If you have participated in an ACLS for Experienced Provider course, you are familiar with the ‘Tank-Tank-Pump-Rate’ mantra for hypotension. If not, consider the following when your patient presents with signs of inadequate perfusion with a normal blood pressure (compensated shock) or an abnormally low pressure (uncompensated shock). ‘Tank1-Tank2-Pump-Rate’ categorizes the types of problems that may decrease perfusion pressure.
As you recall, perfusion pressure relies on blood pressure, which is determined by cardiac output and vascular tone. Cardiac output is the product of heart rate and the stoke volume, the amount of blood the heart ejects with each beat: CO = HR x SV.
There are two tanks noted above, both referring to the vascular container. Tank1 should make us think about a vascular system that is too empty and Tank2 should prod us to consider a vascular system that is too big (vasodilated) or too small (vasoconstricted). We start with a tank that is too empty. Hypovolemia causes a low stroke volume (↓CO = HR x ↓SV). Of course, the heart rate increases to help compensate, so remember that tachycardia may signal early shock. The causes for an empty tank are divided into three categories: too much fluid loss, too little fluid intake, or a combination.
Fluid loss
A common cause of fluid loss is hemorrhage. This can be obvious if you witness a spurting artery or a bloody emesis, but it can be silent as when bleeding occurs in the retroperitoneal space where the kidneys and abdominal aorta reside; this space contains no pain fibers to signal irritation from blood as are present in the abdominal cavity. Burns cause non-blood fluid loss from damaged capillaries and increased evaporation and depending on the extent of the burn, may lose enough fluid to produce shock.
Other non-blood fluid losses include sweating, breathing, diarrhea, vomiting, and excessive urination and may lead to severe dehydration and inadequate perfusion when excessive. These problems are compounded any time we are unable to intake adequate replacement fluids as when nauseated or weak.
The problem of excessive urination requires further explanation and is usually due to diabetes mellitus when the patient experiences excessively high blood sugar and the kidneys try to normalize the glucose level by shunting it into the urine. The problem is that the body has to send a lot of water with the sugar to get it through the kidneys and into the urine. Many times the diabetic (with a high glucose) also has a coexisting illness such as an infection that may interfere with adequate hydration, thus worsening the dehydration. There is another type of diabetes called diabetes insipidus, a problem with ADH, the antidiuretic hormone responsible for regulating water loss through the kidneys. If you don’t make enough ADH or your kidneys are resistant to ADH, you can experience excessive urinary water loss and become severely dehydrated. Patients with either of these conditions may wear some type of medical identification bracelet or necklace, so be sure to look.
Abnormal constrictions and dilations
Even with a normal blood volume, you can experience inadequate perfusion if your Tank2 becomes abnormally constricted as may occur with severe hypertension or abnormally dilated, as discussed here. Vasodilation produces a decrease in stroke volume because the vessels are too big to provide the pressure required to return the blood to the heart so it can be pumped (↓CO = HR x ↓SV). The sympathetic nervous system is responsible for maintaining normal vascular tone by stimulating receptors that cause the arteries to contract. Increased sympathetic stimulation increases arterial pressure, decreased stimulation decreases pressure; remove all stimulation and the pressure plummets as when a patient suffers a spinal cord injury that damages or destroys the sympathetic nerves running through it.
Life-threatening vasodilation can also be caused by the discharge of chemicals into the bloodstream as occurs in anaphylactic shock and septic shock. Allergic reactions release histamine that causes vasodilation, most of the time producing something benign like that congested nose you have each spring; but if histamine is released in larger quantities, it may result in histamine shock, otherwise known as anaphylactic shock. For septic shock, the patient develops an overwhelming infection in the bloodstream resulting in the release of substances into the circulation like nitric acid (the “nitro” in nitroglycerine) that cause vasodilation and decrease perfusion.
Reversible and irreversible problems
Pump problems are divided into two categories — those that are reversible and those that are not. Reversible problems include tension pneumothorax and cardiac tamponade; both compress the heart and interfere with the return of blood to the heart, thus decreasing available stroke volume (↓CO = HR x ↓SV). If the abnormal air in the chest or the misplaced blood in the pericardial sac is removed in a timely manner, the heart can return to normal function. This is not so for irreversible pump problems when a patient has suffered irreparable heart damage from blunt or penetrating trauma, or suffers from cardiomyopathy, a sick heart muscle condition that may be caused by a variety of problems (like viral infections, alcohol abuse, kidney disease, extensive myocardial infarction or long-term hypertension).
Rate problems are either too slow or too fast. Inadequate perfusion can simply be the result of a heart rate that is too slow (↓CO = ↓HR x SV) or a heart rate that beats too fast to allow adequate ventricular filling and thus decreases the stroke volume (↓CO = ↑↑↑HR x ↓SV). Guiding the heart rate back into the normal range should improve perfusion.
Now you are ready to chant ‘Tank-Tank-Pump-Rate’ over your patient in shock and go fill the Tank or squeeze the Tank or relieve the Pump or support the Pump or increase the Rate or decrease the Rate or any combination that will obtain an adequate perfusion pressure for your patient.
References
1. Cummins RO, ed. ACLS for Experienced Providers. American Heart Association; 2003.
2. Inchley O. Histamine Shock. Journal of Physiology. 1926 April: 282-293.
3. Vincent JL, Zhang H, Szabo, C, Preiser JC. Effects of Nitric Oxide in Septic Shock. Am J Respir Crit Care Med. 2000 June;161(6):1781-5
