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The carotid arteries are major blood vessels that provide blood supply to the head. There are two carotid arteries, one on each side of the neck. Each artery splits into 2 branches: the EXternal carotid arteries supplying the face, scalp and neck; and the INternal carotid arteries supplying the brain.
Carotid STENOSIS is a progressive NARROWING of carotid arteries caused by fatty deposits, or cholesterol plaques. Narrowed blood vessels RESTRICT blood flow to the brain. The plaques may also rupture, and blood clots may form, leading to a COMPLETE blockage. A stroke occurs when the blood supply to the brain is interrupted or seriously reduced.
Carotid endarterectomy is a surgical procedure performed to remove plaques from a carotid artery, with the goal of preventing strokes. This treatment is usually recommended for patients who have experienced symptoms of reduced blood flow, known as mini-strokes or transient ischemic attacks, which are described as episodes of dizziness, numbness, confusion or paralysis.
In this procedure, an incision is made in the neck to access the artery. Clamps are used to temporarily stop blood flow through the affected segment. A small tube, called a shunt, may be used to reroute the blood flow to supply the brain during the procedure. An incision is made in the artery and the plaques are removed. At the end, the shunt is removed and incisions are closed.
Carotid endarterectomy can be effective in preventing future strokes but the procedure may not be suitable for everyone; the risks are generally higher in patients with overall poor health.
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As arritmias cardíacas podem ser classificadas de acordo com o local de origem: ritmos sinusais são originários no nódulo sinoatrial ou nódulo SA; os ritmos atriais são originários nos átrios; ritmos ventriculares são originários nos ventrículos.
O ritmo sinusal é o ritmo normal do coração definido pelo marcapasso natural no nódulo SA. Em um coração saudável, o nódulo SA dispara 60 a 100 vezes por minuto, resultando na frequência cardíaca normal de 60 a 100 batimentos por minuto. As variações mais comuns do ritmo sinusal incluem:
* Bradicardia sinusal: quando o nódulo SA dispara menos de 60 vezes por minuto, resultando em uma frequência cardíaca mais lenta, com menos de 60 batimentos por minuto.
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* Taquicardia sinusal: quando o nódulo SA dispara mais de 100 vezes por minuto, gerando uma frequência cardíaca mais rápida, com mais de 100 batimentos por minuto.
A bradicardia sinusal e a taquicardia sinusal podem ser normais ou clínicas, dependendo da causa subjacente. Por exemplo, a bradicardia sinusal é considerada normal durante o sono e a taquicardia sinusal pode ser normal durante os exercícios físicos.
As arritmias cardíacas originárias de outras partes dos átrios são sempre patológicas. As mais comuns incluem: flutter atrial, fibrilação atrial e Taquicardia atrioventricular Reentrante Nodal. Estas são formas de taquicardia supraventricular ou TSV.
O flutter atrial ou flutter auricular é causado por um impulso elétrico que gira em torno de um ciclo localizado que se autoperpetua, mais comumente localizado no átrio direito. Isso é chamado de circuito REENTRANTE. Para cada ciclo, há uma contração dos átrios. A frequência atrial é regular e rápida, entre 250 e 400 batimentos por minuto. A frequência ventricular, ou frequência cardíaca, no entanto, é mais lenta, graças às propriedades REFRATÁRIAS do nódulo AV. O nódulo AV evita que parte dos impulsos atriais cheguem aos ventrículos. Neste exemplo, apenas um em cada TRÊS impulsos atriais segue o caminho para os ventrículos. Portanto, a frequência ventricular é 3 vezes MENOR do que a frequência atrial. A frequência ventricular em flutter atrial geralmente é regular, mas também pode ser IRREGULAR. Em um ECG, flutter atrial é caracterizado pela ausência de ondas P normais. Em vez disso, são observadas ondas flutter ou ondas f com um padrão serrilhado.
