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How Does Acidosis Affect The Heart?

Acidosis And Contractility Of Heart Muscle.

Acidosis And Contractility Of Heart Muscle.

Acidosis and contractility of heart muscle. The contractility of heart muscle is sensitive to small and physiological changes of extracellular pH. The reduction of contractility associated with an acidosis is determined by the fall of pH in the intracellular fluid. The function of many organelles within the cardiac cell is affected by hydrogen ions. The tension generated by isolated myofibrils at a fixed calcium concentration is reduced at low pH. The dominant mechanism for the reduction of contractility in whole tissue is competitive inhibition of the slow calcium current by hydrogen ions. The reduction of the slow calcium current is similar when the same fall of developed tension is induced by acidosis or by a reduction of extracellular calcium concentration. Measurement of tissue pH with fast-responding extracellular electrodes show that, in myocardial ischaemia, tissue acidosis develops at the same time or only seconds before the onset of contractile failure. Much of the reduced contractility can be accounted for by the severity of the acidosis. Although a mild acidosis can delay or prevent damage to the myocardium from ischaemia or hypoxia, a severe acidosis is not beneficial and may even cause tissue necrosis. Continue reading >>

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects A metabolic acidosis can cause significant physiological effects, particularly affecting the respiratory and cardiovascular systems. Hyperventilation ( Kussmaul respirations ) - this is the compensatory response Shift of oxyhaemoglobin dissociation curve (ODC) to the right Decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) Sympathetic overactivity (incl tachycardia, vasoconstriction,decreased arrhythmia threshold) Resistance to the effects of catecholamines Increased bone resorption (chronic acidosis only) Shift of K+ out of cells causing hyperkalaemia 5.4.2 Some Effects have Opposing Actions. The cardiac stimulatory effects of sympathetic activity and release of catecholamines usually counteract the direct myocardial depression while plasma pH remains above 7.2. At systemic pH values less than this, the direct depression of contractility usually predominates. The direct vasodilatation is offset by the indirect sympathetically mediated vasoconstriction and cardiac stimulation during a mild acidosis. The venoconstriction shifts blood centrally and this causes pulmonary congestion. Pulmonary artery pressure usually rises during acidosis. The shift of the oxygen dissociation curve to the right due to the acidosis occurs rapidly. After 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Acidosis is commonly said to cause hyperkalaemia by a shift of potassium out of cells. The effect on potassium levels is extremely variable and indirect effects due to the type of acidosis present are much more important. For example hyperkalaemia is due to renal failure in uraemic acidosis rather than the acidosis. Significant potassium loss du Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Adverse Effects Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Adverse Effects Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

The Effects Of Acid-base Disturbances On Cardiovascular And Pulmonary Function - Sciencedirect

The Effects Of Acid-base Disturbances On Cardiovascular And Pulmonary Function - Sciencedirect

The effects of acid-base disturbances on cardiovascular and pulmonary function Author links open overlay panel Jere H.Mitchell1 Disturbances in acid-base balance are commonly met problems in clinical medicine and decisions about their treatment are of great importance in patients with cardiopulmonary problems, in whom acid-base disturbances may be especially critical.Similarly, cardiopulmonary function may be significantly compromised even in patients with no intrinsic heart or lung disease, in the face of acid-base disturbances.It is essential, therefore, to understand the physiological consequences of these disturbances on the cardiovascular and pulmonary system. Of major importance is the effect of acid-base disturbances on the delivery of oxygen to the various tissue cells of the body.In order to understand all the pathophysiological mechanisms involved it is necessary to review the effects of acid-base changes on the heart, the peripheral vessels, the lungs, and the diffusion of oxygen between air, blood, and tissues. The requirement for oxygen by the various tissue cells of the body is met by the combined cardiovascular and pulmonary systems, which function as a unit termed the oxygen transport system of the body.The movement of oxygen from the ambient air to the tissue cells involves ventilation, pulmonary perfusion, diffusion, oxygen-carrying capacity of hemoglobin, cardiac output (including cardiac muscle performance), systemic distribution of flow, and finally the oxygen delivery capacity of hemoglobin.It is important to understand the effects of changes in pH on each of these steps in the chain. Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

