Renal Physiology and Acid Base Balance

Disconnect the patient from the dialysis machine.

Clamp the abdominal catheter and cap it if possible; if unable to cap, cover with sterile gauze.

An increase in blood osmolality and hypotension.

ADH directly stimulates vasoconstriction and increases the permeability of the distal convoluted tubule (DCT) and collecting duct (CD) to water, allowing for more reabsorption of water and increasing stroke volume (SV).

The three key components of DKA are hyperglycaemia, ketosis, and metabolic acidosis.

Chronic renal failure refers to the loss of kidney function over months or years. In advanced stages, dangerous levels of wastes and fluids back up in the body, leading to serious complications.

The renal system consists of the kidneys, ureters, bladder, and urethra. Its primary functions include:

1. Filtration: Removing waste products and excess substances from the blood.
2. Regulation: Maintaining fluid and electrolyte balance, blood pressure, and acid-base homeostasis.
3. Hormone Production: Producing hormones such as erythropoietin and renin that regulate blood pressure and red blood cell production.

The signs and symptoms of chronic renal failure include:

• Fluid retention
• Polyuria
• Anuria
• Hyperkalaemia
• Hypertension (HTN)
• Shortness of breath (SOB)
• Nausea and vomiting (N & V)
• Restless legs
• Pruritis

Renal pathophysiology can significantly impact pharmacokinetics in the following ways:

• Absorption: Altered gastrointestinal function may affect drug absorption.
• Distribution: Changes in body fluid composition can influence drug distribution.
• Metabolism: Renal impairment can reduce the metabolism of drugs, leading to increased plasma concentrations.
• Excretion: Impaired renal function decreases the elimination of drugs, necessitating dosage adjustments to avoid toxicity.

The RAAS plays a crucial role in regulating blood pressure and fluid balance through the following components:

• Renin: Released by the kidneys in response to low blood pressure, it converts angiotensinogen to angiotensin I.
• Angiotensin II: A potent vasoconstrictor that increases blood pressure and stimulates aldosterone release.
• Aldosterone: Promotes sodium and water reabsorption in the kidneys, increasing blood volume and pressure.
• ADH (Antidiuretic Hormone): Enhances water reabsorption in the kidneys, further contributing to fluid balance.

Loop Diuretics in ACPO:

• Actions: Inhibit sodium and chloride reabsorption in the ascending loop of Henle, leading to increased urine output.
• Rationale for Use: Rapidly reduce fluid overload and pulmonary congestion in ACPO.
• Indications: Used in patients with ACPO to relieve symptoms of dyspnea and improve oxygenation.
• Adverse Effects:
  • Electrolyte imbalances (e.g., hypokalemia)
  • Dehydration
  • Ototoxicity (at high doses)
  • Renal impairment (if used excessively)

Frusemide, a loop diuretic, works by inhibiting the Na-K-2Cl symporter in the thick ascending limb of the loop of Henle, leading to increased excretion of sodium, potassium, and chloride, which results in diuresis.

Frusemide is indicated for conditions such as heart failure, pulmonary edema, hypertension, and renal impairment where fluid overload is present.

Contraindications for Frusemide include hypersensitivity to the drug, severe electrolyte depletion, anuria, and caution in patients with renal impairment or hepatic dysfunction.

Common adverse effects of Frusemide include electrolyte imbalances (hypokalemia, hyponatremia), dehydration, hypotension, and ototoxicity at high doses.

Acid-base balance is crucial for maintaining homeostasis, influencing enzyme activity, oxygen transport, and overall metabolic processes. It is regulated by buffers, respiratory control, and renal function.

Conditions related to acid-base disorders include metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis, hyperkalemia, BRASH syndrome, and diabetic ketoacidosis (DKA).

The main functions of renal filtration include:

1. Removal of metabolic waste products from the body, primarily urea and uric acid.
2. Regulation of electrolyte balance, including sodium, potassium, and calcium.
3. Osmoregulation, which controls blood volume and body water content.
4. Blood pressure homeostasis, where the renal system alters water retention and thirst to maintain normal blood pressure.
5. Regulation of acid-base homeostasis and blood pH, in conjunction with the respiratory system.

Nephrons are the main functional component of the kidneys.

The respiratory and cardiovascular systems have certain functions that overlap with renal system functions.

Metabolic wastes and excess ions are filtered out of the blood, combined with water, and leave the body in the form of urine.

A complex network of hormones controls the renal system to maintain homeostasis.

Chronic renal disease can lead to serious complications, including:

• High blood pressure
• Fluid build-up in the lungs or other areas
• Vitamin D deficiency, affecting bone health
• Nerve damage that can lead to seizures

Common complications of haemodialysis include:

• Hypotension: Low blood pressure during the procedure.
• Cramps: Muscle cramps can occur.
• Nausea and Vomiting (N&V): Patients may experience nausea and vomiting.
• Headaches: Some patients report headaches during or after treatment.

