Download Free Medical Acid-Base Balance PowerPoint Presentation

Acid-Base Balance PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Acid – base balance".

This medical PowerPoint presentation is about acid-base balance, the regulation of hydrogen ion (H+) concentration in the body fluids. The pH of the blood and other bodily fluids must be maintained within a narrow range to support proper physiological function.

The pH scale ranges from 0 to 14, with a pH of 7 considered neutral. A pH below 7 is acidic, while a pH above 7 is alkaline or basic. In humans, the pH of the blood is tightly regulated between 7.35 and 7.45, slightly on the alkaline side.

Acids are substances that can donate H+ ions, while bases are substances that can accept H+ ions. The body has various mechanisms for regulating the balance between acids and bases in the blood, including the lungs, kidneys, and buffer systems.

The lungs regulate the amount of carbon dioxide (CO2) in the blood, which can affect pH. When CO2 levels increase, the body increases breathing to eliminate excess CO2 and maintain pH.

The kidneys help to regulate the levels of acids and bases in the blood by excreting excess acids or bases in the urine.

Buffer systems in the blood also help to regulate pH by binding excess H+ ions or releasing H+ ions as needed.

An imbalance in acid-base balance can lead to acidosis (low pH) or alkalosis (high pH), which can cause various symptoms and health problems. Examples of conditions that can disrupt acid-base balance include kidney disease, diabetes, and respiratory disorders.

Tags : acid-base balance, regulation of hydrogen ion (H+) concentration in the body fluids, Otolaryngology, Otolaryngology PowerPoint presentation

Published on : Jun 23, 2023 | Views : 2785 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Acid – base balance Basic facts – repetition Regulation of A-B balance Pathophysiology of clinically important disorders
Slide 2-

Acids vs. Bases definition: Bronsted-Lowry (1923) normal A:B ratio  1:20 strength is defined in terms of the tendency to donate (or accept) the hydrogen ion to (from) the solvent (i.e. water in biological systems) Acid: H+ donorBase: H+ acceptor
Slide 3-

pH pH is and indirect measure of [H+] CAVE! Hydrogen ions (i.e. protons) do not exist free in solution but are linked to adjacent water molecules by hydrogen bonds (H3O+) [H+] by a factor of 2 causes a  pH of 0.3 neutral vs. normal plasma pH pH 7.4 (7.36-7.44)  normal pH 7.0  neutral but fatal!!! pH=-log [H+] pH 7.40  40 nM pH 7.00  100 nM pH 7.36  44 nM pH 7.44  36 nM
Slide 4-

Buffers extracellular carbonic acid / bicarbonate (H2CO3 / HCO3-) haemoglobin intracellular proteins phosphoric acid / hydrogen phosphate (H3PO4 / H2PO4- + HPO42-) Henderson-Hasselbalch equation: pH = 6.1 + log([HCO3-] / 0.03 pCO2)
Slide 5-

Organs involved in the regulation of A-B-balance Equilibrium with plasma High buffer capacity Haemoglobin – main buffer for CO2 Excretion of CO2 by alveolar ventilation: minimally 12,000 mmol/day Reabsorption of filtered bicarbonate: 4,000 to 5,000 mmol/day Excretion of the fixed acids (acid anion and associated H+): about 100 mmol/day
Slide 6-

Organs involved in the regulation of A-B-balance CO2 production from complete oxidation of substrates 20% of the body’s daily production metabolism of organic acid anions such as lactate, ketones and amino acids metabolism of ammonium conversion of NH4+ to urea in the liver results in an equivalent production of H+ Production of plasma proteins esp. albumin contributing to the anion gap Bone inorganic matrix consists of hydroxyapatite crystals (Ca10(PO4)6(OH)2] bone can take up H+ in exchange for Ca2+, Na+ and K+ (ionic exchange) or release of HCO3-, CO3- or HPO42-
Slide 7-

pH is constantly “impaired” by metabolism Total CO2: = [HCO3] + [H2CO3] + [carbamino CO2] + [dissolved CO2]
Slide 8-

Why is pH so important ? All the known low molecular weight and water soluble biosynthetic intermediates possess groups that are essentially completely ionised at neutral pH’ pH-dependent ionisation (i.e. charge) serves to an efficient intracellular trapping of ionised compounds within the cell and its organelles Exceptions: macromolecules (proteins) mostly charged anyway or size-trapping or hydrophobic lipids those needed intarcellularly are protein-bound waste products pH has an effects on protein function
Slide 9-

The most important pH for the body is the intracellular pH
Slide 10-

The most important pH for the body is the intracellular pH Intracellular pH is maintained at about the pH of neutrality (6.8 at 37˚C) because this is the pH at which metabolite intermediates are all charged and trapped inside the cell Extracellular pH is higher by 0.5 to 0.6 pH units and this represents about a fourfold gradient favouring the exit of hydrogen ion from the cell to maintain it at a stable value because of the powerful effects of intracellular [H+] on metabolism maintaining a stable intracellular pH by: ‘Intracellular buffering’ (chemical, metabolic, organelles) Adjustment of arterial pCO2 Loss of fixed acids from the cell into the extracellular fluid pN  [H+] = [OH-] pN=7.0 at 25˚C for pure H2O pN=6.8 at 37˚C in cell
Slide 11-

Respiratory system - CO2 differences in the stimulation of respiration by pCO2, H+ and pO2 alveolar ventilation disturbances acidemia  respiratory centre of the brain  alveolar ventilation  CO2 alkalemia  respiratory centre of the brain   alveolar ventilation   CO2
Slide 12-