Merck And The Merck Manuals

Merck And The Merck Manuals

Acidosis is caused by an overproduction of acid in the blood or an excessive loss of bicarbonate from the blood (metabolic acidosis) or by a buildup of carbon dioxide in the blood that results from poor lung function or depressed breathing (respiratory acidosis). If an increase in acid overwhelms the body's acid-base control systems, the blood will become acidic. As blood pH drops (becomes more acidic), the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing (respiratory compensation). Breathing faster and deeper increases the amount of carbon dioxide exhaled. The kidneys also try to compensate by excreting more acid in the urine. However, both mechanisms can be overwhelmed if the body continues to produce too much acid, leading to severe acidosis and eventually heart problems and coma. The acidity or alkalinity of any solution, including blood, is indicated on the pH scale. Metabolic acidosis develops when the amount of acid in the body is increased through ingestion of a substance that is, or can be broken down (metabolized) to, an acid—such as wood alcohol (methanol), antifreeze (ethylene glycol), or large doses of aspirin (acetylsalicylic acid). Metabolic acidosis can also occur as a result of abnormal metabolism. The body produces excess acid in the advanced stages of shock and in poorly controlled type 1 diabetes mellitus (diabetic ketoacidosis). Even the production of normal amounts of acid may lead to acidosis when the kidneys are not functioning normally and are therefore not able to excrete sufficient amounts of acid in the urine. Major Causes of Metabolic Acidosis Diabetic ketoacidosis (buildup of ketoacids) Drugs and substances such as acetazolamide, alcohols, and aspirin Lactic acidosis (buildup of lactic acid Continue reading >>

Effects Of Changes Of Ph On The Contractile Function Of Cardiac Muscle.

Effects Of Changes Of Ph On The Contractile Function Of Cardiac Muscle.

1. Am J Physiol. 1990 Jun;258(6 Pt 1):C967-81. Effects of changes of pH on the contractile function of cardiac muscle. (1)Department of Physiology, University of Leeds, United Kingdom. It has been known for over 100 years that acidosis decreases the contractility ofcardiac muscle. However, the mechanisms underlying this decrease are complicated because acidosis affects every step in the excitation-contraction couplingpathway, including both the delivery of Ca2+ to the myofilaments and the responseof the myofilaments to Ca2+. Acidosis has diverse effects on Ca2+ delivery.Actions that may diminish Ca2+ delivery include 1) inhibition of the Ca2+current, 2) reduction of Ca2+ release from the sarcoplasmic reticulum, and 3)shortening of the action potential, when such shortening occurs. Conversely, Ca2+delivery may be increased by the prolongation of the action potential that issometimes observed and by the rise of diastolic Ca2+ that occurs during acidosis.This rise, which will increase the uptake and subsequent release of Ca2+ by thesarcoplasmic reticulum, may be due to 1) stimulation of Na+ entry via Na(+)-Ca2+ exchange; 2) direct inhibition of Na(+)-Ca2+ exchange; 3) mitochondrial releaseof Ca2+; and 4) displacement of Ca2+ from cytoplasmic buffer sites by H+.Acidosis inhibits myofibrillar responsiveness to Ca2+ by decreasing thesensitivity of the contractile proteins to Ca2+, probably by decreasing thebinding of Ca2+ to troponin C, and by decreasing maximum force, possibly by adirect action on the cross bridges. Thus the final amount of force developed byheart muscle during acidosis is the complex sum of these changes. Continue reading >>

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some people's bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus , especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acidosis is higher in people with diabetes who Continue reading >>

Effects Of Acidosis On Myocardial Contractility And Metabolism*

Effects Of Acidosis On Myocardial Contractility And Metabolism*

The effects of increased H+ concentration and the competition between H+ and Ca2+ on cardiac contractile function and metabolism have been investigated using the perfused rat heart. A working heart preparation was established by cannulating the aorta and left atrium. Fluid ejection from the left ventricle passed into a small closed air space and escaped through the coronary circulation, thereby allowing a minimum dead space between changes of perfusion fluid. Respiratory acidosis (high pCO2,) to pH 6.6 produced a rapid fall of left ventricular pressure with a half time of 5 sec. This effect could be fully counteracted by an increase of the Ca2+ concentration in the perfusion fluid. Calcium titration curves against left ventricular pressure are shown illustrating a shift of the curves towards higher Ca2+ concentrations with decreased pH or verapamil addition and a shift towards low Ca2+ concentrations with epinephrine. In contrast to effects obtained with respiratory acidosis, an extracellular pH of 6.6 induced by metabolic acidosis (low HCO3) or artificial buffers caused a small and much slower decline of left ventricular pressure development. Under the latter conditions, intracellular pH decreased much less than with respiratory acidosis. Studies with isolated cardiac sarcolemma showed that both high and low affinity Ca2+ binding was inhibited at pH 6.6 relative to pH 7.4. Verapamil inhibited only low affinity Ca2+ binding. From these and other data, it is concluded that increased extracellular H+ in the presence of high pCO2 causes a rapid fall of intra cellular pH and exerts a negative inotropic effect primarily by competing with Ca2+ for intracellular calcium binding sites, although extracellular sites are also involved. It is proposed that H+ interferes with that Continue reading >>