The main anatomical features of the kidney include:

The nephron consists of several key components:

1. Glomerulus: A network of capillaries where filtration of blood occurs.
2. Bowman's Capsule: Encases the glomerulus and collects the filtrate.
3. Proximal Convoluted Tubule: Responsible for the reabsorption of water, ions, and nutrients.
4. Loop of Henle: Creates a concentration gradient in the renal medulla, essential for water reabsorption.
5. Distal Convoluted Tubule: Further adjusts the filtrate composition through secretion and reabsorption.
6. Collecting Duct: Final site for water reabsorption and urine concentration.
7. Afferent and Efferent Arterioles: Regulate blood flow into and out of the glomerulus.
8. Peritubular Capillaries and Vasa Recta: Supply blood to the nephron and assist in reabsorption and secretion processes.

NFP = GHP – (OP + CHP) where:

• GHP = Glomerular Hydrostatic Pressure
• OP = Osmotic Pressure
• CHP = Capsular Hydrostatic Pressure

The main components of the Renal Corpuscle include:

• Afferent arteriole
• Juxtaglomerular cells
• Distal convoluted tubule
• Macula Densa
• Efferent arteriole
• Glomerular space
• Glomerular capsule
• Mesangium
• Glomerulus capillaries
• Podocyte
• Proximal tubule

Glomerular Hydrostatic Pressure (GHP) is crucial as it drives the filtration of blood through the glomerulus, facilitating the formation of urine. In this context, GHP is typically around 55 mmHg.

Blood Colloid Osmotic Pressure (OP) and Capsular Hydrostatic Pressure (CHP) oppose filtration:

• OP (30 mmHg) pulls water back into the capillaries, reducing filtration.
• CHP (15 mmHg) exerts pressure against the filtration process, also reducing filtration. Thus, both pressures decrease the NFP, which is calculated as GHP minus the sum of OP and CHP.

Acute Kidney Failure:

• Develops within hours or days.
• Chance of kidney function recovery is possible.
• Possible causes include:
  • Traumatic (e.g., post-surgical)
  • Acute intoxications
  • Part of multiorgan failure
  • Various other diseases (e.g., infections)

Chronic Kidney Failure:

• Develops over years.
• Irreversible at the end stage.
• Possible causes include:
  • Secondary to high blood pressure and/or diabetes
  • Chronic bacterial inflammation of the kidneys
  • Cystic kidneys
  • Various autoimmune diseases

The three types of renal failure are:

Causes of pre-renal acute renal failure include:

• Cardiac failure
• Sepsis
• Blood loss
• Dehydration
• Vascular occlusion

Conditions that can lead to intra-renal acute renal failure include:

• Glomerulonephritis
• Small-vessel vasculitis
• Acute tubular necrosis (due to drugs, toxins, prolonged hypotension)
• Interstitial nephritis (due to drugs, toxins, inflammatory disease, infection)

Common causes of post-renal acute renal failure include:

• Urinary calculi (kidney stones)
• Retroperitoneal fibrosis
• Benign prostatic enlargement
• Prostate cancer
• Cervical cancer
• Urethral stricture/valves
• Meatal stenosis/phimosis

Pre-renal and post-renal causes can lead to intra-renal failure by impairing kidney perfusion or causing obstruction, which may result in direct damage to kidney tissues and subsequent renal dysfunction.

The stages of kidney function in chronic renal failure are as follows:

The initial imbalances caused by chronic kidney disease include:

1. Sodium and water balance
2. Potassium balance
3. Elimination of nitrogenous wastes
4. Erythropoietin production
5. Acid-base balance
6. Activation of vitamin D
7. Phosphate elimination

The consequences of impaired sodium and water balance in chronic kidney disease include:

• Hypertension
• Increased vascular volume
  • Leads to Edema
  • Can result in Heart failure
    • May also lead to Pericarditis

Hyperkalemia is a significant consequence of impaired potassium balance in chronic kidney disease, which can lead to serious cardiac complications and requires careful monitoring and management to prevent life-threatening arrhythmias.

Chronic kidney disease leads to decreased erythropoietin production, resulting in:

• Anemia
• Coagulopathies
  • Can lead to Bleeding

Impaired acid-base balance in chronic kidney disease can lead to:

• Skeletal buffering
• Acidosis

Impaired activation of vitamin D and phosphate elimination in chronic kidney disease can lead to:

• Hypocalcemia
  • Results in Hyperparathyroidism

The final outcomes of chronic kidney disease that converge from heart failure, uremia, acidosis, and hyperparathyroidism include:

• Osteodystrophies
• Impaired immune function
• Skin disorders
• Gastrointestinal manifestations
• Neurologic manifestations
• Sexual dysfunction

Chronic renal failure significantly reduces nonrenal clearance and alters the bioavailability of drugs that are predominantly metabolized by the liver and intestine. This can lead to increased drug levels and potential toxicity.

