Metabolic alkalosis

Last updated: August 08, 2023

Metabolic alkalosis

Watch later

Watch later

Parathyroid hormone
Calcitonin
Vitamin D
Insulin
Glucagon
Diabetes mellitus
Diabetes mellitus: Pathology review
Pancreatic neuroendocrine neoplasms
Hyperparathyroidism
Hypoparathyroidism
Parathyroid disorders and calcium imbalance: Pathology review
Insulins
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Osteoporosis medications
Hypertrophic cardiomyopathy
Pigmentation skin disorders: Pathology review
Albinism
Thymus histology
Glomerular filtration
Measuring renal plasma flow and renal blood flow
Thyroglossal duct cyst
Bowel obstruction
Platelet plug formation (primary hemostasis)
Anatomy of the abdominal viscera: Kidneys, ureters and suprarenal glands
Anatomy of the perineum
Thiazide and thiazide-like diuretics
Vaginal and vulvar disorders: Pathology review
Alpha-thalassemia
Spleen histology
Fallopian tube and uterus histology
Mammary gland histology
Ovary histology
Brucella
Oral cancer
Oxygen binding capacity and oxygen content
Obstructive lung diseases: Pathology review
Ehrlichia and Anaplasma
Myeloproliferative disorders: Pathology review
Nervous system anatomy and physiology
Hyperkalemia
Dementia: Pathology review
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Mediastinum
Infectious endocarditis: Clinical sciences
Infective endocarditis: Clinical
Endocarditis
Endocarditis: Pathology review
Development of the respiratory system
Adenovirus
Anatomy of the arm
Perinatal infections: Clinical
Dyslipidemias: Pathology review
Acyanotic congenital heart defects: Pathology review
Blood pressure, blood flow, and resistance
ECG basics
Development of the cardiovascular system
Fetal circulation
Calcium channel blockers
Anatomy of the eye
Introduction to the cranial nerves
Cranial nerve pathways
Anatomy of the olfactory (CN I) and optic (CN II) nerves
Anatomy of the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Anatomy of the trigeminal nerve (CN V)
Anatomy of the facial nerve (CN VII)
Anatomy of the vestibulocochlear nerve (CN VIII)
Anatomy of the glossopharyngeal nerve (CN IX)
Anatomy of the vagus nerve (CN X)
Anatomy of the spinal accessory (CN XI) and hypoglossal (CN XII) nerves
Anatomy clinical correlates: Facial (CN VII) and vestibulocochlear (CN VIII) nerves
Anatomy clinical correlates: Glossopharyngeal (CN IX), vagus (X), spinal accessory (CN XI) and hypoglossal (CN XII) nerves
Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Anatomy clinical correlates: Olfactory (CN I) and optic (CN II) nerves
Anatomy clinical correlates: Trigeminal nerve (CN V)
Actinomyces israelii
Clostridium botulinum (Botulism)
Clostridium tetani (Tetanus)
Haemophilus influenzae
Listeria monocytogenes
Mycobacterium tuberculosis (Tuberculosis)
Neisseria meningitidis
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus agalactiae (Group B Strep)
Streptococcus pneumoniae
Central nervous system histology
Peripheral nervous system histology
Eye and ear histology
Coxsackievirus
Cytomegalovirus
Eastern and Western equine encephalitis virus
Epstein-Barr virus (Infectious mononucleosis)
Herpes simplex virus
JC virus (Progressive multifocal leukoencephalopathy)
Lymphocytic choriomeningitis virus
Measles virus
Mumps virus
Poliovirus
Rabies virus
Varicella zoster virus
West Nile virus
Acute disseminated encephalomyelitis
Central pontine myelinolysis
Multiple sclerosis
Transverse myelitis
Charcot-Marie-Tooth disease
Guillain-Barre syndrome
Adult brain tumors
Neurofibromatosis
Pediatric brain tumors
Pituitary adenoma
Sympathomimetics: Direct agonists
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Cardiac muscle histology
Mesothelioma
Nasal polyps
Nasopharyngeal carcinoma
Pancoast tumor
Superior vena cava syndrome
Cystic fibrosis: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Pneumonia: Pathology review
Tuberculosis: Pathology review
Lung cancer and mesothelioma: Pathology review
Nasal, oral and pharyngeal diseases: Pathology review
Restrictive lung diseases: Pathology review
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Respiratory distress syndrome: Pathology review
Adrenergic antagonists: Presynaptic
Adrenergic receptors
Cholinergic receptors
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympatholytics: Alpha-2 agonists
Introduction to the immune system
Gallbladder disorders: Pathology review
Anatomy of the thyroid and parathyroid glands
Acute coronary syndrome: Clinical sciences
Approach to chest pain: Clinical sciences
Approach to dyspnea: Clinical sciences
Approach to hypertension: Clinical sciences
Coronary artery disease: Clinical sciences
Diabetes mellitus (Type 1): Clinical sciences
Diabetes mellitus (Type 2): Clinical sciences
Dyslipidemia: Clinical sciences
Essential hypertension: Clinical sciences
Tobacco use: Clinical sciences
Ketone body metabolism
Kidney histology
Ureter, bladder and urethra histology
Bladder exstrophy
Horseshoe kidney
Hydronephrosis
Hypospadias and epispadias
Potter sequence
Renal agenesis
Alport syndrome
Goodpasture syndrome
IgA nephropathy (NORD)
Lupus nephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
Amyloidosis
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Membranoproliferative glomerulonephritis
Membranous nephropathy
Minimal change disease
Acute tubular necrosis
Renal papillary necrosis
Acute pyelonephritis
Chronic pyelonephritis
Lower urinary tract infection
Postrenal azotemia
Prerenal azotemia
Renal azotemia
Chronic kidney disease
Kidney stones
Renal tubular acidosis
Angiomyolipoma
Medullary cystic kidney disease
Medullary sponge kidney
Multicystic dysplastic kidney
Polycystic kidney disease
Beckwith-Wiedemann syndrome
Nephroblastoma (Wilms tumor)
Non-urothelial bladder cancers
Renal cell carcinoma
Transitional cell carcinoma
WAGR syndrome
Neurogenic bladder
Posterior urethral valves
Urinary incontinence
Vesicoureteral reflux
Renal artery stenosis
Renal cortical necrosis
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Hypercalcemia
Hypermagnesemia
Hypernatremia
Hyperphosphatemia
Hypocalcemia
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypophosphatemia
Congenital renal disorders: Pathology review
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal failure: Pathology review
Renal tubular acidosis: Pathology review
Renal tubular defects: Pathology review
Renal and urinary tract masses: Pathology review
Urinary incontinence: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Appendicitis
Abdominal hernias
Inguinal hernias: Clinical sciences
Femoral hernias: Clinical sciences
Umbilical hernias: Clinical sciences
Ventral and incisional hernias: Clinical sciences
Inguinal hernia
Femoral hernia
Acute pancreatitis: Clinical sciences
Cholecystitis: Clinical sciences
Peptic ulcer disease: Clinical sciences
Anticoagulants: Warfarin
Factor V Leiden