Renal system – fixed H+ & HCO3- Proximal tubular mechanisms: reabsorption of HCO3- filtered at the glomerulus production of NH4+ Distal tubular mechanisms: net excretion of H+ normally 70mmol/day max. 700mmol/day together with proximal tubule excretion of H+ could increase up to 1000x!!! (pH of urine 4.5) Formation of titratable acidity (TA) Addition of NH4+ to luminal fluid Reabsorption of remaining HCO3-
Slide 13-

Assessment of A-B balance
Slide 14-

Disorders of A-B balance Acidosis: abnormal condition lowering arterial pH before secondary changes in response to the primary aetiological factor Alkalosis: abnormal condition raising arterial pH before secondary changes in response to the primary aetiological factor Simple A-B disorders: there is a single primary aetiological acid-base disorder Mixed A-B disorders: more primary aetiological disorders are present simultaneously Acidaemia: arterial pH<7.36 (i.e. [H+]>44 nM) Alkalaemia: arterial pH>7.44 (i.e. [H+]<36 nM)
Slide 15-

Causes Respiratory abnormal processes which tend to alter pH because of a primary change in pCO2 levels acidosis alkalosis Metabolic abnormal processes which tend to alter pH because of a primary change in [HCO3-] acidosis alkalosis
Slide 16-

Respiratory acidosis (RA) primary disorder is a pH due to PaCO2 (>40 mmHg), i.e. hypercapnia time course: acute (pH) chronic (pH or normalisation of pH) renal compensation – retention of HCO3-, 3-4 days causes: decreased alveolar ventilation (presence of excess CO2 in the inspired gas) (increased production of CO2 by the body) paCO2 = VCO2 / VA
Slide 17-

Most cases of RA are due to decreased alveolar ventilation !!!! the defect leading to this can occur at any level in the respiratory control mechanism A rise in arterial pCO2 is a potent stimulus to ventilation so a respiratory acidosis will rapidly correct unless some abnormal factor is maintaining the hypoventilation
Slide 18-

RA - inadequate alveolar ventilation Central respiratory depression & other CNS problems drug depression of respiratory center (e.g. by opiates, sedatives, anaesthetics) CNS trauma, infarct, haemorrhage or tumour hypoventilation of obesity (e.g. Pickwick syndrome) cervical cord trauma or lesions (at or above C4 level) high central neural blockade poliomyelitis tetanus cardiac arrest with cerebral hypoxia Nerve or muscle disorders Guillain-Barre syndrome Myasthenia gravis muscle relaxant drugs toxins e.g. organophosphates, snake venom various myopathies Lung or chest wall defects acute on COPD chest trauma -contusion, haemothorax pneumothorax diaphragmatic paralysis pulmonary oedema adult respiratory distress syndrome restrictive lung disease aspiration Airway disorders upper airway obstruction laryngospasm bronchospasm / asthma External factors Inadequate mechanical ventilation
Slide 19-

RA - rare causes Over-production of CO2 in hypercatabolic disorders malignant hyperthermia sepsis Increased intake of CO2 re-breathing of CO2-containing expired gas addition of CO2 to inspired gas insufflation of CO2 into body cavity (e.g. for laparoscopic surgery)
Slide 20-

RA - metabolic effects (hypercapnia!) depression of intracellular metabolism cerebral effects cardiovascular system extremely high hypercapnia: anaesthetic effects (pCO2>100mmHg) hypoxaemia An arterial pCO2>90 mmHg is not compatible with life in patients breathing room air: pAO2 = [0.21x(760-47)]-90/0.8 = 37 mmHg
Slide 21-

RA - compensation Acute RA - buffering only! about 99% of this buffering occurs intracellularly proteins (haemoglobin and phosphates) are the most important intravascular buffers for CO2 but their concentration is low relative to the amount of carbon dioxide requiring buffering the bicarbonate system is not responsible for any buffering of a respiratory acid-base disorder - system cannot buffer itself Chronic RA - renal bicarbonate retention takes 3 or 4 days to reach its maximum paCO2  pCO2 in proximal tubular cells  H+ secretion into the lumen:  HCO3 production which crosses the basolateral membrane and enters the circulation (so plasma [HCO3] increases)  Na+ reabsorption in exchange for H+  NH3 production to 'buffer' the H+ in the tubular lumen (so urinary excretion of NH4Cl increases)
Slide 22-

RA - correction (i.e. treatment) the pCO2 rapidly returns to normal with restoration of adequate alveolar ventilation treatment needs to be directed to correction of the primary cause if this is possible rapid fall in pCO2 (especially if the RA has been present for some time) can result in: severe hypotension ‘post hypercapnic alkalosis’
Slide 23-

Metabolic acidosis (MA) primary disorder is a pH due to HCO3-:  fixed [H+] = high anion gap loss or  reabsorption of HCO3- = normal anion gap AG = [Na+] - [Cl-] - [HCO3-]
Slide 24-

MA - causes ketoacidosis diabetic, alcoholic, starvation lactic acidosis acute renal failure toxins renal tubular acidosis GIT loss of HCO3 diarrhoea drainage of pancreatic or bile juice
Slide 25-

MA - metabolic effects respiratory hyperventilation shift of haemoglobin dissociation curve to the right decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) cardiovascular others increased bone resorption (chronic acidosis only) shift of K+ out of cells causing hyperkalaemia