Week 7: Acid-Base Balance Flashcards
Explain the cellular ion exchange mechanisms in the regulation of pH
To maintain the body’s normal pH (7.35-7.45), hydrogen must be either neutralized by bicarbonate (HCO3-) or excreted from the body. As hydrogen ion increases, the pH decreases and becomes more acidic. As hydrogen ion decreases, pH increases and becomes more alkaline. Imbalances are classified by the effect of pH (i.e. acidic or alkaline) and the cause (i.e., metabolic or respiratory). A pH below 6.8 and above 7.8 is lethal. pH is regulated by 4 mechanisms:
- Chemical buffers (i.e., carbonic acid-bicarbonate buffering through association and dissociation)
- Respiratory buffering (regulates retention and elimination of CO2 and therefore H2CO3 concentration)
- Renal buffering (i.e., bicarb reabsorption and regeneration, ammonia formation, and phosphate buffering)
- RBCs (i.e., hydrogen ions combine with hemoglobin that has released its oxygen to form HHb, which buffers the hydrogen ion
Describe the intracellular compensatory mechanisms for buffering changes in body pH
Potassium and hydrogen are both positively charged “cations”, they move freely between the ICF and ECF. Each fluid compartment is electrically neutral and this must be maintained. There are cellular shifts of potassium in exchange for hydrogen during states of alkalosis or acidosis, but this shifting will impact the body and influence serum potassium.
Compare and contrast the causes, diagnostics, manifestations, and treatment of potassium electrolyte imbalances
Potassium is a major intracellular cation and the sodium-potassium ATPase pump maintains concentration within a narrow range of 3.5-5 mmol/L. Kidneys regulate potassium balance tightly as it is essential for transmission and conduction of nerve impulses, normal cardiac rhythms, skeletal and smooth muscle contraction and regulates ICF osmolality.
Hypokalemia: potassium level of <3.5 mmol/L and is caused by reduced potassium intake and entry into cell or increased loss (typically due to loop diuretics). Manifestations include:
- decreased neuromuscular excitability
- skeletal muscle weakness
- smooth muscle atony
- cardiac dysrhythmias
- u wave on electrocardiogram (ECG)
Treatment involves replacing potassium orally or intravenously (slowly!)
Hyperkalemia: potassium level of > 5.0 mmol/L, is considered rare as kidneys are efficient at excreting potassium. Can be caused by increased intake, acidosis, a shift of potassium from the cells to the ECF, renal pathology, insulin deficiency, and cell trauma/hypoxia. Manifestations include:
- tingling of lips and fingers
- restlessness
- intestinal cramping
- diarrhea
- T waves on the ECG
Treatment includes calcium gluconate, insulin and/or glucose, buffered solutions dialysis
Determine acid-base imbalances through analysis of arterial blood gases
pH: 7.35-7.45
PCO2: 35-45 mm Hg
Bicarbonate: 22-26 mmol/L
PO2: 80-100 mm Hg
SO2 = 96-98%
ABGs can tell us:
1. Is there an acid base imbalance?
2. Which system is causing the imbalance?
3. Which system is trying to compensate for the imbalance?
4. What is the alternate system doing? (i.e., fully compensating)
Identify common causes of metabolic and respiratory acidosis and metabolic and respiratory alkalosis
Metabolic Alkalosis: hydrogen diffuses out of the cells and into the blood, but potassium moves into the cells to maintain electroneutrality. The kidneys reabsorb hydrogen and secrete potassium. As a result, the physiological response to metabolic alkalosis causes hypokalemia. Resulting from an increase in HCO3- , often from an excessive loss of metabolic acids.
Metabolic Acidosis: hydrogen leaves the blood and diffuses into the cells and potassium moves into the cells to maintain electroneutrality. The kidneys secrete hydrogen but also reabsorb potassium. As a result, the physiological response to metabolic acidosis causes hyperkalemia. Resulting from a decrease in HCO3-, often from an increase in metabolic acids.
Respiratory Acidosis: resulting from an increase of PCO2 and will result in hypoventilation. Carbon dioxide mixes with H20 to make carbonic acid; retaining CO2 is like a bad friend, will hook up with hydrogen to make carbonic acid (toxic situation)
Respiratory Alkalosis: resulting from a decrease in PCO2 and results in hyperventilation.
Compare and contrast clinical manifestations and treatment of metabolic and respiratory alkalosis and acidosis
Respiratory acidosis is typically caused by hypoventilation which may result from a depressed CNS (i.e., opioid overdose) or if you have respiratory muscle problems (i.e., chest wall disorders or COPD). Clinical manifestations might include headache, restlessness, convulsions, or coma. To treat you will need to supply adequate ventilation and may need mechanical ventilation or oxygen therapy.