Transcript

Watch video only

With metabolic alkalosis, “alkalosis” refers to a process that raises blood pH above 7.45, and “metabolic” refers to the fact that it’s caused by an increase in the concentration of bicarbonate HCO3− in the blood.

Normally, blood pH depends on the balance or ratio between the concentration of bases, mainly bicarbonate HCO3−, which increases the pH, and acids, which decrease the pH.

The blood pH needs to be constantly between 7.35 and 7.45.

Now, metabolic alkalosis can typically happen from two main causes - loss of hydrogen H+ ions and gain of HCO3− bicarbonate ions, or, most often, a combination of these two.

Loss of hydrogen H+ ions can occur either from the gastrointestinal tract or from the kidneys.

The first case most commonly happens during vomiting, because the gastric secretions are very acidic, meaning that they have lots of hydrogen H+ ions.

On top of that, normally, as gastric secretions flow into the pancreas, they’re met with HCO3− bicarbonate secretions which neutralize the acid so that the various pancreatic enzymes like trypsin and chymotrypsin, can work effectively.

So during vomiting, not only is the stomach acid lost, but in addition the pancreas doesn’t secrete HCO3− bicarbonate into the intestines, and so it builds up in the blood instead.

Another way that hydrogen H+ ions can be lost is through the urine, in the context of having too much of the hormone aldosterone.

This can happen, when there’s an adrenal tumor that secretes excess aldosterone.

The aldosterone makes the α- intercalated cells of the distal convoluted tubule and collecting duct dump out hydrogen H+ ions and reabsorb more bicarbonate HCO3− ions.

The result is that the urine becomes more acidic and the blood becomes more basic.

Now, the second cause - a primary gain of HCO3− bicarbonate ions - is usually caused by an increased reabsorption of HCO3− bicarbonate ions from the kidneys.

There are various things that could stimulate the kidneys to do that.

One of them is volume contraction or excessive loss of extracellular fluid, which can happen with loop diuretics and thiazide diuretics, as well as in cases of severe dehydration.

The resulting alkalosis is called a contraction alkalosis.

Sometimes, dehydration occurs in combination with other causes of metabolic alkalosis, like prolonged vomiting.

Another stimulus is hypokalemia, or decreased levels of potassium in the blood, which can be due to excessive loss from the gastrointestinal tract, like in diarrhea, or from the kidneys due to diuretic use.

In any case, when there’s less volume or less potassium in the extracellular space, it triggers the renin-angiotensin-aldosterone mechanism.

As a result, angiotensin II and aldosterone levels rise, and the kidneys start to retain water and reabsorb more bicarbonate HCO3− ions in the proximal convoluted tubule.

In addition, the α- intercalated cells of the distal convoluted tubule and the collecting ducts secrete some hydrogen H+ ions into the urine, but, most importantly, also make new bicarbonate HCO3− ions, which will again get reabsorbed.

Now, in other cases, excess bicarbonate HCO3− ions don’t come from within our bodies at all, but are ingested in large amounts, usually in the form of antacids, like NaHCO3 sodium bicarbonate.

Key Takeaways

Metabolic alkalosis is a condition in which the blood pH is above 7.45, following an increase in blood HCO3 concentration to over 27 mEq/L. Common causes of metabolic alkalosis include excessive loss of hydrogen ions like when vomiting, abnormal renal function, loop, and thiazide diuretics, excessive use of antacids, etc. Symptoms of metabolic alkalosis include nausea, vomiting, muscle weakness, and confusion.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2017)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "Respiratory alkalosis" Respir Care (2001)
  6. "Respiratory Alkalosis: A Quick Reference" Veterinary Clinics of North America: Small Animal Practice (2008)
  7. "Metabolic alkalosis" J Am Soc Nephrol (1997)
  8. "A Quick Reference on Metabolic Alkalosis" Veterinary Clinics of North America: Small Animal Practice (2017)