A fibrilação atrial é causada por múltiplos impulsos elétricos que são iniciados ALEATORIAMENTE de muitos focos ECTÓPICOS, dentro e ao redor dos átrios, geralmente perto das raízes das veias pulmonares. Esses sinais elétricos caóticos e não sincronizados fazem com que os átrios tremem ou fibrilhem ao invés de se contraírem. A frequência atrial durante a fibrilação pode ser EXTREMAMENTE alta, mas a maioria dos impulsos elétricos NÃO passam através do nódulo AV para os ventrículos, novamente, graças às propriedades refratárias do nódulo AV. Aqueles que passam são IRREGULARES. A frequência ventricular ou frequência cardíaca é, portanto, IRREGULAR e pode variar de lento, menor que 60, a rápido, mais de 100 batimentos por minuto. Em um ECG, a fibrilação atrial caracteriza-se por ausência de ondas P e presença de complexos QRS ESTREITOS e irregulares. A linha de base pode parecer ondulada ou totalmente plana, dependendo do número de focos ectópicos nos átrios. Em geral, um número maior de focos ectópicos resulta em uma linha de base mais plana.
A Taquicardia Atrioventricular Reentrante Nodal, ou TAVRN, é causada por um pequeno circuito de reentrada que envolve DIRETAMENTE o nódulo AV. Toda vez que o impulso passa através do nódulo AV, ele é transmitido para os ventrículos. A frequência atrial e a frequência ventricular são, portanto, idênticas. A frequência cardíaca é regular e rápida, variando de 150 a 250 batimentos por minuto.
Os ritmos ventriculares são os mais perigosos, sendo ameaças para a vida.
A taquicardia ventricular é mais comumente causada por um foco de disparo ou circuito, sendo FORTE e ÚNICO em um dos ventrículos. Geralmente ocorre em pessoas com problemas cardíacos estruturais, como cicatrizes de um ataque cardíaco prévio ou anormalidades nos músculos cardíacos. Os impulsos que começam nos ventrículos produzem batimentos ventriculares PREMATUROS que são regulares e rápidos, variando de 100 a 250 batimentos por minuto. Em um ECG, a taquicardia ventricular é caracterizada por complexos QRS largos e estranhos. A onda P está ausente. A taquicardia ventricular pode ocorrer com episódios curtos de menos de 30 segundos e não causar nenhum ou poucos sintomas. A taquicardia ventricular SUSTENTADA dura mais de 30 segundos e requer tratamento imediato para prevenir uma parada cardíaca. A taquicardia ventricular também pode progredir para a fibrilação ventricular.
A fibrilação ventricular, ou FV, é causada por MÚLTIPLOS e FRACOS focos ectópicos nos ventrículos. Esses sinais elétricos não sincronizados fazem com que os ventrículos sofram FIBRILAÇÃO em vez de se contraírem. O coração bombeia pouco ou nenhum sangue. A FV pode rapidamente levar a uma parada cardíaca. O ECG da FV é caracterizado por formas de onda IRREGULAR e aleatória de amplitude variável, NÃO é possível identificar a onda P, o complexo QRS ou onda T. A amplitude diminui com o tempo, desde a FV GROSSEIRA inicial até a FV FINA e, finalmente, até a linha plana.
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Huntington’s disease, or HD, is an INHERITED neurodegenerative disorder in which brain cells are damaged and die over time, leading to progressive loss of mental and physical abilities.
The disease is caused by an ABnormal version of the gene huntingtin, or HTT. The normal HTT gene has a stretch of 10 to 35 repeats of C-A-G nucleotide triplets, which encode for the amino acid glutamine. In people with HD, the HTT gene has MORE than 36 CAG repeats. The ABnormally LONG stretch of poly-glutamine ALTERS the structure of HTT protein, causing fragmentation and aggregation, forming a MIS-folded protein that is TOXIC to nerve cells. The resulting neuronal cell death is most prominent in the basal ganglia of the brain, especially in the striatum. Because the striatum’s function in motor control is to INHIBIT unwanted movements, its degeneration results in UNcontrollable dance-like movements, known as Huntington’s CHOREA, characteristic of the disease.
A person has 2 copies of the HTT gene but ONE ABnormal copy is sufficient to cause the disease. Children of an affected parent have a 50% chance of receiving the abnormal copy, hence a 50/50 chance of inheriting the disease. This pattern of inheritance is known as autosomal dominant.
