to-back waves - sawtooth apperance |
Atrial Flutter
|
|
Treatment for Atrial Flutter
|
- Class Ia & Ic
- Class III |
|
Electrocardiogram (ECG) Tracing
- prolong PR interval (>200 msec) - asymotomatic |
First degree Heart block
|
|
Electrocardiogram (ECG) Tracing
- progressive lengthening of the PR interval until a beat is "dropped" - P wave not followed by a QRS complex - "asymptomatic" |
Second degree heart block
(Mobitz type I) |
|
Treatment for Second degree heart block (Mobitz type I).
|
Atropine
|
|
Electrocardiogram (ECG) Tracing
- Dropped beats w/no length chance of PR interval |
Second degree heart block
(Mobitz type II) |
|
Treatment for Second degree heart block (Mobitz type II)
|
Pacemaker
|
|
Electrocardiogram (ECG) Tracing
- atria and ventricles beat independently - both P and QRS present (but bear no relation) - atrial rate faster than ventricles |
Third degree Heart block
|
|
Electrocardiogram (ECG) Tracing
- complete erratic rhythm w/no identifiable wave - fatal arrhythmia w/out intervention |
Ventricular fibrillation
|
|
Treatment for ventricular fibrillation
|
- CPR
- Shock (defib) |
|
Receptors in the aortic arch responses to?
|
increase in BP only
|
|
Receptors in the carotid sinus responses to?
|
both increase and decrease in BP
|
|
Aortic arch receptors are transmitted via?
|
Vagus
|
|
Carotid sinus receptors are transmitted via?
|
Glossopharyngeal
|
|
Peripheral chemoreceptors in the carotid and aortic bodies respond to?
|
- decrease oxygen
- decrease pH of blood |
|
Central chemoreceptors in the brain respond to?
|
- changes in pH and CO2
|
|
Cushing triad
|
- increase intracranial pressure
- bradycardia - respiratory depression |
|
Circulation through organ
- largest share of system cardiac output |
Liver
|
|
Circulation through organ
- highest blood flow per gram of tissue |
Circulation through organ
- |
|
Circulation through organ
- large arteriovenous oxygen difference (100% extraction) |
Heart
|
|
Autoregulation
Factor: local metabolites- O2, adenosine, NO |
Heart
|
|
Autoregulation
Factor: Local metabolites- CO2 (pH) |
Brain
|
|
Autoregulation
Factor: Myogenic and tubuloglomerular feedback |
Kidney
|
|
Autoregulation
Factor: Hypoxia cause vasoconstriction |
Lungs
|
|
Autoregulation
Factor: Local metabolites- lactate, adenosine, K+ |
Skeletal Muscle
|
|
Autoregulation
Factor: sympathetic stimulation; regulates temp. |
Skin
|