Acidosis And Heart Disease

Acidosis And Heart Disease

As weve discussed in other articles, acidosis is a systemic lowering of the pH of the naturally alkaline organs, fluids and tissues of the body. Naturally, the stomach is acidic and at times, needs to remain so. The predominant terrain in the body needs to be slightly alkaline, with the blood and lymph being around 7.365 to 7.42 pH. Although the primary cause of acidosis in the body is dietary habits, environmental pollutants, car emissions, pesticides, herbicides, preservatives, vegetable and fruit dyes and waxes, artificial sweeteners, food additives, water pollutants, contaminated soils, tap water additives add to acidosis and toxicity in the body. Heart disease is one of the leading causes of death in North America. Studies show that most of those deaths are premature. In other words, lifestyle changes could save lives, giving those with heart disease a better quality of life and a long life span. The main cause of heart disease has its root in acidosis. Just as acid rain eats into marble, acidosis irritates and inflames tissue. The acids wear away at the cell membranes, the insides of arteries and veins and the very fabric of the heart. This continuing process weakens the heart and the arteries and veins to the point where they could break down. Acidosis isnt organ or location specific. It affects all the tissues in the body as all tissues are sensitive to this corroding acid. Just as you are sensitive to chemicals in your environment, acidosis is a condition that acts like corrosive chemicals inside your body. The muscle cells of your heart and the tubular muscles of your arteries and veins come in direct contact with the metabolic acids in the blood stream. Since the bodys piping system helps regulate blood flow and blood pressure, it is imperative that they rem Continue reading >>

Re: Does Blood Ph Affect Heart Rate, And, If So, How?

Re: Does Blood Ph Affect Heart Rate, And, If So, How?

Re: Does blood pH affect heart rate, and, if so, how? Posted By: Amit Agarwal, Grad student, Neuroscience/Neurogenetics, Dear Casey, Its indeed an interesting question, which still keeps manyscientific minds busy. Many researchers working in the field of cardiacbiology are trying to understand detailed electrophysiological andneurochemical mechanisms which can affect heart rate and its efficiency.There are several studies available on rodents which outline factorsresponsible for the maintenance of normal heart rate. Your question alsotargets one of the aspects of such studies. Several studies have shown thatacidosis can lead to reduced heart rate. So before going ahead letsunderstand what is acidosis? When breathing is restricted, the body cannot eliminate carbon dioxide asit should, and the amount of carbon dioxide in the blood increases. Carbondioxide (CO2) and water (H2O) exist in equilibrium with carbonic acid(H2CO3) in a reaction catalyzed by an enzyme called carbonic anhydrase.CO2 + H2O --> H2CO3 A molecule of carbonic acid dissociates on its own into a moleculebicarbonate (HCO3-) and an (acidic) hydrogen ion. (H+) H2CO3 <> HCO3- and H+ Thus the overall pattern is: H2O + CO2 <> H2CO3 <> HCO3- + H+ Therefore, if breathing is restricted, CO2 builds up and the reactionshifts to the right in an attempt to balance things out, ultimately makingthe blood more acidic and thus decreasing its pH. This is calledrespiratory acidosis. As you can see, either a build-up in the blood ofcarbon dioxide or a decrease in the blood of oxygen will cause the pH ofthe blood to fall. If both occur at the same time, as they do in cases ofsuffocation, the pH of the blood will plummet to life-threatening levelswithin a very few minutes. The pH of normal human blood is in the 7.35 to7.45 ran Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild metabolic acidosis impairs the -adrenergic response in isolated human failing myocardium Schotola et al.; licensee BioMed Central Ltd.2012 Pronounced extracellular acidosis reduces both cardiac contractility and the -adrenergic response. In the past, this was shown in some studies using animal models. However, few data exist regarding how the human end-stage failing myocardium, in which compensatory mechanisms are exhausted, reacts to acute mild metabolic acidosis. The aim of this study was to investigate the effect of mild metabolic acidosis on contractility and the -adrenergic response of isolated trabeculae from human end-stage failing hearts. Intact isometrically twitching trabeculae isolated from patients with end-stage heart failure were exposed to mild metabolic acidosis (pH 7.20). Trabeculae were stimulated at increasing frequencies and finally exposed to increasing concentrations of isoproterenol (0 to 1 10-6 M). A mild metabolic acidosis caused a depression in twitch-force amplitude of 26% (12.1 1.9 to 9.0 1.5 mN/mm2; n = 12; P < 0.01) as compared with pH 7.40. Force-frequency relation measurements yielded no further significant differences of twitch force. At the maximal isoproterenol concentration, the force amplitude was comparable in each of the two groups (pH 7.40 versus pH 7.20). However, the half-maximal effective concentration (EC50) was significantly increased in the acidosis group, with an EC50 of 5.834 10-8 M (confidence interval (CI), 3.48 10-8 to 9.779 10-8; n = 9), compared with the control group, which had an EC50 of 1.056 10-8 M (CI, 2.626 10-9 to 4.243 10-8; n = 10; P < 0.05), indicating an impaired -adrenergic force response. Our data show that mild metabolic acidosis reduces cardiac contractility and significantly impairs the -adrenerg Continue reading >>

