Cardiovascular system anatomy and physiology

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Cardiovascular system anatomy and physiology

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Anatomy of the larynx and trachea
Bones and joints of the thoracic wall
Vessels and nerves of the thoracic wall
Anatomy of the lungs and tracheobronchial tree
Muscles of the thoracic wall
Anatomy of the pleura
Development of the respiratory system
Nasal cavity and larynx histology
Bronchioles and alveoli histology
Trachea and bronchi histology
Respiratory system anatomy and physiology
Ventilation-perfusion ratios and V/Q mismatch
Ventilation
Alveolar surface tension and surfactant
Upper respiratory tract infection
Sinusitis
Retropharyngeal and peritonsillar abscesses
Laryngitis
Bacterial epiglottitis
Anatomy of the pharynx and esophagus
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Regulation of pulmonary blood flow
Zones of pulmonary blood flow
Airflow, pressure, and resistance
Breathing cycle and regulation
Lung volumes and capacities
Pulmonary edema
Anatomic and physiologic dead space
Pulmonary shunts
Diffusion-limited and perfusion-limited gas exchange
Alveolar gas equation
Gas exchange in the lungs, blood and tissues
Anatomy clinical correlates: Thoracic wall
Anatomy clinical correlates: Pleura and lungs
Otitis media
Eustachian tube dysfunction
Corynebacterium diphtheriae (Diphtheria)
Haemophilus influenzae
Bacterial tracheitis
Pediatric upper airway conditions: Clinical
Rhinovirus
Adenovirus
Moraxella catarrhalis
Streptococcus pyogenes (Group A Strep)
Streptococcus pneumoniae
Human parainfluenza viruses
Epstein-Barr virus (Infectious mononucleosis)
Influenza virus
Pediatric ear, nose, and throat conditions: Clinical
Alpha 1-antitrypsin deficiency
Compliance of lungs and chest wall
Combined pressure-volume curves for the lung and chest wall
Breathing cycle
Allergic rhinitis
Nasopharyngeal carcinoma
Oral cancer
Nasal polyps
Warthin tumor
Sjogren syndrome
Nasal, oral and pharyngeal diseases: Pathology review
Choanal atresia
Sialadenitis
Aphthous ulcers
Sleep apnea
Thoracic outlet syndrome
Neonatal respiratory distress syndrome
Cystic fibrosis
Cystic fibrosis: Clinical
Cystic fibrosis: Pathology review
Restrictive lung diseases
Restrictive lung diseases: Pathology review
Idiopathic pulmonary fibrosis
Sarcoidosis
Hypersensitivity pneumonitis
Obstructive lung diseases: Pathology review
Chronic bronchitis
Emphysema
Asthma
Asthma: Clinical
Bronchiectasis
Type I hypersensitivity
Pharmacodynamics: Desensitization and tolerance
Pneumonia: Pathology review
Pneumonia
Pneumonia: Clinical
Mycoplasma pneumoniae
Pulmonary changes at high altitude and altitude sickness
Oxygen-hemoglobin dissociation curve
Bronchodilators: Leukotriene antagonists and methylxanthines
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Mycobacterium tuberculosis (Tuberculosis)
Antituberculosis medications
Tuberculosis: Pathology review
Respiratory syncytial virus
Lung cancer
Lung cancer: Clinical
Lung cancer and mesothelioma: Pathology review
Pancoast tumor
Horner syndrome
Superior vena cava syndrome
Chronic obstructive pulmonary disease (COPD): Clinical
Chlamydia pneumoniae
Coxiella burnetii (Q fever)
Klebsiella pneumoniae
Streptococcus pneumoniae
Pseudomonas aeruginosa
Chronic granulomatous disease
Bordetella pertussis (Whooping cough)
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Pleural effusion: Clinical
Pleural effusion
Pneumothorax: Clinical
Pneumothorax
Acute respiratory distress syndrome
Acute respiratory distress syndrome: Clinical
Pulmonary hypertension
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Pulmonary embolism
Pulmonary hypoplasia
Congenital diaphragmatic hernia
Mesothelioma
Respiratory distress syndrome: Pathology review
Pulmonary changes during exercise
Pulmonary chemoreceptors and mechanoreceptors
Pulmonary corticosteroids and mast cell inhibitors
Syncope: Clinical