The onset and progression of the disease depends on the number of CAG repeats – the greater the number of repeats, the earlier the age of onset and the faster the progression.
The high degree of sequence repetition also INcreases the likelihood of INaccurate DNA replication. Repeating sequences may form loops which cause the DNA polymerase to add more repeats as it replicates the DNA. This means a phenotypically-NORMAL father with 30-35 repeats MAY give his child a 40-repeats gene that would produce the disease. As the size of the polyglutamine stretch INcreases from generation to generation, the onset of symptoms gets earlier with each generation. This phenomenon is known as genetic ANTICIPATION.
An average person with a 40-50 CAG repeats in the HTT gene usually develops symptoms in their 40s. People with more than 60 repeats may start to show signs of the disease in their childhood. The first signs are SUBTLE mental and cognitive disturbances that may go unnoticed. As the disease progresses, chorea becomes prominent, followed by motor speech disorders, rigidity, swallowing difficulty, dysphagia, personality changes, memory loss, and other cognitive and psychiatric impairments.
Diagnosis is by genetic testing. Genetic counseling is available for people with family history of HD.
Life expectancy in HD is generally around 10 to 20 years following the onset of symptoms. Most life-threatening complications result from problems in muscle coordination, of which pulmonary aspiration is the most common cause of death. Currently there is no cure for Huntington’s disease, but treatments can relieve symptoms and improve quality of life.
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ANTI-Arrhythmic agents are drugs used to SUPPRESS abnormal rhythms of the heart. They act to either:
– interfere with the dynamics of cardiac action potentials by blocking a certain ion channel,
or
– block the sympathetic effects of the autonomic nervous system on the heart, to slow down heart rate.
There are 5 classes of antiarrhythmic drugs:
Class I: Sodium-channel blockers: these drugs bind to and block the fast sodium channels that are responsible for the DE-polarizing phase in contractile myocytes. The result is a SLOWER depolarization with a smaller amplitude. Slower influx of sodium results in a SMALLER flow of positive ions through gap junctions to adjacent cells; the adjacent cells take LONGER to reach the threshold required to generate a new action potential, ultimately resulting in a SLOWER propagation of action potentials through the myocardium. This REDUCED conduction velocity helps to SUPPRESS formation of re-entrant circuits, hence the use of these drugs for treating re-entrant tachycardias.
Class I agents are divided further into subclass IA, IB and IC. These subclasses differ in the STRENGTH of sodium channel blockage, and in their effect on the duration of action potentials and the effective refractory period, the ERP. While subclass IC has no effect on ERP, IA prolongs and IB shortens ERP, respectively. Changes in ERP may have different outcomes for different types of arrhythmias. A longer ERP generally reduces cardiac excitability, but prolonged repolarizations may increase the risk of torsades de pointes, a type of tachycardia caused by afterdepolarizations.
Class II: Beta-blockers: these drugs bind to beta1-adrenergic receptorsand block the sympathetic influences that act through these receptors. Sympathetic nerves release catecholamines which act to increase SA node firing rate and cardiac conductibility, especially at the AV node. These activities may precipitate arrhythmias. Beta-blockers SUPPRESS sympathetic effects, thereby decreasing heart rate and SLOWING down conduction through the AV node. The latter is particularly useful in treatment of tachycardias that originate upstream of the AV node, known as supraventricular tachycardias, or SVT. Note should be taken, however, that beta-blocker treatment may cause AV blocks.
Class III: Potassium-channel blockers: these agents block the potassium channels responsible for the repolarizing phase. The result is a SLOWED repolarization, hence a PROLONGED duration of action potentials and refractory period. This reduces the heart’s excitability and suppresses re-entrant However, these drugs may also CAUSE arrhythmias because slow repolarizations are associated with LONGER QT intervals and INcreased risks of torsades de pointes.
Class IV: Calcium-channel blockers: these drugs block calcium channels that are responsible for DE-polarization in SA and AV nodal cells. Blocking these channels results in a LOWER sinus rate and SLOWER conduction through the AV node. However, because calcium is also involved in cardiac myocyte contraction, these agents also reduce contractility of the heart and should not be used in case of systolic heart failures.