Renal clearance of drugs depends mainly on Glomerular Filtration Rate (GFR), tubular absorption, and tubular secretion. Changes in any of these variables can affect the renal clearance rate of a substance.

Drug doses should usually be reduced in renal disease in proportion to the predicted reduction in clearance of the active drug moiety to avoid toxicity and ensure efficacy.

Examples of drugs that may require dose adjustments in renal disease include digoxin, lithium, morphine, metformin, and some antibiotics.

Dialysis is an external filtering process that uses semi-permeable tubes running through a plasma-like solution. During dialysis:

1. Waste diffuses down its gradient out of the blood.
2. The cleaned blood is then returned to the body.
3. Water balance is maintained through osmosis.

It is important to select the right dialysis for the right person to ensure effective treatment.

The primary function of dialysis fluid in peritoneal dialysis is to facilitate the movement of water, salts, and waste products from the blood into the dialysis solution through the peritoneal membrane.

The peritoneal cavity, covered by a thin membrane containing many small blood vessels, is significant in peritoneal dialysis as it allows for the exchange of substances between the blood and the dialysis fluid.

Haemodialysis involves the following steps:

1. Blood circulation: Blood is slowly pumped out of the body into a dialysis machine.
2. Filtration: The blood passes through a filter membrane in the machine for cleaning.
3. Return: After filtration, the blood is returned to the body through the same vascular access.

Vasopressin

1. Clamp the catheter.
2. Disconnect the lines.
3. Cap the catheter ends with IV bung (note: both lumens are venous).

1. Turn the dialysis machine off.
2. Clamp the lines.
3. Cap the ends.
4. If unable to detach lines, decannulate the patient (remove needles from fistula) and apply direct pressure due to high pressure in the fistula.

• Dyspnoea
• Medical Hypoperfusion/Hypovolaemia
• Hypoglycaemia
• Hyperglycaemia
• Abdominal Pain (consider peritonitis in peritoneal dialysis patients)
• Suspect venous air embolism if air is seen in the venous line and patient has cardiovascular collapse.

Paramedics may use either dialysis port, but a pump set is essential due to high pressure in the 'arterialised' veins.

Avoid using the fistula arm for cannulation; if necessary, cannulate at least 2cm proximal to the fistula.

It helps to identify trends, clinical deterioration, and/or response to treatment.

The use of blood pressure cuffs or tourniquets should be avoided on the arm containing the fistula.

1. Open the blood pump door to stop the machine.
2. Then turn off or unplug the machine from the wall.

The RAAS regulates blood pressure by controlling blood volume and vascular resistance. It responds to a drop in blood pressure by initiating a series of hormonal responses that ultimately lead to increased blood pressure.

The key components of RAAS include:

1. Renin - an enzyme released by the kidneys in response to low blood pressure.
2. Angiotensinogen - a protein produced by the liver that is converted to Angiotensin I by renin.
3. Angiotensin I - a precursor that is converted to Angiotensin II by the Angiotensin-converting enzyme (ACE) in the lungs.
4. Angiotensin II - a potent vasoconstrictor that increases blood pressure and stimulates the release of aldosterone.
5. Aldosterone - a hormone that promotes sodium and water retention by the kidneys, further increasing blood volume and blood pressure.

The RAAS can be manipulated through various pharmacological agents to manage conditions such as hypertension (HTN), heart failure (HF), acute myocardial infarction (AMI), and diabetes mellitus (DM). Common classes of medications include:

• ACE inhibitors - block the conversion of Angiotensin I to Angiotensin II, reducing blood pressure.
• Angiotensin II receptor blockers (ARBs) - prevent Angiotensin II from binding to its receptors, lowering blood pressure.
• Direct renin inhibitors - inhibit renin activity, decreasing the production of Angiotensin I and II.

The juxtaglomerular cells produce renin in response to three mechanisms:

1. Baroreceptor mechanism: Decreased blood pressure in the afferent arteriole.
2. Sympathetic nerve mechanism: Activation of Beta 1 adrenergic nerves.
3. Macular densa mechanism: Decreased NaCl concentration passing through the distal convoluted tubule (DCT) stimulates renin production.

