Hypoxia

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Hypoxia

Cardiothoracic Disease

Cardiothoracic Disease

Respiratory system anatomy and physiology
Lung volumes and capacities
Anatomic and physiologic dead space
Ventilation
Alveolar gas equation
Compliance of lungs and chest wall
Combined pressure-volume curves for the lung and chest wall
Alveolar surface tension and surfactant
Airflow, pressure, and resistance
Breathing cycle
Breathing control
Pulmonary chemoreceptors and mechanoreceptors
Ideal (general) gas law
Boyle's law
Dalton's law
Henry's law
Fick's laws of diffusion
Graham's law
Diffusion-limited and perfusion-limited gas exchange
Hypoxia
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Erythropoietin
Carbon dioxide transport in blood
Regulation of pulmonary blood flow
Zones of pulmonary blood flow
Pulmonary shunts
Ventilation-perfusion ratios and V/Q mismatch
Pulmonary changes during exercise
Pulmonary changes at high altitude and altitude sickness
Diffuse parenchymal lung disease: Clinical
Restrictive lung diseases: Pathology review
Restrictive lung diseases
Idiopathic pulmonary fibrosis
Sarcoidosis
Lung cancer: Clinical
Lung cancer and mesothelioma: Pathology review
Mesothelioma
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Cardiac cycle
Normal heart sounds
Abnormal heart sounds
Blood pressure, blood flow, and resistance
Resistance to blood flow
Laminar flow and Reynolds number
Compliance of blood vessels
Pressures in the cardiovascular system
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Measuring cardiac output (Fick principle)
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Stroke volume, ejection fraction, and cardiac output
Frank-Starling relationship
Pressure-volume loops
Changes in pressure-volume loops
Cardiac work
Cardiac preload
Cardiac afterload
Law of Laplace
Baroreceptors
Renin-angiotensin-aldosterone system
Chemoreceptors
Cardiac conduction system
Action potentials in pacemaker cells
Action potentials in myocytes
Cardiac conduction velocity
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac contractility
Cerebral circulation
Coronary circulation
Control of blood flow circulation
Microcirculation and Starling forces
Cardiomyopathies: Clinical
Cardiomyopathies: Pathology review
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Restrictive cardiomyopathy
Sleep apnea
Apnea of prematurity
Aortic aneurysms and dissections: Clinical
Aortic dissections and aneurysms: Pathology review
Aortic dissection
Aneurysms
Marfan syndrome
Peripheral vascular disease: Clinical
Peripheral artery disease: Pathology review
Peripheral artery disease
Arterial disease
Deep vein thrombosis
Leg ulcers: Clinical
Chronic venous insufficiency
Thrombophlebitis
Vasculitis: Pathology review
Vasculitis
Kawasaki disease
Behcet's disease
Nutcracker syndrome
Superior mesenteric artery syndrome
Subclavian steal syndrome
Coronary steal syndrome
Lymphedema
ECG basics
ECG normal sinus rhythm
ECG rate and rhythm
ECG intervals
ECG axis
ECG QRS transition
ECG cardiac hypertrophy and enlargement
ECG cardiac infarction and ischemia
Heart blocks: Pathology review
Premature ventricular contraction
Premature atrial contraction
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Atrioventricular block
Bundle branch block
Long QT syndrome and Torsade de pointes
Ventricular tachycardia
Brugada syndrome
Ventricular fibrillation
Pulseless electrical activity
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Positive inotropic medications
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Adrenergic antagonists: Presynaptic
cGMP mediated smooth muscle vasodilators
Calcium channel blockers
Heart failure: Clinical
Heart failure: Pathology review
Heart failure
Cor pulmonale
Pulmonary hypertension
Pulmonary edema
Anatomy of the coronary circulation
Asthma: Clinical
Obstructive lung diseases: Pathology review
Asthma
Chronic obstructive pulmonary disease (COPD): Clinical
Chronic bronchitis
Emphysema
Alpha 1-antitrypsin deficiency
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Pulmonary corticosteroids and mast cell inhibitors
Non-corticosteroid immunosuppressants and immunotherapies
Cystic fibrosis: Pathology review
Cystic fibrosis
Bronchiectasis
Anatomy of the heart
Anatomy clinical correlates: Heart
Cardiac muscle histology
Marfan syndrome
Ehlers-Danlos syndrome
Arteriole, venule and capillary histology
Cardiac muscle histology
Artery and vein histology
Trachea and bronchi histology
Bronchioles and alveoli histology
Nasal cavity and larynx histology
Coarctation of the aorta
Mitral valve disease
Pulmonary valve disease
Tricuspid valve disease
Aortic valve disease
Ventricular arrhythmias: Pathology review
Supraventricular arrhythmias: Pathology review
Coronary artery disease: Clinical
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Arterial disease
Angina pectoris
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome

