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 >>
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 >>
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 >>
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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 >>
Acidosis And The Preterm, Effects On Heart And Lungs
Acidosis and the preterm, effects on heart and lungs Noori S, Wu T-W, Seri I. pH Effects on Cardiac Function and Systemic Vascular Resistance in Preterm Infants. The Journal of pediatrics. 2013;162(5):958-63.e1 . This study examined the effects of pH on ventricular outputs and calculated vascular resistance. There was little effect detectable on contractility or outputs or SVR in the first few days, but a reduction in SVR with lower pH after the first 3 days, which is accompanied by an increase in systemic flow. Animal models show different effects of respiratory acidosis and metabolic acidosis, probably largely because of differential effects on intracellular pH, the authors here find no effect of CO2 in the first 3 days, but increasing flow with decreased SVR as CO2 increases thereafter. I find the study reasssuring, but I am not sure how good we are at measuring true contractility with ultrasound, the indices that are measured are highly derived, nevertheless Noori and colleagues find no effect of pH on contractility. This may not be very surprising, they quote a review article Orchard CH, Kentish JC. Effects of changes of pH on the contractile function of cardiac muscle. American Journal of Physiology Cell Physiology. 1990;258(6):C967-C81 . (open access) which examines the mechanisms, if you read it you will notice, on the few occasions that actual pH values are discussed, they show that the major effects of changes in intracellular acidosis are when the pH is less than 7, sometimes as low as 6.6 or even 6.0! There is not much effect in these animal models in general of pH over 7.0. Nevertheless I think these studies can help us to feel less worried about acidosis in our babies, it is so common for small preterm babies to develop metabolic, mixed and respiratory ac Continue reading >>
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 >>
How Acidity Interferes With The Heart Beat
How acidity interferes with the heart beat How acidity interferes with the heart beat Modulation of hERG potassium channel function by extracellular acidosis: single channel effects and underlying basis Start date: 16 December 2013 (Duration 3 years) The hearts ability to pump blood round the body depends on co-ordinated electrical activity generated by small proteins in heart cells called ion channels. When blood flow to the heart is blocked off, for example, because of coronary heart disease or a heart attack, the blood becomes acidic. This acidity alters cardiac ion channel function and can predispose the heart to develop an irregular heartbeat or arrhythmia. An ion channel called hERG is central to normal cardiac activity. There is evidence that acidity (acidosis) impairs hERG function in ways that increase arrhythmia risk but the underlying mechanisms are incompletely understood. This project aims to provide, for the first time, detailed insight into how acidosis alters the electrical activity of individual hERG channel proteins. Genetic methods will be used to investigate which parts of the ion channel protein are affected by acidosis to modify hERG function. The results of this study could explain how acidosis could interfere with the effectiveness of drugs used to treat arrhythmia. Continue reading >>
Metabolic Acidosis And Its Correction In Patients Undergoing Open-heart Operation
Metabolic Acidosis and Its Correction in Patients Undergoing Open-Heart Operation Cleveland Clinic Journal of Medicine. 1957 October;24(4):193-203 THE occurrence of metabolic acidosis in patients undergoing open-heart operation has been recognized by Lillehei and his associates.1 According to our observations, the most significant changes in blood pH occur not during, or immediately after operation, but about three hours postoperatively. As long-as the patient is under anesthesia and his respiration is helped by the anesthetist, an excess of CO2 is blown off and the pH does not fall significantly. While the patients circulation is being maintained by the heart-lung machine, the removal of CO2 via the oxygenator also helps to keep the pH within normal limits. However, three or more hours after completion of the operation the blood pH occasionally falls to a level that is incompatible with life. Whatever the underlying cause, the mechanism of death in some cases seems to be an acidosis leading to respiratory failure followed by cardiac arrest. It has been suggested that these unfavorable acid-base imbalances are caused by damage to the blood itself by the pump-oxygenator during the period of bypass. This hypothesis, however, is not supported by the data in this paper. Our experimental results demonstrate that the blood pH and the CO2 content can be lowered simply by reducing the cardiac output. Our clinical results show that the occurrence of reduced blood pH and CO2 content in patients treated with a heart-lung machine is correlated with corresponding periods of hypotension before, during, or after the period of bypass. Furthermore, unfavorable changes in blood pH and CO2 content are known to . . . Continue reading >>
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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 >>
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Acidosis
When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s processes produce acid. Your lungs and kidneys can usually compensate for slight pH imbalances, but problems with these organs can lead to excess acid accumulating in your body. The acidity of your blood is measured by determining its pH. A lower pH means that your blood is more acidic, while a higher pH means that your blood is more basic. The pH of your blood should be around 7.4. According to the American Association for Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight, these numerical differences can be serious. Acidosis can lead to numerous health issues, and it can even be life-threatening. There are two types of acidosis, each with various causes. The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, depending on the primary cause of your acidosis. Respiratory acidosis Respiratory acidosis occurs when too much CO2 builds up in the body. Normally, the lungs remove CO2 while you breathe. However, sometimes your body can’t get rid of enough CO2. This may happen due to: chronic airway conditions, like asthma injury to the chest obesity, which can make breathing difficult sedative misuse deformed chest structure Metabolic acidosis Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t eliminate enough acid or when they get rid of too much base. There are three major forms of metabolic acidosis: Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your body lacks enough insulin, keton 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 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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Thiamine Deficiency, Lactic Acidosis And Heart Disease.
Thiamine Deficiency, Lactic Acidosis and Heart Disease. Am J Physiol Heart Circ Physiol. 2010 Jun;298(6):H2039-45. Gioda, CR., et al. Federal Univ. of Minas Gerais, Belo Horizonte, MG, Brazil. Beriberi is the result of thiamine deficiency (TD), causing neurological and cardiovascular disease. TD causes a reduction in the ability of heart muscle to contract. Thiamine is a cofactor for a number of metabolic enzymes, and while much research has focused on the nervous system effects of beriberi, little is known about the effects on the heart. TD is reported to cause heart failure, but little is known about the mechanism. TPP (thiamine pyrophosphate) is the biologically active form of thiamine in the body and is a cofactor for various enzymes. Rats fed a TD diet for 35 days underwent extensive blood testing while on the diet. The animals were dissected and the hearts were studied. They were found to have whole body deficiency of oxygen consumption and increased lactate levels. Low oxygen consumption often causes increased lactate levels. Reactive oxygen species (ROS), superoxide and H2O2 (hydrogen peroxide) were measured at the cellular levels in the heart muscles. Superoxide levels were increased by 40% and H2O2 levels were 2.5 times normal, consistent with damage to the cells. ROS results from a disruption in oxygen metabolism as was seen above. Antioxidants are the defense against ROS. SOD (superoxide dismutase) is an antioxidant which works against the ROS superoxide. Antioxidant enzyme activity was tested to check for the response to this strong oxidation. The proper proteins were produced, but this did not result in increased SOD enzyme activity in the cells. The SOD enzyme should modulate the superoxide, but could not do so in the TD cells. Importantly, TD cells had Continue reading >>
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 >>
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 >>
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 >>
