NCM 3114 Acid Base Imbalance PDF

Summary

This document provides an overview of acid-base imbalances in the human body. It discusses the mechanisms and chemistry behind acid-base regulation, including the role of buffer systems, kidneys, and lungs. It's ideal for a physiology based learning experience.

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1. ACID-BASE IMBALANCES  Acid-base balance occurs through control of hydrogen ion (H+) production and elimination.  Plasma pH – is an indicator of hydrogen ion (H+) concentration.  The level of free hydrogen ions, formed from acids, must be rigidly controlled for proper...

1. ACID-BASE IMBALANCES  Acid-base balance occurs through control of hydrogen ion (H+) production and elimination.  Plasma pH – is an indicator of hydrogen ion (H+) concentration.  The level of free hydrogen ions, formed from acids, must be rigidly controlled for proper function. Even small changes in the free hydrogen ion level or pH of the body fluids can cause major problems in function.  Keeping the pH within the normal range involves balancing acids and bases in body fluids.  Normal pH ranges from 7.35 to 7.45  controlled by the homeostatic mechanisms. These Mechanisms Consist of:  Buffer systems  The kidneys  The lungs  The hydrogen ion concentration is extremely important:  The greater the concentration, the more acidic the solution and the lower the pH.  The lower the H+ concentration, the more alkaline the solution and the higher the pH.  Keeping the pH of the blood within the normal range is important because changes from normal interfere with many normal physiologic functions. These changes include:  Changing the shape and reducing the function of hormones and enzymes  Changing the distribution of other electrolytes, causing fluid and electrolyte imbalances  Changing excitable membranes, making the heart, nerves, muscles, and the GI tract either less or more active than normal  Decreasing the effectiveness of many drugs  Fortunately, the body has many mechanisms to ensure minimal changes in free hydrogen ion level. ACID-BASE CHEMISTRY ACIDS are substances that release hydrogen ions when dissolved in water (H2O). An acid in solution  increases the amount of free hydrogen ions in that solution.  A strong acid such as hydrochloric acid (HCL) – separates completely in water and readily releases all of its hydrogen ions.  A weak acid such as acetic acid (CH3COOH) – does not completely separate in water; it releases only some of its hydrogen ions. BASES A base is a substance that binds free hydrogen ions in solution. Bases are “hydrogen acceptors” that reduce the amount of free hydrogen ions in solution.  Strong bases include sodium hydroxide (NaOH) and ammonia (NH3) – bind hydrogen ions easily.  Weak bases such as aluminum hydroxide (AlOH3) and bicarbonate (HCO3) – bind hydrogen ions less readily.  Although bicarbonate is a weak base, bicarbonate ions in the body prevent major changes in body fluid pH. ACID-BASE REGULATORY MECHANISMS BUFFER SYSTEMS  Buffer systems are the first line of defense and prevent major changes in the pH of body fluids by removing or releasing H+  they can act quickly to prevent excessive changes in H+ concentration.  Hydrogen ions are buffered by both intracellular and extracellular buffers.  Bicarbonate-carbonic acid buffer system – is the body’s major extracellular buffer system which is assessed when arterial blood gasses are measured.  Normally, there are 20 parts of bicarbonate (HCO3) to one part of carbonic acid (H2CO3)  if this ratio is altered, the pH will change.  If either bicarbonate or carbonic acid is increased or decreased so that the 20:1 ratio is no longer maintained  results in an acid-base imbalance.  Less important buffer systems in the ECF include the inorganic phosphates and the plasma proteins.  Intracellular buffers include proteins, organic and inorganic phosphates, and in red blood cells, haemoglobin. RESPIRATORY ACID-BASE CONTROL MECHANISMS  When chemical buffers alone cannot prevent changes in blood pH, the respiratory system is the second line of defense against changes.  Breathing controls the amount of free hydrogen ions by controlling the amount of carbon dioxide (CO2) in arterial blood.  The lungs, under the control of the medulla, control the CO2 and thus the carbonic acid content of the ECF  by adjusting ventilation in response to the amount of CO2 in the blood.  A rise in the partial pressure of CO2 in arterial blood (PaCO2) is a powerful stimulant of respiration.  The partial pressure of oxygen in arterial blood (PaO2)  also influences respiration. However, its effect is not as marked as that produced by the PaCO2.  