CASE K Sports Physiology
A 35-year-old man was brought to the
ER by emergency medical services.
One hour ago:
- progressively worsening
headache
- nausea and vomiting,
- lethargy,
- eventual obtundation
Ambulance arrived:
- disoriented,
- unresponsive to verbal
interaction,
- responsive only to pain stimuli
Vital signs:
- HR 72 bpm normal
- RR 18 breaths/minute; normal
- BP, 120/69 mm Hg; normal
- temperature, 37.4C slightly
elevated
En route to the ER:
- received intravenous fluids ~ 1 L
of normal saline
History provided by brother:
- previously in good health
Exercise-associated hyponatremia
Several risk factors have been linked with EAH. The main risk
factors include:
- preexercise overhydration
- excessive drinking (>1.5 L/h) during an athletic event
- low body weight
- female gender
- exercise duration >4 hours
- use of nonsteroidal anti-inflammatory drugs,
- and a hot environment (4).
The study from the 2002 Boston Marathon found that specific
predictors for the development of hyponatremia were:
- a fluid intake of >3 L
- a postrace weight greater than prerace weight
- water loading prior to the event,
- fluid intake during the race
The 2015 Third International Exercise-Associated Hyponatremia
Consensus Development Conference defined exercise-associated
hyponatremia (EAH) as hyponatremia (serum or plasma sodium below the
normal reference range of the laboratory) occurring during or up to 24
hours after prolonged physical activity
- uptodate.com
Obtundation:
A condition in which the senses have been dulled by trauma,
mistreatment, or psychological stress.
-Medical Dictionary for the Health Professions and Nursing
Normal vital sign:
- HR: 60 to 100 beats per minute
- RR: 12 to 18 breaths per minute
- BP 90/60 to 120/80 mm/Hg.
- Temperature: 97.8F to 99.1F (36.5C to 37.3C)/average
98.6F (37C)
Normal Saline: Rep
 - no pre-existing illnesses
- met patient at gym around noon

Completed a 2-hour workout Physical stress non-osmotic release of AVP increase in fluid
- tennis and weight-lifting volume
- tennis game was outdoors on a
humid 38C summer day Exposure to heat release of AVP increase in fluid volume

Had not eaten breakfast predictors for the development of hyponatremia were a fluid intake
Hydration: drunk 4 L of water before and of >3 L
during exercise

Following the tennis game,

- continued his workout indoors in
the weight room
- developed a headache
- Assumed that the headache was
related to dehydration
- he had not urinated
- continued drinking water

Completed the weight-training workout

- headache worsened
- assumed migraine

He went home:
- headache continued to worsen
- felt something was seriously
wrong
- began to vomit; bro called ambu
- became disoriented and
unresponsive to verbal interaction

Lab tests: Normal:

- sodium, 123 mEq/L (LOW) - Sodium: 135-145 mmol/L

During exercise, and particularly during exercise in the heat, urine
production declines 2060% from resting values due to a
decrease in kidney blood flow, which results in a decreased rate of
urine production (Zambraski, 1990). At the same time, the kidneys
are reabsorbing both sodium and water in response to sympathetic
nerve stimuli and to exercise-induced increases in aldosterone
(Zambraski, 1990). As a result, exercising humans have a reduced
capacity to excrete water, a normal physiological response that
nevertheless increases the risk that excessive drinking will lead to
hyponatremia.

- chloride, 95 mEq/L - Chloride: 95-105 mmol/L

- potassium, 3.9 mEq/L - Potassium: 3.5-5 mmol/L

- calcium, 6.6 mg/dL (LOW) - Calcium: 8.5 to 10.2 mg/dL

 May be due to dysfunction of Na Ca pump

- creatine phosphokinase, 223 U/L - CPK: 22 to 198 U/L

(HIGH) Creatine kinase or creatine phosphokinase is an enzyme chiefly
found in the brain, skeletal muscles, and heart. An elevated level of
creatine kinase is seen in heart attacks, when the heart muscle is
damaged, or in conditions that produce damage to the skeletal
muscles or brain.

Rhabdomyolysis is characterized by the destruction of skeletal

muscle tissue, and its main causes are trauma, toxic substances
and electrolyte disturbances. Among the latter is hyponatremia-
induced rhabdomyolysis, a rare condition that occurs mainly in
patients with psychogenic polydipsia

- hematocrit, 26.4% (LOW) - Hematocrit: 40%-52% (men),

- hemoglobin, 9.9 g/dL (LOW) - Hemoglobin: 13-17 g/dL (men)

- Urinalysis revealed urinary - Urinary Sodium: 3090 mEq/L

sodium of 190 mEq/L (HIGH) The cause of hyponatremia is typically classified by a person's fluid
status into low volume, normal volume, and high volume.

Low volume hyponatremia can occur from diarrhea, vomiting,

diuretics, and sweating.

Normal volume hyponatremia is divided into cases with dilute

urine and concentrated urine. Cases in which the urine is dilute
include adrenal insufficiency, hypothyroidism, and drinking too
much water or too much beer.