Transcript

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So by this point, you’re probably aware that your body needs oxygen to survive, right?

In fact, every cell in your body needs that precious oxygen.

Those cells use the oxygen to produce energy in the form of ATP, or adenosine triphosphate, a super super important molecule, sometimes even called “the molecular unit of currency”.

The cells use it to basically pay the molecules inside the cell to do their specific jobs.

It’s like one big factory with a bunch of workers that all have specific jobs needed to run the factory, and they only take ATP as payment.

Now the mitochondrion of the cell takes in oxygen and makes ATP to pay the workers, through a process called oxidative phosphorylation, the mitochondrion’s like the factory’s payroll department, right?

When the cell doesn’t get enough oxygen, and so payroll can’t produce the ATP that they need to pay the workers to do their jobs, the whole cellular factory can be damaged or even die, and we call that process hypoxia, where hypo means “less than normal” and oxia means “oxygenation”.

When the oxygen comes in, typically it goes straight to payroll, specifically to the inner mitochondrial membrane where oxidative phosphorylation takes place.

Oxygen’s used in one of the last steps, and serves as an electron acceptor, and this allows the process to finish and produce ATP.

So without oxygen, we can’t finish oxidative phosphorylation and produce ATP.

But why does the whole factory fall apart when payroll stops making ATP? Why don’t they just pause for a bit? Take a little break?

Well, when certain workers stop doing their jobs...things get a little out of hand.

One super important worker is the sodium potassium pump on the cell’s membrane, pretty much like the bouncer that makes sure there isn’t too much sodium diffusing into the cell, basically by pumping it back out every time it diffuses in and maintaining a concentration gradient, this process also keeps too many water molecules from passively diffusing into the cell; think of it like this: water molecules want to go every which way and are constantly moving back and forth, inside and outside the cell, but the all these sodium ions on this side tend to physically block more of them from leaving that side, so over time more water molecules get retained, or almost trapped, on the side with more sodium—in short, the more sodium molecules: the more water molecules.

But, our pump doesn’t do all this for free, and it needs ATP.

So without ATP, it stops pumping sodium back out, and sodium diffuses in...and keeps diffusing in and the concentration gradient goes away, now with less sodium particles on the outside blocking the water molecules from going into the cell, water follows sodium in, which causes the cell to swell up.

When the cell swells up, a couple things happen.

First, usually you have these really tiny microvilli on the cell’s membrane, which look sort of like little fingers that help increase the cell’s surface area and therefore help the cell absorb more things, when the cell swells up and gets all bloated, the water sort of fills these little fingers and reduces the surface area, which makes it harder to absorb molecules since there’s less surface area, right?

Also, sort of along the same lines, the cell can bleb, or bulge outward from all this water, this is a sign that the cell’s cytoskeleton or this structural framework is beginning to fail, and is letting water slip through.

Sources

  1. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  2. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  3. "Yen & Jaffe's Reproductive Endocrinology E-Book" Elsevier Health Sciences (2017)
  4. "Bates' Guide to Physical Examination and History Taking" LWW (2016)
  5. "Robbins Basic Pathology" Elsevier (2017)
  6. "The laws of combination of haemoglobin with carbon monoxide and oxygen" The Journal of Physiology (1912)
  7. "Cellular Stress Responses: Cell Survival and Cell Death" International Journal of Cell Biology (2010)
  8. "Oxygen enrichment of room air to relieve the hypoxia of high altitude" Respiration Physiology (1995)