In metabolic acidosis  the respiratory rate increases, causing greater elimination of CO2 (to reduce the acid load).  In metabolic alkalosis  the respiratory rate decreases, causing CO2 retention (to increase the acid load).  Hyperventilation  increase in rate and depth of breathing  decreased CO2.  Hypoventilation  decrease in rate and depth of breathing  increased CO2. RENAL ACID-BASE CONROL MECHANISMS  The kidneys are the third line of defense against wide changes in body fluid pH.  Renal mechanisms are stronger for regulating acid-base balance but take longer than chemical and respiratory mechanisms to completely respond  they take 24 to 48 hours to respond.  The kidney movement of bicarbonate is the first renal control mechanism.  Much of the bicarbonate made in other body areas is excreted in the urine.  When blood hydrogen ion levels are low, the bicarbonate remains in the urine and is excreted.  When hydrogen ion excess occurs, the kidney tubules also can make additional bicarbonate that will be reabsorbed.  Formation of acids is the second renal control mechanisms. It occurs through the phosphate-buffering system inside the cells of the kidney tubules.  Once the hydrogen ion is in the urine, it binds to phosphate ions  forming an acid, H2PO4  which is excreted in the urine.  Formation of ammonium is the third renal control mechanisms.  Ammonia (NH3) – which is formed during normal protein breakdown converted into ammonium (NH+4).  The ammonia is secreted into the urine, where it can combine with hydrogen ions to form ammonium.  The ammonium “traps” the hydrogen ions and then allows them to be excreted in the urine  the result is a loss of hydrogen ions and an increase in blood pH. COMPENSATION  In the process of compensation – the body adapts to attempt to correct changes in blood pH. The ability of the body to adapt to change.  A pH below 6.9 or above 7.8 – is always fatal.  The normal pH range for human ECF is 7.35 to 7.45.  Both the kidneys and the lungs can compensate for acid-base imbalances, but they are not equal in their compensatory responses.  The respiratory system is much more sensitive to acid-base changes and can begin compensation efforts within seconds to minutes after a change in pHhowever; these efforts are limited and can be overwhelmed easily.  The renal compensatory mechanisms are much more powerful and result in rapid changes in ECF composition  however; these more powerful mechanisms are not fully triggered unless the acid-base imbalance continues for several hours to several days.  Respiratory compensation occurs through the lungs, usually correct for acid-base imbalances from metabolic problems.  To bring the pH level to normal  breathing is triggered in response to increased CO2 levels  both the rate and depth of respiration is increase  these respiratory efforts cause the blood to lose CO2 with each exhalation  so ECF levels of CO2 and free hydrogen ions gradually decrease.  When the lungs can fully compensate  the pH returns to normal.  Renal compensation results when a healthy kidney works to correct for changes in the blood pH that occur when the respiratory system is either overwhelmed or is not healthy.  For example: A person with COPD, the respiratory system cannot exchange gasses adequately  CO2 is retained continually and the blood pH falls (become acidic).  To oppose the process, the kidney excretes more hydrogen ions and increases the reabsorption of bicarbonate back in the blood  as a result, the blood pH remains either within or closer to the normal range.  When these backup mechanisms are completely effective  acid-base problems are fully compensated  and the pH of the blood returns to normal even though the levels of oxygen and bicarbonate are abnormal.  Sometimes, the respiratory problem causing the acid-base imbalance is so severe that the kidney actions can only partially compensate  the pH is not quite normal.  Partial compensation is helpful because it prevents the acid-base imbalance from becoming severe or life-threatening. ACID-BASE IMBALANCES Acid-base imbalances are changes in the blood hydrogen ion level or pH  these changes are caused by problems with the acid-base regulatory mechanisms of the body or by exposure to dangerous conditions.  Acidosis – reflects an imbalance in which the blood pH is below normal.  Alkalosis – reflects an imbalance in which the blood pH is above normal.  Acid-base imbalances impair the function of many organs and can be life-threatening. ACIDOSIS Pathophysiology:  In acidosis  the acid-base balance of the blood and other ECF is upset by an excess of hydrogen ion (H+).  This problem is reflected as an arterial blood pH below 7.35.  Acidosis is not a disease; it is a condition caused by a disorder or pathologic processes.  