Anatomy of the heart
Anatomy of the coronary circulation
ECG rate and rhythm
ECG normal sinus rhythm
ECG QRS transition
Cardiac conduction system
Normal heart sounds
Vasculitis: Clinical
Aortic aneurysms and dissections: Clinical
Vascular tumors
Aneurysms
Aortic dissection
Aortic dissections and aneurysms: Pathology review
Raynaud phenomenon
Deep vein thrombosis
Deep vein thrombosis and pulmonary embolism: Pathology review
Thrombophlebitis
Lymphedema
Angiosarcomas
Cardiac and vascular tumors: Pathology review
Sturge-Weber syndrome
Vasculitis: Pathology review
Kawasaki disease
Kawasaki disease: Clinical
Mitral valve disease
Tricuspid valve disease
Aortic valve disease
Pulmonary valve disease
Introduction to the cardiovascular system
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Arteriole, venule and capillary histology
Artery and vein histology
Cardiovascular system anatomy and physiology
Coronary circulation
Lymphatic system anatomy and physiology
Blood pressure, blood flow, and resistance
Laminar flow and Reynolds number
Compliance of blood vessels
Pressures in the cardiovascular system
Resistance to blood flow
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Frank-Starling relationship
Stroke volume, ejection fraction, and cardiac output
Cardiac afterload
Cardiac preload
Law of Laplace
Cardiac contractility
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Pressure-volume loops
Cardiac work
Changes in pressure-volume loops
Abnormal heart sounds
Action potentials in myocytes
Excitability and refractory periods
Action potentials in pacemaker cells
Cardiac excitation-contraction coupling
Cardiac conduction velocity
ECG basics
ECG intervals
ECG axis
ECG cardiac hypertrophy and enlargement
ECG cardiac infarction and ischemia
Transposition of the great vessels
Tetralogy of Fallot
Persistent truncus arteriosus
Total anomalous pulmonary venous return
Hypoplastic left heart syndrome
Patent ductus arteriosus
Coarctation of the aorta
Ventricular septal defect
Atrial septal defect
Human herpesvirus 8 (Kaposi sarcoma)
Lymphangioma
Chronic venous insufficiency
Vasculitis
Behcet's disease
Aortic dissection
Marfan syndrome
Myocarditis
Endocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Arterial disease
Angina pectoris
Unstable angina
Myocardial infarction
Prinzmetal angina
Hypertension
Hypertensive emergency
Renal artery stenosis
Orthostatic hypotension
Hypotension
Atrial flutter
Atrial fibrillation
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Dyslipidemias: Pathology review
Hypertension: Pathology review
Endocarditis: Pathology review
Pericardial disease: Pathology review
Shock
Shock: Clinical
Shock: Pathology review
Premature atrial contraction
Wolff-Parkinson-White syndrome
Atrioventricular nodal reentrant tachycardia (AVNRT)
Ventricular tachycardia
Premature ventricular contraction
Ventricular fibrillation
Brugada syndrome
Long QT syndrome and Torsade de pointes
Atrioventricular block
Bundle branch block
Heart failure
Cor pulmonale
Heart failure: Clinical
Heart failure: Pathology review
Positive inotropic medications
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Class III antiarrhythmics: Potassium channel blockers
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class IV antiarrhythmics: Calcium channel blockers and others
cGMP mediated smooth muscle vasodilators
Adrenergic antagonists: Beta blockers
Calcium channel blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Ventricular arrhythmias: Pathology review
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Cardiac tumors
Dressler syndrome
Familial hypercholesterolemia
Abetalipoproteinemia
Hypertriglyceridemia
Hyperlipidemia
Pheochromocytoma
Antihistamines for allergies
Mycobacterium avium complex (NORD)
Nocardia
Pneumocystis jirovecii (Pneumocystis pneumonia)
Cryptococcus neoformans
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Blastomycosis
Aspergillus fumigatus