Angiotensin II stimulates:

1. Vasoconstriction
2. Increased reabsorption from renal tubules to increase blood volume
3. Increased sympathetic activity
4. Stimulates aldosterone and ADH secretion

Angiotensin II enhances renal function by:

• Increasing tubular Na+ and Cl- reabsorption
• Promoting K+ excretion
• Leading to H2O retention

Angiotensin II contributes to blood pressure regulation through:

• Arteriolar vasoconstriction, which increases blood pressure
• Stimulation of aldosterone and ADH secretion, promoting fluid retention

Aldosterone is secreted in response to:

• Angiotensin II release
• Hypotension
• Hyperkalaemia

Aldosterone has the following effects on the kidneys:

1. Increased reabsorption of Na+ from filtrate into blood
2. Increased water retention via osmosis from the distal convoluted tubule (DCT) and collecting duct (CD) into capillaries
3. Increased K+ excretion into filtrate

Angiotensin II causes several physiological effects including:

• Sympathetic activity
• Tubular Na+ Cl- reabsorption and K+ excretion
• H2O retention
• Aldosterone secretion
• Arteriolar vasoconstriction, leading to increased blood pressure
• ADH secretion and H2O absorption in the collecting duct

A decrease in renal perfusion triggers the release of renin from the juxtaglomerular apparatus in the kidney. This initiates the conversion of angiotensinogen (released by the liver) to angiotensin I, which is then converted to angiotensin II in the lungs, leading to various physiological responses aimed at increasing blood pressure and restoring perfusion.

The main organs involved in the renin-angiotensin-aldosterone system include:

The primary aim of diuretics is to increase urine production to decrease fluid volume, thereby reducing preload and afterload. This helps in limiting cardiac remodeling.

The five main types of diuretics are:

1. Carbonic Anhydrase Inhibitors
2. Osmotic Diuretics
3. Thiazide & Thiazide-like Diuretics
4. Potassium Sparing Diuretics
5. Loop Diuretics

1. Carbonic anhydrase inhibitors - Act on the proximal tubule to block carbonic anhydrase, promoting bicarbonate excretion.

2. Osmotic diuretics - Such as Mannitol, increase water excretion at the Bowman's capsule and Loop of Henle.

3. Loop diuretics - Block the sodium-potassium-chloride cotransporter in the Loop of Henle, promoting excretion of sodium, potassium, and chloride.

4. Thiazide diuretics - Act on the distal convoluted tubule to inhibit sodium and chloride reabsorption.

5. Potassium-sparing diuretics - Work on the collecting duct to antagonize aldosterone receptors, increasing sodium excretion and retaining potassium.

Diuretics are commonly used for:

• Hypertension
• Congestive Heart Failure (CCF)
• Oedema
• Traumatic Brain Injury (TBI)
• Other conditions may include renal failure and certain liver diseases.

The significant adverse effects of diuretics include:

• Electrolyte imbalances
• Hypernatremia and Hyponatremia
• Hyperkalemia and Hypokalemia

Loop Diuretics inhibit the Na+/K+/2Cl- Symporter in the thick segment of the Ascending Loop of Henle (ALOH), making them very powerful diuretics that cause potassium wasting.

Thiazide diuretics act on the early segment of the Distal Convoluted Tubule (DCT) by inhibiting NaCl absorption through the Na+/Cl- Symporter, leading to an osmotic fluid shift.

K+ Sparing diuretics either compete for binding sites with aldosterone or inhibit its creation/secretion, which prevents Na+ reabsorption and reduces K+/H+ excretion.

Frusemide inhibits the Na+/K+/2Cl- symporter in the thick ascending loop of Henle, leading to the retention of Na, K, Cl, and H2O in the renal tubule. This results in decreased osmolality of the renal medulla and reduced water reabsorption in the descending loop of Henle and collecting ducts, ultimately increasing urine output.

Excessive diuresis from frusemide can lead to hypovolaemic shock and potassium loss, which may precipitate dysrhythmias.

Frusemide should not be administered to patients with systolic blood pressure < 100 mmHg and to patients under 16 years of age.

The initial dose of frusemide for patients aged 16 or over who are not taking oral diuretics is 40mg administered via IV/IM route.

The maximum total dose of frusemide for patients aged 16 or over who are taking oral diuretics is 160mg.

• Early diagnosis
• Early treatment including:
  • GTN (Glyceryl Trinitrate)
  • Oxygen (O2)
  • CPAP (Continuous Positive Airway Pressure)
  • Frusemide

The FAST-FU study indicates that early treatment with intravenous furosemide by EMS and at the ED can significantly impact patient outcomes, including reducing in-hospital and 30-day all-cause mortality rates compared to standard treatment.

Time is critical in the prognosis of ACPO/AHF/CCF, as early intervention can lead to better outcomes, including lower mortality rates and reduced hospitalization duration.

The combination bar graph shows that the FAST-FU group (blue bars) has lower in-hospital and 30-day all-cause mortality rates and reduced rates of prolonged hospitalization compared to the control group (red bars) across different risk categories.

The patient reported shortness of breath and was unable to speak beyond a few words over the telephone.

The crew found the patient struggling to breathe with audible crackles in his lungs.

The patient exhibits increased work of breathing and crackles can be heard upon entering the room.

The patient's respiratory rate is 40 breaths per minute and oxygen saturation level is 78%.

The medications listed for the patient include Slow K, Lasix, Lopressor, Nitroglycerin Spray, and Lanoxin.

The patient's heart rate is 140 beats per minute and blood pressure is 180/100 mmHg.