Respiratory Alkalosis: is caused from losing too much carbon dioxide which may be due to high altitudes, hypermetabolic states (i.e., fever, anemia), salicylate intoxication, anxiety or panic disorder, or the improper use of ventilators. Clinical manifestations include dizziness, lightheadedness, confusion or panic, numbness, convulsions or coma. Treatment may include breathing into a paper bag or re-breather and treating hypoxemia and hypermetabolic states.
Metabolic Acidosis: is cased from the accumulation of hydrogen ions which may result from lactic acidosis, starvation, diabetic ketoacidosis, diarrhea or renal failure. It may clinically manifest in headache, lethargy or kussmaul respirations. Treatment will include a buffering solution administration and treating the underlying causes through base administration and correcting sodium and water deficits.
Metabolic Alkalosis: is caused from the loss of hydrogen and may result from prolonged vomiting (less hydrogen ions - think stomach acid), excessive bicarb intake (i.e., tums), gastric suctioning, or diuretic therapy. It will clinically manifest in weakness, muscle cramps, hyperactive reflexes with signs of hypocalcemia. Treatment includes sodium chloride, potassium, or chloride IV (chloride replaces bicarb)
Describe the Carbonic Acid-Bicarbonate Buffering system
This is the first system to act, when bicarbonate (HCO3-) and carbonic acid (H2C03) increase or decrease proportionately, the 20:1 ratio is maintained. This process involves the kidneys, which can reabsorb bicarbonate or regenerate new bicarbonate from CO2 and H20, and the lungs which can decrease carbonic acid by exhaling CO2. These two systems work very effectively together.
Lungs Kidneys
CO2 + H20 –> H2CO3 –> HCO3- + H+
Carbon dioxide and water together make carbonic acid, if acid is needed OR carbonic acid dissociates into carbon dioxide and water, where the carbon dioxide can be blown off by the lungs if we need to remove acid.
In the kidneys, carbonic acid dissociates into bicarbonate and hydrogen to be excreted by the kidneys OR bicarbonate and hydrogen can make carbonic acid depending on what the body needs.
Describe the respiratory buffering system
Chemoreceptors in the body sense pH and PCO2 changes, as a response the lungs will either blow off or retain CO2. When CO2 is blown off, it can’t combine with H20 and carbonic acid (H2CO3) can’t be formed. By retaining CO2, it can combine with H20 and produce carbonic acid.
respiratory acidosis: respirations will increase
respiratory alkalosis: respirations will decrease
Describe the renal buffering system
The kidneys regulate pH by making new bicarbonate or reabsorbing it from the urine, they can also secret excess hydrogen into the urine by attaching it to phosphate and ammonia.
What are the alternative buffering systems?
- Protein buffering (instantaneous): proteins have negative charges so they can serve as buffers for hydrogen; mainly intracellular buffers with hemoglobin
- Phosphate buffering (hours to days): exchanges of calcium and phosphate, and release of carbonate from the bones
- Cellular ion exchange (2 to 4 hours): exchanges of potassium for hydrogen and vice versa
What happens with hypokalemia?
When hypokalemia develops, potassium ions diffuse out of the cells and into the blood. In response, hydrogen ions move into the cells to maintain electrical neutrality. The kidneys reabsorb the potassium but secrete the hydrogen to also maintain balance. As a result, the physiological response to hypokalemia causes metabolic alkalosis.
What happens with hyperkalemia?
When hyperkalemia develops, potassium ions diffuse out of the blood and into the cells and hydrogen ions leave the cells to maintain neutral electrical balance. Kidneys will also secrete potassium, but also reabsorb more hydrogen to keep electroneutrality. As a result, the physiological response to hyperkalemia causes metabolic acidosis.
Discuss ECG changes in potassium electrolyte imbalances
Hypokalemia: a drop in potassium will result in a more spiked p-wave and the p-r interval will be longer; s-t depression and t was is also more shallow and very prominent spiked u wave (looks like a lazy signature)
Hyperkalemia: wide and flatter p-wave, p-r interval will be more prolonged and r wave will have decreased amplitude; widened qrs, s-t segment is flattened and t wave is very tall and peaked and wide (looks like someone was hyper and wrote their signature really fast)
How is respiratory acidosis compensated?
The metabolic system via the kidneys will compensate by conserving bicarbonate and eliminating hydrogen ions in acidic urine. If the metabolic system fails to compensate, a lactate-containing solution can be administered by IV.
How is respiratory alkalosis compensated?
The metabolic system via the kidneys will compensate by conserving hydrogen ions and eliminating bicarbonate through alkaline urine. If the metabolic system fails to compensate, a chloride-containing solution can be administered by IV. Bicarbonate ions will be replaced by chloride ions.