Class V includes all drugs that act by other or unknown mechanisms.
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The mitral valve serves to ensure ONE-WAY blood flow from the left atrium to the left ventricle of the heart. It OPENS during diastole when the left atrial pressure is higher than the left ventricular pressure, allowing blood to fill the left ventricle; and CLOSES during systole, when the pressure gradient is reversed, to prevent blood from flowing BACK to the atrium as the ventricles contract. The mitral valve has 2 flaps, known as anterior and posterior mitral leaflets, which are supported by a fibrous ring, called mitral annulus. During ventricular contraction, the leaflets are kept from opening in the wrong direction by the action of papillary muscles which attach to the leaflets via cord-like tendons called chordae tendineae, or tendinous chords.
The most common of all heart valve diseases is mitral valve prolapse, or MVP. In MVP, the mitral leaflets bulge into the left atrium every time the ventricles contract. In many people, the reason why this happens is unclear. In others, it is linked to connective tissue disorders such as Ehlers-Danlos or Marfan syndrome. Connective tissue problems are believed to weaken the leaflets, INcrease leaflet area and cause elongation of the chordae tendineae. In most people, MVP is Asymptomatic and does not require treatment. However, it does increase the risks of developing other heart diseases such as arrhythmias, endocarditis, and most frequently, mitral valve regurgitation. In fact, mitral valve prolapse is the most common cause of mitral regurgitation. The billowing leaflets may not fit together properly; elongated chords may also rupture, resulting in a LEAKY valve, which permits BACKflow of the blood to the left atrium when the ventricles contract. When the volume of regurgitated blood is significant, the left side of the heart experiences volume OVERLOAD and eventually fails; blood is backed up to the lungs, causing pulmonary congestion, a hallmark of left-sided heart failure.
Mitral valve prolapse and regurgitation produce characteristic ABNORMAL heart sounds, such as clicks and murmurs, which can be heard during auscultation. Diagnosis is usually confirmed by echocardiography, a procedure in which heart valves and blood flows can be visualized LIVE using ultrasound.
A leaky valve requires surgical repair or replacement. In a typical valve repair surgery, the floppy portion of the valve is removed and the remaining parts are REconnected. The procedure may also include tightening or replacing the mitral annulus, known as annuloplasty. Valve replacement is considered when repair is not possible. Artificial valves can be mechanical or bio-prosthetic. Mechanical valves last longer but usually require life-long administration of anticoagulant medications to prevent formation of blood clots.
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Do ponto de vista do paciente, as moscas volantes são objetos que se deslocam no campo de visão. Elas podem parecer borrões, pequenas linhas ou teias de aranha que se movem com o movimento do olho. É impossível focar a visão nas moscas volantes e elas são visíveis quando se olha para um fundo brilhante, como o céu azul ou uma tela de computador em branco. As moscas volantes são, de fato, partículas suspensas dentro do corpo vítreo – uma estrutura em gel que preenche o espaço entre o cristalino e a retina. O que se vê, no entanto, não são as partículas, mas as sombras que elas fazem sobre a retina. Quanto mais perto da retina, maiores e mais claras aparecem no campo de visão.
Comumente, as moscas volantes se desenvolvem com o processo natural de envelhecimento. Com a idade, o corpo vítreo sofre sinérese – um processo no qual a água é separada dos componentes sólidos, criando grumos percebidos pelo paciente como bolhas ou minhocas. A principal proteína estrutural do corpo vítreo – o colágeno – torna-se desnaturada, aglomerada e pode ser vista como cordas flutuantes ou teias de aranha. Os grumos podem entrar em colapso, fazendo com que o vítreo encolha e se afaste da retina. Essa tração exercida pelo vítreo na retina produz “flashes” luminosos ou fotopsia na visão periférica. Eventualmente, o vítreo é separado da retina. Isso é conhecido como deslocamento do vítreo posterior ou DVP. DVP é muito comum, mas geralmente é benigno e não requer tratamento. As moscas volantes podem ser um incômodo para a visão, mas na maioria das pessoas, o cérebro aprenderá a IGNORÁ-LAS. Complicações podem acontecer, no entanto, em um pequeno número de casos. À medida que o vítreo se desloca, ele pode puxar a retina, resultando em um rasgo na retina. O fluído do vítreo pode então PASSAR ATRAVÉS do rasgo, fazendo com que a retina se separe do tecido subjacente. Isso é conhecido como descolamento de retina e é uma condição que ameaça a visão. Sinais de atenção incluem:
– Aumento súbito no número de moscas volantes, especialmente as menores, pois podem representar pigmentos ou células sanguíneas liberadas da retina danificada ou dos vasos sanguíneos.