The patient's Glasgow Coma Scale (GCS) is 15, indicating full consciousness, and pupils are equal and reactive to light (PEARL).

Pitting edema is noted at the ankles of the patient.

Cardiogenic pulmonary oedema is a condition where the left ventricle of the heart cannot pump effectively, leading to fluid accumulation in the lungs. Underlying causes include:

• Congestive cardiac failure
• Left ventricular failure post acute myocardial infarction (AMI)
• Hypertension
• Pericardial tamponade

If the patient is hypoventilating and/or has inadequate tidal volume, initiate IPPV with PEEP and 100% oxygen via bag valve mask.

Regularly repeating and documenting ABCD physical examinations and physiological observations is crucial to identify trends, clinical deterioration, and/or response to treatment.

Acid-base balance is the equilibrium between acidity and alkalinity of the body fluids, measured using the pH scale, which ranges from 0 (very acidic) to 14 (very alkaline). The normal pH of blood is between 7.35 and 7.45, and it is crucial for proper physiological functioning and health.

An acid is any substance that consists of molecules that can donate hydrogen ions to other molecules.

A solution that contains more acid than base has more hydrogen ions, resulting in a lower pH.

Examples of strong acids include:

1. HCl - hydrochloric acid
2. HNO3 - nitric acid
3. H2SO4 - sulfuric acid

A strong base consists of molecules that can accept hydrogen ions.

A solution that contains more base than acid has fewer hydrogen ions, resulting in a higher pH.

Examples of strong bases include:

1. NaOH - sodium hydroxide
2. KOH - potassium hydroxide
3. Ca(OH)2 - calcium hydroxide

The normal pH range of blood is 7.35 to 7.45.

If the pH changes significantly, enzymes can stop functioning, muscles and nerves can start weakening, and metabolic activities become impaired.

The pH range of urine is 4.5 to 8.

The pH of stomach acid ranges from 1.5 to 3.5.

The pH of saliva ranges from 6.5 to 7.5.

The pH range of the small intestine is 7.2 to 7.5.

The pH range of the colon is 7.9 to 8.5.

The bicarbonate buffering system helps maintain blood pH by neutralizing excess hydrogen ions (H+) and stabilizing pH levels. It involves the conversion of carbon dioxide (CO2) and water (H2O) into carbonic acid (H2CO3), which then dissociates into bicarbonate ions (HCO3-) and hydrogen ions (H+). This process allows the body to respond to changes in pH by adjusting the levels of CO2 and H+ in the blood.

pH sensors detect changes in blood pH, specifically an increase in hydrogen ion (H+) concentration, which indicates a drop in pH. When a drop in pH is detected, these sensors send signals to the brain, prompting the individual to breathe, thereby increasing the elimination of CO2 and helping to restore normal pH levels.

When a person holds their breath, levels of carbon dioxide (CO2) rise in the blood. This increase in CO2 leads to the formation of carbonic acid (H2CO3), which dissociates into bicarbonate ions (HCO3-) and hydrogen ions (H+), resulting in a decrease in blood pH (acidosis).

The onset time for calcium gluconate when administered intravenously is 30 seconds.

1. Holding one's breath causes CO2 levels to rise in the blood.

2. CO2 combines with water to form carbonic acid (H2CO3).

3. Carbonic acid dissociates to form bicarbonate ions (HCO3-) and hydrogen ions (H+).

4. pH sensors detect the increase in H+ concentration, signaling the brain to initiate breathing, which helps restore normal pH levels.

The lungs regulate blood levels of CO2 by combining it with H2O to form carbonic acid (H2CO3-). Increased levels of carbonic acid lead to a decrease in pH. Chemoreceptors in the medulla of the brain sense these pH changes and adjust the rate and depth of breathing to compensate, eliminating more CO2 and raising pH.

The respiratory system is very effective in maintaining acid-base balance, being twice as effective as chemical buffers. It responds within minutes to changes in pH, but this is a temporary measure that requires the renal system for long-term adjustments to pH.

Increased levels of carbonic acid (H2CO3-) from elevated CO2 levels lead to a decrease in pH, making the blood more acidic.

Chemoreceptors in the medulla of the brain sense changes in pH and vary the rate and depth of breathing to compensate for these changes, helping to regulate CO2 levels and maintain acid-base balance.

In response to acidosis, the kidneys reabsorb sodium bicarbonate and increase the excretion of hydrogen ions. This process leads to the formation of more bicarbonate in the renal tubules, which is retained by the body, causing blood bicarbonate levels to rise and the pH to increase.

During alkalosis, the kidneys compensate by excreting bicarbonate and retaining more hydrogen ions. This results in urine becoming more alkaline and a decrease in blood bicarbonate levels.

In metabolic acidosis, the primary change is a decrease in bicarbonate (HCO3) and a decrease in pCO2 as a compensatory mechanism. This results in a decrease in pH.