Cases in which the urine is concentrated include syndrome of

inappropriate antidiuretic hormone secretion (SIADH).
Because of retention of free water, patients actually have mild
(although clinically inap- parent) volume expansion.

High volume hyponatremia can occur from heart failure, liver

failure, and kidney failure.

Learning Objectives for the Case in Sports Physiology:

1. Discuss the effects of exercise and increased metabolic rates on the fluids and electrolytes of the body.

2. Give the physiologic mechanisms of the following signs and symptoms:

A. Headache
B. Lethargy, obtundation
C. Nausea, vomiting

3. Correlate the laboratory results with the case.

In this condition, secondary to head trauma, seizures, other CNS diseases, and neoplastic conditions,
especially lung, breast, and ovarian cancers that secrete ADH-like hormones, the serum sodium is depressed
because of excessive retention of water in the collecting ducts. This results in depletion of water in the renal
tubules, thereby concentrating the urine. Therefore, although the serum is dilute in sodium (hypotonic), the
urine is concentrated to levels >40 mEq/L, and urine osmolality exceeds 300 mOsm/kg, while the serum
osmolality is <280 mOsm/kg.

SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE (SIADH):

Nonphysiologic elevation of ADH levels as a conse- quence of ectopic production, as in malignancy, or
stimulation of excess pituitary production by various pulmonary or central nervous system (CNS) diseases.

e. Syndrome of inappropriate antidiuretichormone (SIADH)gain of water

is also called hyposmotic volume expansion.
(1) The osmolarity of ECF decreases because excess water is retained.
(2) ECF volume increases because of the water retention. Water shifts into the cells; as a result of this shift,
ICF osmolarity decreases until it equals ECF osmolarity, and ICF volume increases.
(3) Plasma protein concentration decreases because of the increase in ECF volume.

Although hematocrit might also be expected to decrease, it remains unchanged because water shifts into the
RBCs, increasing their volume and offsetting the diluting effect of the gain of ECF volume.

Normal
1. Vasopressin (Anti-Diuretic Hormone) is produced by the hypothalamus in response to increased serum
osmolality.

2. Vasopressin is then transported to the posterior pituitary gland.

3. It is then released into the circulatory system via the posterior pituitary gland.

4. It then travels to the kidneys where it binds to vasopressin receptors on the distal convoluted tubules.

5. This causes Aquaporin-2 channels to move from the cytoplasm into the apical membrane of the tubules:

These aquaporin-2 channels allow water to be reabsorbed out of the collecting ducts and back into the
bloodstream.
 This results in both a decrease in volume and an increase in osmolality (concentration) of the urine
being excreted.
6. The extra water that has been reabsorbed re-enters the circulatory system, reducing the serum
osmolality.

7. This reduction in serum osmolality is detected by the hypothalamus and results in decreased production
of vasopressin.

Deranged physiology in SIADH

SIADH has a number of potential causes. These are demonstrated in the diagram below. The important difference
in SIADH, is the lack of any negative feedback mechanism, resulting in an inability to reduce or stop ADH
production. As a result, ADH is continually produced, regardless of what the serum osmolality is. This ultimately
results in abnormally low levels of serum sodium and relatively high levels of urinary sodium, giving rise to the
characteristic symptoms and signs associated with SIADH

4. Discuss how the management of this case had contributed to the patients signs and symptoms.
- received intravenous fluids ~ 1 L of normal saline
- Because this individual is stuporous and the sodium level is severely decreased, hypertonic saline is
required with fairly rapid partial cor- rection. This therapy is not benign and requires monitoring in
 intensive care unit (ICU). Also, the target is not correction of the sodium level to normal but rather to a
level of safety, such as 120 to 125 mmol/L.
- Patients with severe neurologic symptoms, such as seizures or coma, require rapid partial correction of
the sodium level. The treatment of choice is hypertonic (eg, 3%) saline. When there is concern that the
saline infusion might cause volume overload, the infusion can be administered with a loop diuretic such
as furosemide. The diuretic will cause the excretion of hypotonic urine that is essentially half-normal
saline, so a greater portion of sodium than water will be retained, helping to correct the serum sodium
level.
- When hyponatremia occurs for any reason, especially when it occurs slowly, the brain adapts to
prevent cerebral edema. Solutes leave the intra- cellular compartment of the brain over hours to days,
so patients may have few neurologic symptoms despite very low serum sodium levels. If the serum
sodium level is corrected rapidly, the brain does not have time to readjust, and it may shrink rapidly as it
loses fluid to the extracellular space. It is believed that this rapid shrinkage may trigger demyelination of
the cerebellar and pontine neurons.
- Nevertheless, the risk of rapid correction of hyponatremia is lower than the risk caused by a delay in the
correction of symptomatic hyponatremia. Hyponatremia guidelines have been recently revised, and an
increase of 5mEq in the first hour is currently recommended. Through the use of hypertonic saline (3%
NaCl) and subsequently normal saline (0.9% NaCl), a target of 10mEq in the first 24 hours can be
reached, and thereafter, the goal is 8mEq/L per day.(9) Higher corrections increase the risk of pontine
myelinolysis, which can lead to death.

5. Make a concept map.