– Sombra ou cortina de visão – um sinal de perda de visão da parte deslocada da retina.
As pessoas com alto grau de miopia correm maior risco de ter DVP. A forma mais longa do globo ocular na miopia aumenta a probabilidade de DVP e também o risco de complicações na retina. Isso ocorre porque a retina é esticada sobre uma superfície maior e torna-se mais fina e mais vulnerável aos rasgos. Outros fatores de risco para DVP incluem inflamação intraocular, trauma, cirurgia ocular prévia, diabetes e histórico familiar.
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Hyperosmolar hyperglycemic state, or HHS, is another ACUTE and life-threatening complication of diabetes mellitus. It develops slower than DKA, typically in the course of several days, but has a much higher mortality rate. Like DKA, HHS is triggered when diabetic patients suffer from ADDITIONAL physiologic stress such as infections, other illness, inadequate diabetic treatment or certain drugs. Similar to DKA, the RISE in COUNTER-regulatory hormones is the major culprit. These hormones stimulate FURTHER production and release of glucose into the blood, causing it to overflow into urine, resulting in excessive LOSS of water and electrolytes.
The major DIFFERENCE between HHS and DKA is the ABSENCE of acidosis in HHS. This is because, unlike DKA, the level of insulin in HHS patients is HIGH enough to SUPPRESS lipolysis and hence ketogenesis. This explains why HHS occurs more often in type 2 diabetics, who have more or less normal level of circulating insulin. Reminder: type 2 diabetics DO produce insulin but their cells do NOT respond to insulin and therefore cannot use glucose.
Because symptoms of acidosis are NOT present, development of HHS may go UNnoticed until blood glucose levels become EXTREMELY high. Severe dehydration results in INcreased concentrations of solutes in the blood, raising its osmolarity. HyPERosmotic blood plasma drives water OUT of body’s tissues causing cellular dysfunction.
Primary symptom of HHS is ALTERED consciousness due to excessive dehydration of brain tissues. This can range from confusion to coma. Emergency treatment consists of intravenous fluid, insulin and potassium similar to those used in DKA.
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Diabetic ketoacidosis, DKA, is an ACUTE and potentially life-threatening complication of diabetes mellitus. DKA is commonly associated with type 1 but type 2 diabetics are also susceptible. DKA is caused by a critically LOW INSULIN level and is usually triggered when diabetic patients undergo further STRESS, such as infections, INadequate insulin administration, or cardiovascular diseases. It may also occur as the FIRST presentation of diabetes in people who did NOT know they had diabetes and therefore did NOT have insulin treatment.
Glucose is the MAJOR energy source of the body. It comes from digestion of carbohydrates and is carried by the bloodstream to various organs. Insulin is a hormone produced by beta-cells of the pancreas and is responsible for DRIVING glucose INTO cells. When insulin is DEFICIENT, glucose can NOT enter the cells; it stays in the blood, causing HIGH blood sugar levels while the cells are STARVED. In response to this metabolic starvation, the body increases the levels of COUNTER-regulatory hormones. These hormones have 2 major effects that are responsible for clinical presentation of DKA:
– First, they produce MORE glucose in an attempt to supply energy to the cells. This is done by breaking down glycogen into glucose, and synthesizing glucose from NON-carbohydrate substrates such as proteins and lipids. However, as the cells CANNOT use glucose, this response ONLY results in MORE sugar in the blood. As blood sugar level EXCEEDS the ability of the kidneys to REabsorb, it overflows into urine, taking water and electrolytes along with it in a process known as OSMOTIC DIURESIS. This results in large volumes of urine, dehydration and excessive thirst.