In respiratory alkalosis, there is a decrease in pCO2 and a compensatory increase in bicarbonate (HCO3). This leads to an increase in pH.

In respiratory acidosis, there is an increase in pCO2 and a compensatory increase in bicarbonate (HCO3). This results in a decrease in pH.

In metabolic alkalosis, there is an increase in bicarbonate (HCO3) and a compensatory increase in pCO2. This results in an increase in pH.

• Rapid, shallow respirations
• Decreased blood pressure with vasodilation
• Dyspnea
• Headache
• Hyperkalemia
• Dysrhythmias (increased potassium)
• Drowsiness, dizziness, disorientation
• Muscle weakness and hyperreflexia

• Decreased respiratory stimuli (e.g., anesthesia, drug overdose)
• Chronic Obstructive Pulmonary Disease (COPD)
• Pneumonia
• Atelectasis

Respiratory acidosis is characterized by a decreased pH (below 7.35) and an increased pCO2 (above 45 mm Hg) due to the retention of CO2 by the lungs.

• Seizures
• Deep, Rapid Breathing
• Hyperventilation
• Tachycardia
• ↓ or Normal BP
• Hypokalemia
• Numbness & Tingling of Extremities
• Lethargy & Confusion
• Light Headedness
• Nausea, Vomiting

• Hyperventilation (due to Anxiety, Pulmonary Embolism, Fear)
• Mechanical Ventilation

Respiratory alkalosis is characterized by an increase in pH (greater than 7.45) and a decrease in pCO2 (less than 35 mm Hg) due to loss of CO2 from the lungs.

• Headache
• Decreased BP
• Hyperkalemia
• Muscle Twitching
• Warm, Flushed Skin (due to vasodilation)
• Nausea, Vomiting, Diarrhea
• Changes in LOC (Confusion, increased drowsiness)
• Kussmaul Respirations (Compensatory Hyperventilation)

• Diabetic Ketoacidosis (DKA)
• Severe Diarrhea
• Renal Failure
• Shock

• Restlessness followed by Lethargy
• Dysrhythmias (Tachycardia)
• Compensatory Hypoventilation
• Confusion (LOC, Dizzy, Irritable)
• Nausea, Vomiting, Diarrhea
• Tremors, Muscle Cramps, Tingling of Fingers & Toes
• Hypokalemia

• Severe Vomiting
• Excessive GI Suctioning
• Diuretics
• Excessive NaHCO3

The three components of acid-base balance are cellular (chemical) factors, respiratory factors, and metabolic factors.

Respiratory acidosis is caused by an increase in CO2 levels in the blood and body fluids due to respiratory malfunction.

Respiratory alkalosis results from hyperventilation.

Metabolic acidosis is caused by anaerobic metabolism and lactic acidosis.

Metabolic alkalosis is considered rare.

A key factor to remember regarding metabolic acidosis is the usage of ETCO2 (end-tidal carbon dioxide).

Compensation in acid-base balance occurs from a cellular level through to a visceral functional level, indicating the body's efforts to maintain homeostasis.

Many clinical presentations can cause disturbances in acid-base balance.

The patient presents with bradycardia (HR 38) and hypotension (BP 85/47), which are critical signs indicating potential cardiovascular instability. This could be related to his history of atrial fibrillation and chronic renal failure, necessitating immediate evaluation and intervention.

BRASH syndrome is a synergistic process created by a combination of hyperkalaemia and medications that block the atrioventricular (AV) node, producing bradycardia and reduced perfusion that worsen renal function and potassium handling.

Potential adverse effects include increased myocardial and cerebral damage due to elevated intracellular calcium levels, tissue necrosis from extravasation, and dysrhythmias.

BRASH syndrome is a clinical syndrome in which the combination of AV‑nodal blocking medications and hyperkalaemia leads to profound bradycardia, reduced cardiac output (shock), and worsening renal failure. Components: Bradycardia, Renal failure, AV‑node blocker overdose, Shock, Hyperkalaemia.

The PCT provides ~60% of K+ reabsorption primarily via paracellular pathways (between cells) through solvent drag and paracellular K+ channels.

Renin is secreted by the kidney in response to stimuli (including ↑K+). It catalyses angiotensin production, which stimulates adrenal aldosterone secretion to increase renal K+ excretion.

To identify trends, detect clinical deterioration early, and document the response to treatment.

Peaked T waves due to repolarisation abnormalities are commonly seen in this range; other changes may begin to appear as potassium rises.

Progressive atrial paralysis is seen: widening and flattening of P waves, PR prolongation, and eventual disappearance of P waves as levels increase.

At potassium levels between 7.0 and 9.0 mmol/L, conduction abnormalities can include:

1. Bradyarrhythmias: Sinus bradycardia, high-grade AV block with slow junctional and ventricular escape rhythms, slow atrial fibrillation.
2. Conduction blocks: Bundle branch block, fascicular blocks.
3. Prolonged QRS interval with bizarre QRS morphology.