Acidosis can be caused by metabolic problems, respiratory problems, or both.  Patients at greater risk for acute acidosis are those with problems that impair breathing.  Older adults with chronic health problems are at a greater risk for developing acidosis.  Acidosis can result from an actual or relative increase in the amount or strength of acids.  An actual acid excess result in acidosis by either overproducing acids (and release of hydrogen ions) or undereliminating normally produced acids (retention of hydrogen ions).  Examples of problems that actually increase acid production are: diabetic ketoacidosis and seizures.  Examples of problems that actually decrease acid elimination are: respiratory impairment and renal impairment.  In relative acidosis – the amount or strength of acids does not increase, instead, the amount or strength (or both) of the bases decreases (to create a base deficit)  which makes the fluid relatively acidic than basic  caused by either overeliminating bases (bicarbonate ions [HCO-3]) or overproducing bases.  Examples of problems that underproduce bases are: pancreatitis and dehydration.  A condition that overeliminates bases is: diarrhea.  Regardless of its origin, acidosis causes major changes in body function.  The main problems are related to the fact that hydrogen ions are positively charged ions  an increase in H+ creates imbalances of other positively charged electrolytes, especially potassium.  These electrolyte imbalances then disrupt the functions of the nerves, cardiac muscle and skeletal muscle.  The early manifestations of acidosis first appear in the: musculoskeletal, cardiac, respiratory, and central nervous systems.  Even slight increases in blood hydrogen ion levels reduce the activity of many hormones and enzymes  leading to death.  Many drugs are less effective during acidosis.  Acidosis can be caused by metabolic problems, respiratory problems, or combined metabolic and respiratory problems. 1.1.Metabolic Acidosis  Four processes can result in metabolic acidosis: 1. Overproduction of hydrogen ions – can occur with excessive breakdown of fatty acids, anaerobic (lactic acidosis), and excessive intake of acids.  Excessive breakdown of fatty acids occurs with diabetic ketoacidosis or starvation. = When glucose is not available for fuel  the body breaks down fats (lipids)  the products of excessive fatty acids breakdown  are strong acids (ketoacids)  which release large amounts of hydrogen ions.  Lactic acidosis occurs when cells are forced to use glucose without adequate oxygen (anaerobic metabolism)  as a result; glucose is incompletely broken down  and forms lactic acid. = Lactic acid leaves the cell, enters blood, and releases hydrogen ions  causing acidosis. = Lactic acidosis occurs whenever the body has too little oxygen such as during heavy exercise, seizure activity, fever and reduced oxygen intake.  Excessive intake of acids floods the body with hydrogen ions. = Agents that cause acidosis when ingested in excess include: alcoholic beverages, methyl alcohol, and acetylsalicylic acid (aspirin). 2. Underelimination of hydrogen ions – leads to acidosis when hydrogen ions are produced at the normal rate but are not removed at the same rate they produced.  Most hydrogen ion loss occurs through the lungs and the kidneys. = Kidney failure causes acidosis when the kidney tubules cannot secrete hydrogen ions into the urine  as a result; too many hydrogen ions are retained. 3. Underproduction of bicarbonate ions (base deficit) – leads to acidosis when hydrogen ion production and removal are normal but too few bicarbonate ions are present to balance the hydrogen ion.  Such base deficits occur when bicarbonate ions are not produced at the normal rate  because bicarbonate is made in the kidneys and in the pancreas, renal failure and impaired liver or pancreatic function  can cause base-deficit acidosis. 4. Overelimination of bicarbonate ions (base-deficit) – leads to acidosis when hydrogen ion production and removal are normal but too many bicarbonate ions have been lost.  One cause of base-deficit acidosis is diarrhea. 1.2.RESPIRATORY ACIDOSIS Respiratory acidosis – results any area of the respiratory function is impaired  reducing the exchange of oxygen (O2) and carbon dioxide (CO2)  causing CO2 retention – because any increase in CO2 levels causes the same increase in hydrogen ion levels, CO2 retention  leads to acidosis.  Unlike metabolic acidosis, respiratory acidosis results from only one mechanism – retention of CO2 causing increased production of free hydrogen ions.  Respiratory acidosis is caused by four types of problems: 1. Respiratory depression – caused by reduced function of the brainstem neurons that trigger breathing movements  resulting in a reduced rate and depth of breathing  leading to poor gas exchange and retention of carbon dioxide.  