– Second, they activate lipolysis and fatty acid metabolism for ALTERNATIVE fuel. In the liver, metabolism of fatty acids as an alternative energy source produces KETONE bodies. One of these is acetone, a volatile substance that gives DKA patient’s breath a characteristic SWEET smell. Ketone bodies, unlike fatty acids, can cross the blood-brain barrier and therefore can serve as fuel for the brain during glucose starvation. They are, however, ACIDIC, and when produced in LARGE amounts, overwhelm the buffering capacity of blood plasma, resulting in metabolic ACIDOSIS. As the body tries to reduce blood acidity by EXHALING MORE carbon dioxide, a deep and labored breathing, known as Kussmaul breathing may result. Another compensation mechanism for high acidity MOVES hydrogen ions INTO cells in exchange for potassium. This leads to increased potassium levels in the blood; but as potassium is constantly excreted in urine during osmotic diuresis, the overall potassium level in the body is eventually depleted. A blood test MAY indicate too much potassium, or hyperkalemia, but once INSULIN treatment starts, potassium moves BACK into cells and hypokalemia may result instead. For this reason, blood potassium level is monitored throughout treatment and potassium replacement is usually required together with intravenous fluid and insulin as primary treatment for DKA.
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The cardiac cycle refers to the sequence of events that occur and repeat with every heartbeat. It can be divided into 2 major phases: SYSTOLE and DIASTOLE, each of which SUBdivides into several smaller phases. Systole and diastole, when not specified otherwise, refer to VENTRICULAR contraction and relaxation, respectively.
Basic principles:
– Blood flows from HIGHER to lower pressure.
– Contraction INcreases the pressure within a chamber, while relaxation lowers the pressure.
– AV valves OPEN when atrial pressures are HIGHER than ventricular pressures and CLOSE when the pressure gradient is REVERSED. Similarly, semilunar valves OPEN when ventricular pressures are HIGHER than aortic/pulmonary pressures, and close when the reverse is true.
The cycle is initiated with the firing of the SA node that stimulates the atria to depolarize. This is represented by the P-wave on the ECG. Atrial contraction starts shortly after the P-wave begins, and causes the pressure within the atria to increase, FORCING blood into the ventricles. Atrial contraction, however, only accounts for a FRACTION of ventricular filling, because at this point, the ventricles are ALREADY almost full due to PASSIVE blood flow DOWN the ventricles through the OPEN AV valves.
As atrial contraction completes, atrial pressure begins to FALL, REVERSING the pressure gradient across the AV valves, causing them to CLOSE. The closing of the AV valves produces the first heart sound, S1, and marks the beginning of SYSTOLE. At this point, ventricular DE-polarization, represented by the QRS complex, is half way through, and the ventricles start to contract, RAPIDLY building UP pressures inside the ventricles. For a moment, however, the semilunar valves remain closed, and the ventricles contract within a CLOSED space. This phase is referred to as isovolumetric contraction, because NO blood is ejected and ventricular volume is unchanged.
Ventricular ejection starts when ventricular pressures EXCEED the pressures within the aorta and pulmonary artery; the aortic and pulmonic valves OPEN and blood is EJECTED out of the ventricles. This is the RAPID ejection phase.
As ventricular RE-polarization, reflected by the T-wave, begins, ventricular pressure starts to FALL and the force of ejection is REDUCED.
When ventricular pressures drop BELOW aortic and pulmonary pressures, the semilunar valves CLOSE, marking the end of systole and beginning of diastole. Closure of semilunar valves produces the second heart sound, S2.
The first part of diastole is, again, isovolumetric, as the ventricles relax with ALL valves CLOSED. Ventricular pressure drops RAPIDLY but their volumes remain unchanged.
Meanwhile, the atria are being filled with blood and atrial pressures RISE slowly. Ventricular FILLING starts when ventricular pressures drop BELOW atrial pressures, causing the AV valve to open, allowing blood to flow DOWN the ventricles PASSIVELY.