When potassium levels exceed 9.0 mmol/L, the ECG changes can include:

• Development of sine wave appearance (pre-terminal rhythm)
• Asystole
• Ventricular fibrillation
• PEA with bizarre, wide complex rhythm

This encompasses all previous changes as well.

• Mild hyperkalaemia leads to:
  • Peaked T waves due to faster repolarisation (enhanced Phase 3).
  • Increased excitability and instability of the heart.

• Moderate hyperkalaemia results in:
  • Slower conduction due to impaired Phase 0.
  • Widened QRS complex.
  • Bradycardia.

• Severe hyperkalaemia can lead to:
  • Failure of depolarisation.
  • Cardiac arrest.

• The resting membrane potential (RMP) becomes less negative due to increased potassium levels.

• Hyperkalaemia causes fewer Na+ channels to be active, leading to a slowed conduction velocity and resulting in a widened QRS complex and prolonged PR intervals.

The primary role of calcium gluconate is to stabilize the cardiac membrane in patients with hyperkalemia.

Calcium gluconate antagonizes the effects of hyperkalemia on the heart.

The recommended initial dose for patients aged 16 and older is 1g administered over 2 minutes.

If precipitate is present in the calcium gluconate solution, it should not be used, and the solution must be clear before administration.

The maximum total dose for patients under 16 years old is 210mg/kg or 3g, whichever is less.

Sodium bicarbonate reverses metabolic acidosis by buffering hydrogen ions.

Sodium bicarbonate reduces plasma potassium by altering pH and causing intracellular movements of potassium ions.

Adverse effects include metabolic alkalosis, heart failure, and hypokalaemia, which may cause dysrhythmias.

The initial dose is 1mmol/kg bolus, with a maximum bolus of 100mmol.

There are no contraindications for sodium bicarbonate use in NSW Ambulance.

Flush the line between administration of sodium bicarbonate and calcium gluconate to prevent precipitation.

• Age: 66 years old
• Heart Rate (HR): 32 bpm (bradycardic)
• Blood Pressure (BP): 111/76 mmHg
• Glasgow Coma Scale (GCS): 15 (alert)
• Oxygen Saturation (SaO2): 95%
• Respiratory Rate (RR): 22 breaths per minute
• Blood Glucose Level (BGL): 9.5 mmol/L
• Temperature (T): 35.4°C (hypothermic)
• Symptoms: Chest pain, pale/yellow appearance, malaise, generalized weakness

A regular heart rhythm on an ECG indicates that the electrical activity of the heart is functioning normally, with consistent intervals between heartbeats.

The note indicates that the patient requires dialysis treatment, which is critical for managing kidney function, especially in cases of acute or chronic renal failure.

ST-segment elevation in the ECG may indicate cardiac ischemia, which is a condition where the heart muscle does not receive enough blood and oxygen. This can be a sign of a heart attack or other serious cardiac conditions.

The irregular waveforms and very fast heart rate observed in the ECG suggest ventricular tachycardia, a potentially life-threatening arrhythmia that can lead to decreased cardiac output and may require immediate medical intervention.

The 12-lead electrocardiogram (ECG) represents the electrical activity of the heart as seen from different angles through various leads. Each lead provides a unique perspective on the heart's electrical function, allowing for comprehensive assessment of cardiac health.

The different leads in an ECG tracing represent the electrical activity of the heart from various angles. Each lead provides unique information about the heart's rhythm and can help identify abnormalities. For example:

• Lead II: Commonly used for rhythm monitoring.
• Lead aVL: Provides information about the left side of the heart.
• Lead V2: Monitors the anterior wall of the heart.
• Lead V5: Assesses the lateral wall of the heart.
• Lead aVF: Looks at the inferior wall of the heart.
• Lead V3: Also monitors the anterior wall, positioned between V2 and V4.
• Lead V6: Monitors the left lateral wall of the heart.

An idioventricular rhythm indicates that the heart's ventricles are generating electrical impulses independently of the atria, typically occurring when the normal pacemaker (the sinoatrial node) fails. This can lead to a slower heart rate, as seen in the ECG with a ventricular rate of 30 BPM.

A non-specific intra-ventricular conduction block suggests that there is a delay or obstruction in the electrical conduction pathways within the ventricles. This can be associated with various cardiac conditions and may indicate underlying heart disease or structural abnormalities.

The phrase 'Cannot rule out Anterior infarct, age undetermined' indicates that there may be signs of a previous heart attack affecting the anterior wall of the heart. This finding necessitates further investigation to assess the extent of damage and to guide treatment decisions.

An abnormal ECG indicates deviations from normal cardiac electrical activity and may reflect arrhythmias, ischaemia, conduction defects, electrolyte abnormalities, or structural heart disease; it signals the need for further clinical evaluation and appropriate management.