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Cardiovascular system anatomy and physiology

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The circulatory system is also called the cardiovascular system, where “cardi” refers to the heart, and “vascular” refers to the blood vessels. So, these are the two key parts: the heart, which pumps blood, and the blood vessels, which carry blood to the body and return it back to the heart again. Ultimately, this is how nutrients like O2, or oxygen, get pushed out to the organs and tissues that need it, and how waste like CO2, or carbon dioxide, which is the main byproduct of cellular respiration, gets removed.

The heart is about the size of a person’s fist, which makes sense: a bigger person has a bigger fist and, therefore, a bigger heart.And it’s shaped like a cone, and sits slightly shifted over to the left side, in the mediastinum, which is the middle of the chest cavity, or thorax.It sits on top of the diaphragm, which is the main muscle that helps with breathing, behind the sternum, or breastbone, in front of the vertebral column, squished in between the two lungs, and protected by the ribs.

If you look more closely, you can see that the heart sits inside a sac of fluid that has two walls, called the serous pericardium. The outer layer is called the parietal layer. It gets stuck tightly to another layer called the fibrous pericardium, which is made of tough, dense connective tissue, which holds the heart in place and prevents it from overfilling with blood. The inner layer is called the visceral layer, and it gets stuck tightly to the heart itself, forming the epicardium, or the outer layer of the heart. The cells of the serous pericardium, both the parietal and visceral layer -- secrete a protein-rich fluid that fills the space between those layers and serves as a lubricant for the heart, allowing it to move around a bit with each heartbeat without feeling too much friction.

So, moving from the outside to the inside of the heart, after the epicardium, there’s the myocardium, which is the muscular middle layer. This forms the bulk of the heart tissue because those cardiac muscle cells contract and pump blood. In addition to cardiac muscle cells, there are crisscrossing connective tissue fibers, which are made of collagen, that together form the fibrous cardiac skeleton, which helps supports the muscle tissue. The myocardium also has dedicated blood vessels - called coronary vessels - which lay on the outside of the heart and then penetrate into the myocardium to bring blood to that layer because it needs a lot of energy to pump blood. Finally, there’s the innermost layer of the heart, called the endocardium, which is made of a relatively thin layer of endothelium, which is the same layer of cells that line the blood vessels. This endocardium lines the heart chambers and heart valves.

All right, so on the right side of the heart, deoxygenated blood enters either through the top, through a blood vessel called the superior vena cava, or the bottom, through another blood vessel called the inferior vena cava, in the right atrium, where “atrium” means “entryway.”. Both vena cavas are veins, which bring blood towards the heart. There’s also a tiny third opening into the right atrium called the coronary sinus, which collects blood from coronary vessels returning from the myocardium.

Now, all of that blood then goes through the first of two atrioventricular valves that separate the atria from the ventricles. This one is called the tricuspid valve, and it allows blood into the right ventricle. The tricuspid valve has three little flaps or ‘cusps’, and each cusp looks kind of like a parachute because it has tiny little strings called chordae tendinae coming off of it that tether the cusp to a small muscle called a papillary muscle. When the heart contracts, that papillary muscle keeps the chordae tendinae taut, and both of these help to prevent regurgitation of blood back into the atrium, allowing it to only flow out next valve.

That being said, that contraction pumps the blood out the pulmonary valve which like the tricuspid valve has three cusps and also prevents blood from going backwards - but unlike the tricuspid valve, the pulmonary valve doesn’t have any of those chordae tendinae. Once it’s past the pulmonary valve, the blood goes into the pulmonary arteries which carry the blood away from the heart to the left and right lung. Just remember that arteries start with “a” and carry blood “away” from the heart.