The atria contract to finish the filling phase and the cycle repeats itself.
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pH is an indicator of acidity. The body’s blood pH is strictly regulated within a narrow range between 7.35 and 7.45. This is because even a minor change in acidity may have devastating effects on protein stability and biochemical processes.
Normal cellular metabolism constantly produces and excretes carbon dioxide into the blood. Carbon dioxide combines with water to make carbonic acid which dissociates into hydrogen ions and bicarbonate.
CO2 + H2O = H2CO3 = H+ + HCO3−
This is an equilibrium, meaning all the components of the left and right sides co-exist at all times, and the concentration of any component is determined by that of others at any given moment. The rule of thumb is: an increase in concentration of ANY component on ONE side will shift the equation to the OTHER side, leading to INCREASED concentrations of all components on THAT side, and vice versa. This equilibrium is central to understand acid-base regulation. CONTINUED carbon dioxide production by all cells of the body drives the equilibrium to the right to generate more hydrogen ions. Because pH is basically a function of hydrogen ion concentration, more hydrogen means higher acidity and lower pH. Normal metabolism, therefore, constantly makes the blood more acidic. The body must react to keep the blood pH within the normal limits. This is achieved by 2 mechanisms:
Elimination of carbon dioxide through exhalation. The amount of carbon dioxide exhaled by the lungs is regulated in response to changes in acidity. A decrease in pH is sensed by central or arterial chemoreceptors and leads to deeper, faster breathing; more carbon dioxide is exhaled, less hydrogen is made, blood acidity decreases and blood pH returns to normal. Pulmonary regulation is fast, usually effective within minutes to hours.
Excretion of hydrogen ions and reabsorption of bicarbonate through the kidneys. The kidneys control blood pH by adjusting the amount of excreted acids and reabsorbed bicarbonate. Renal regulation is slower; it usually takes days to respond to pH disturbances.
Renal regulation: Although all of the plasma bicarbonate is filtered in the glomerulus during the first step of urine formation, virtually ALL of it is REabsorbed BACK into the blood. Most of this reabsorption happens in the proximal tubule. The amount of reabsorbed bicarbonate in the proximal tubule is regulated, via a number of mechanisms, in response to changes in blood pH. It increases during acid loads and decreases during alkali loads. While the proximal tubule basically RETURNS FILTERED bicarbonate back to the blood, the downstream collecting ductgenerates NEW bicarbonate by ACTIVELY SECRETING acids. As protons are depleted from the distal tubular cells, the equation shifts to the right, producing MORE bicarbonate which then exits into the blood. Hydrogen ions secreted into the lumen combine with urinary buffers, mainly filtered phosphate, and ammonia, to be excreted in urine. The ammonia buffering system is particularly important because unlike phosphate, which is filtered in FIXED amounts from the plasma and can be depleted during high acid loads, ammonia production is regulated in response to changes in acidity and its concentration may increase several folds when necessary. Blood pH is the main regulator of acid excretion, but potassium, chloride concentrations and several hormones also play important roles.
Pathologic changes may cause acid-base disturbances. Acidosis refers to a process that causes increased acidity, while alkalosis refers to one that causes increased alkalinity. It’s not uncommon for a patient to have several processes going on at once, some of them in opposite directions. The resulting plasma pH may be normal; too acidic, called acidemia; or too basic, called alkalemia.
Acidosis may result from INadequate function of the lungs which causes arterial carbon dioxide to accumulate. This is RESPIRATORY acidosis. On the other hand, METABOLIC acidosis may result from excessive production of metabolic acids, DEcreased ability of the kidneys to excrete acids, ingestion of acids, or loss of alkali. Metabolic acidosis is characterized by primary DEcrease in plasma bicarbonate.
Alkalosis can also be either respiratory or metabolic. Respiratory alkalosis is caused by INcreased ventilation resulting in excessive exhalation of carbon dioxide. Metabolic alkalosis can result from excess loss of acids through the kidneys or gastrointestinal tract, bicarbonate retention, or ingestion of alkali. Metabolic alkalosis is characterized by primary increase in plasma bicarbonate.