Respiration can be depressed also by anesthetic drugs (especially opioids) and poisons such as methyl alcohol, pesticides, and botulinus toxin.  Physical depression of respiration occurs when neurons are damaged or destroyed by trauma or when problems in other areas of the brain increases the ICP  causing edema which presses on the respiratory center located in the brainstem. = Problems causing cerebral edema and respiratory depression include: brain tumors, cerebral aneurysm, stroke, and overhydration. 2. Inadequate chest expansion – reduces gas exchange and leads to acidosis.  Chest expansion can be restricted by skeletal muscle trauma or deformities, respiratory muscle weakness, or external constriction. = Respiratory muscle weakness – caused by electrolyte imbalances, fatigue, muscle dystrophy, muscle damage or breakdown  reduces chest movement. = External conditions such as body casts, tight scar tissue around the chest, obesity and ascitis  can restrict chest movement and gas exchange. 3. Airway obstruction – prevents air movement into and out from the lungs  leading to poor gas exchange, CO2 retention and acidosis.  The upper airway can be obstructed externally by clothing, neck edema, and local lymph node enlargement.  Internal obstruction of the upper airway can be caused by aspiration of foreign objects, bronchoconstriction, mucus and edema. 4. Reduced alveolar-capillary diffusion – causes poor gas exchange  leading to CO2 retention and acidosis.  Disorders that reduce diffusion include: pneumonia, pneumonitis, tuberculosis, emphysema, acute respiratory distress syndrome, chest trauma, pulmonary emboli, pulmonary edema and drowning. Combined Metabolic and Respiratory Acidosis  Metabolic and respiratory acidosis can occur at the same time.  Uncorrected acute respiratory acidosis always leads to poor oxygenation and lactic acidosis.  Combined acidosis is more severe than either metabolic acidosis or respiratory acidosis alone.  Cardiac arrest – is an example of problem leading to combined metabolic and respiratory acidosis. Clinical Manifestations:  Manifestations of acidosis are similar whether the cause is metabolic or respiratory.  These are changes in the excitable membranes of neurons, skeletal muscle and gastric smooth muscle.  Central Nervous System (CNS) Changes – include depression of CNS function.  Problems may range from lethargy to confusion – especially in older patients.  Stuporous and unresponsive – as acidosis worsens. = Assess the patient’s mental status.  Neuromuscular Changes – with acidosis include:  Reduced muscle tone and deep tendon reflexes (hyporeflexia) – the cause of these changes are high blood levels of potassium (hyperkalemia) along with acidosis.  Skeletal muscle weakness – is bilateral from acidosis.  Flaccid paralysis – which may progress.  Cardiovascular Changes – are first seen wild acidosis and are more severe as the condition worsens.  Early changes include: increased heart rate and cardiac output.  With worsening acidosis or with acidosis and hyperkalemia: decreased heart rate, tall and peaked T waves, widened QRS complexes.  Thready peripheral pulses – may be hard to find and are easily blocked  Hypotension – may occur as a result of vasodilation.  Respiratory Changes – may cause the acidosis and can be caused by the acidosis.  Kussmaul respiration – breaths are deep and rapid and not under voluntary control (in metabolic acidosis with respiratory compensation).  Shallow and rapid respiration – if acidosis is caused by respiratory problems breathing efforts are reduced.  Muscle weakness makes this problem worse.  Skin Changes – occur with metabolic and respiratory acidosis.  Skin and mucous membranes warm, dry and pink – caused by vasodilation due to metabolic acidosis.  Pale to cyanotic and dry skin – in respiratory acidosis. Psychosocial Assessment:  It is vital to complete a psychosocial assessment because behavioural changes may be the first manifestations of acidosis. = Observe and document patient’s behaviour by description (objectively) rather than by interpretation (subjectively). Ex: you should state that “the patient does not recognize close family members” rather than “the patient is confused”. = Ask family members if the patient’s behaviour is typical for him or her, and establish a baseline for comparison with later assessment findings. Laboratory Assessment:  Arterial blood pH is less than 7.35  indicate acidosis.  Other laboratory data: ABG and blood levels of electrolytes  Metabolic acidosis = The pH is low (

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