Acidosis And Contractility

Acidosis And Contractility

how does acidosis cause reduced contractility? how does acidosis cause reduced contractility? If you are acidotic then H+ is going to be coming into the cell from the extracellular space which will cause K+ to efflux out. In heart tissue this means that K+ will be leaving the cell causing the resting membrane potential to become more negative and thus less excitable. thanks you guys that makes perfect sense!! I think (in addition to the HyperK+) the H+ ions also protonate and inactivate Na Channels. The idea that acidosis (i.e. incr [H+]) leads to efflux of K+ from cardiac myocytes --> hyperpolarization and thus decreased contractility makes sense, but is there such thing as a H+/K+ exchanger on such cell types? I've looked in BRS Physiology, but can't find one. There is a Na+/H+ exchanger, but that's different. Plus, this article states that "the dominant mechanism for the reduction of contractility in whole tissue is competitive inhibition of the slow calcium current by hydrogen ions." I know this is an old thread, but would anyone care to shed some light on this issue? Thanks! There are some other conjectures which can be found here . I always thought that the effects of acidosis and alkalosis on muscle (tetany / low contractility) were via Ca++. I was told that: H+ and Ca++ ions compete for binding sites on albumin, so in acidotis the Ca++ will be displaced by additional H+ --> More free Ca++ in circulation --> inhibition of muscle Na+ channels by Ca++ (this is the paradoxical step, as you'd expect more Ca++ to increase contractility. I'm not sure what the mechanism of inhibition is here.) The reverse being true of alkalosis causing tetany - less H+ allows Ca++ to bind to albumin, releasing the inhibition of Na+ channels causing tetany and paraesthesia (due to a si Continue reading >>

Effects Of Clinically Relevant Acute Hypercapnic And Metabolic Acidosis On The Cardiovascular System: An Experimental Porcine Study

Effects Of Clinically Relevant Acute Hypercapnic And Metabolic Acidosis On The Cardiovascular System: An Experimental Porcine Study

Effects of clinically relevant acute hypercapnic and metabolic acidosis on the cardiovascular system: an experimental porcine study Stengl et al.; licensee BioMed Central Ltd.2013 Hypercapnic acidosis (HCA) that accompanies lung-protective ventilation may be considered permissive (a tolerable side effect), or it may be therapeutic by itself. Cardiovascular effects may contribute to, or limit, the potential therapeutic impact of HCA; therefore, a complex physiological study was performed in healthy pigs to evaluate the systemic and organ-specific circulatory effects of HCA, and to compare them with those of metabolic (eucapnic) acidosis (MAC). In anesthetized, mechanically ventilated and instrumented pigs, HCA was induced by increasing the inspired fraction of CO2 (n = 8) and MAC (n = 8) by the infusion of HCl, to reach an arterial plasma pH of 7.1. In the control group (n = 8), the normal plasma pH was maintained throughout the experiment. Hemodynamic parameters, including regional organ hemodynamics, blood gases, and electrocardiograms, were measured in vivo. Subsequently, isometric contractions and membrane potentials were recorded in vitro in the right ventricular trabeculae. HCA affected both the pulmonary (increase in mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance (PVR)) and systemic (increase in mean arterial pressure (MAP), decrease in systemic vascular resistance (SVR)) circulations. Although the renal perfusion remained unaffected by any type of acidosis, HCA increased carotid, portal, and, hence, total liver blood flow. MAC influenced the pulmonary circulation only (increase in MPAP and PVR). Both MAC and HCA reduced the stroke volume, which was compensated for by an increase in heart rate to maintain (MAC), or even increase (HCA), Continue reading >>

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