A widened and distorted QRS complex in those leads suggests abnormal ventricular conduction such as ventricular hypertrophy, bundle branch block, or prior/acute myocardial injury; it may impair ventricular synchrony and warrant further investigation.

The presence of wide QRS complexes suggests a ventricular conduction abnormality or ventricular-origin rhythm (e.g., bundle branch block, ventricular tachycardia) and should prompt correlation with clinical status and further cardiac assessment.

An irregular rhythm may indicate arrhythmias such as atrial fibrillation, frequent ectopic beats, or variable AV conduction; these can cause haemodynamic compromise, increase thromboembolic risk, and require targeted management.

Key components:

• P wave: atrial depolarisation (atrial electrical activity)
• PR interval: AV nodal conduction time
• QRS complex: ventricular depolarisation (ventricular activation)
• ST segment and T wave: ventricular repolarisation These elements are used to assess cardiac rhythm, conduction, ischaemia, and electrolyte effects.

Generalised weakness, severe muscle pains, abdominal cramps. Vital signs: HR 66 bpm, BP 159/97 mmHg, SaO2 97%, RR 15/min, T 37.2°C, GCS 15.

History of Conn's syndrome due to bilateral adrenal adenomas; taking spironolactone. No known drug allergies (NKDA).

Conn's syndrome (primary hyperaldosteronism) can cause hypokalaemia leading to muscle weakness and cramps. Spironolactone is potassium-sparing and treats aldosterone effects but can cause hyperkalaemia if overused or in renal impairment; either electrolyte disturbance may contribute to generalized weakness and muscle pain.

A wide QRS complex with flattened T waves is most suggestive of hypokalaemia-related ECG changes; correlate with serum potassium and clinical context.

The tracing in leads V1–V6 is consistent with ventricular tachycardia, characterised by rapid, wide, and abnormal QRS complexes representing abnormal ventricular activation.

Limb leads I, II, and III demonstrate normal sinus rhythm with consistent P–QRS–T morphology, indicating preserved atrial to ventricular conduction in those leads.

Wide and bizarre QRS complexes indicate abnormal ventricular conduction and are characteristic of ventricular tachycardia; this is a potentially life‑threatening arrhythmia requiring urgent management.

Drowsiness, generalized abdominal pain, vomiting, fever (39°C), tachypnoea (RR 29), diaphoresis, pallor, dry mucous membranes, poor skin turgor, and wheezes/crackles in the right lower chest.

Current vital signs and relevant measurements:

• HR: 104 bpm (tachycardic)
• RR: 29/min (tachypnoeic)
• BP: 100/70 mmHg (low‑normal; may reflect volume depletion)
• SaO2: 98% (adequate oxygenation)
• T: 39°C (fever)
• GCS: 14 (mildly altered consciousness)
• BGL: 25 mmol/L (marked hyperglycaemia)
• ETCO2: 15 mmHg (low, consistent with hyperventilation/Kussmaul breathing) These findings support severe metabolic disturbance (eg, DKA) with dehydration and systemic illness.

Type 1 diabetes predisposes to diabetic ketoacidosis (DKA), especially during illness or insulin omission; the history explains the marked hyperglycaemia, dehydration, and risk of ketosis and acid‑base disturbance.

DKA develops from an absolute or relative lack of insulin, causing increased counter‑regulatory hormones (eg, glucagon), enhanced hepatic glucose production, lipolysis, and ketogenesis.

Excess glucose leads to osmotic diuresis with polyuria, polydipsia and consequent dehydration (often with tachycardia and orthostatic hypotension).

During relative metabolic starvation, increased lipolysis leads to hepatic production of ketone bodies (acetoacetate, beta‑hydroxybutyrate and acetone), causing metabolic acidosis.

Acidosis, insulin deficiency and hyperosmolality drive potassium out of cells into the extracellular space, so measured serum potassium may be high despite total body potassium depletion.

The biggest concern when treating children with DKA is cerebral oedema.

Common signs and symptoms of DKA include polyuria, polydipsia, dehydration (tachycardia, orthostasis), abdominal pain, nausea/vomiting, fruity (acetone) breath, Kussmaul respirations, and altered mental status (confusion to coma).

Search for precipitating or contributing factors such as infection, myocardial ischaemia/AMI, insulin omission or non‑adherence, recent surgery or trauma, and drug or alcohol use; identifying and treating the trigger is essential.

The cardinal features are hyperglycaemia, ketosis, and metabolic acidosis.

Severity is indicated by the degree of volume depletion, the severity of acidosis (pH and bicarbonate), level of consciousness, renal function, and concurrent electrolyte disturbances—especially abnormalities of potassium homeostasis.

Marked hyperkalaemia is uncommon in DKA but can occur from acidosis, insulin deficiency, hyperosmolality, severe dehydration and reduced renal excretion; clinical context and serum potassium must guide treatment.