The blood goes from the pulmonary artery into a pulmonary arteriole, which is a bit smaller, and finally into a capillary, which is the smallest. In the lungs, the capillary lines up alongside a small sack of air called an alveolus - and when you have a lot of them they’re called alveoli. Up until now the blood has been loaded with carbon dioxide, which makes the blood look dark red rather than blue, which is how it’s usually drawn, and how we’ll still draw it to stay consistent. Now, at this point in the journey, the carbon dioxide moves from the capillary to the alveolus and oxygen moves from the alveolus to the capillary, giving the blood that nice bright red color.

Now, in the blood, each red blood cell has millions of hemoglobin proteins, and each of these hemoglobins can bind to four oxygen molecules, so each red blood cell can carry millions of oxygen molecules when fully loaded! The oxygen-rich blood moves into a venule and then eventually into a pulmonary vein that dumps the blood into the left atrium. This trip -- from the right ventricle of the heart through the pulmonary artery to the lungs and back to the left atrium of the heart -- is called the pulmonary circulation.

After entering the left atrium, the blood goes through the second atrioventricular valve, called the mitral valve, into the left ventricle. The mitral valve has only two cusps or leaflets, one in front called the anterior leaflet that’s a little smaller and one behind it called the posterior leaflet. Both of these have chordae tendinae coming off of them that tether the valve to papillary muscles in the left ventricle. Similar to the right side of the heart, when it contracts, this prevents blood from going backwards.

Finally, blood in the left ventricle gets pumped out through the aortic valve, which normally has three cusps, out to the aorta, the largest artery in the body. Just like in the lungs, the aorta branches into arterioles which are smaller arteries and finally into capillaries which are the smallest, and at that point they’re at the organs and tissues. In the organs, the red blood cells line up alongside tissue cells and drop off oxygen and pick up carbon dioxide, basically the reverse of what happened with the alveolus in the lung. Loaded up with carbon dioxide, the blood turns that dark red color again, shown as blue, and starts the return journey to the heart by going into small venules and then larger veins. Now, the lower half of the body drains into the inferior vena cava, and the upper half drains into the superior vena cava, both of which dump blood back into the right atrium.

So this trip -- from the left ventricle of the heart to the body and back to the right atrium of the heart -- is called the systemic circulation. Now, relative to the pulmonary circulation, the systemic has a lot more blood vessels, which means there’s about a 5 times greater resistance to blood flow, which essentially meaning it’s a lot harder to pump blood through, even though it’s the same amount of blood being pumped as the pulmonary side. Because of this difference, the left ventricle needs to be stronger, and so the muscular layer of the left ventricle wall - or its myocardium - is three times thicker than the right ventricle’s myocardium.

Okay so let’s talk a little bit about that pumping. Every heartbeat, sounds something like, “lub dub, lub dub, lub dub.” So the first heart sound - “lub”, is called S1, and the noise comes from the tricuspid and mitral valves snapping shut when the left and right ventricles contract which happens at about the same time. Right after the S1 sound, the aortic valve and pulmonic valve open up, allowing blood to get pushed out to the body, and this period of time is called systole. The second heart sound - “dub”, is called S2, and the noise comes from the aortic and pulmonic valves snapping shut to prevent blood from flowing backwards after it leaves the ventricles - effectively ending systole. Right after the S2 sound, the tricuspid and mitral valves open back up, allowing blood to fill up the ventricles again, and this period of time is called diastole. That’s it, each heartbeat can be broken into systole and diastole. So a systolic blood pressure is the pressure in the arteries when the ventricles are squeezing out blood under high pressure, and diastolic blood pressure is when the ventricles are filling up with more blood, so it’s going to be slightly lower pressure.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2018)
  4. "Principles of Anatomy and Physiology" Wiley (2014)