Question

A 45-year-old male is transferred from the Emergency department of a NYC hospital into the critical care setting. At arrival he requires initiation of mechanical ventilation due to Acute Respiratory Distress Syndrome (ARDS). Invasive hemodynamic monitoring is started with an EV1000 Monitor. He works as an International Business manager and recently traveled to Madrid, Spain and Berlin, Germany. At arrival he conducted with auto isolation due to the COVID-19 public health sanitary emergency. At 5 days from arrival he started with fever and dry cough. He got in contact with his family physician and stayed at home with general support measures but on day 7 he started with shortness of breath and arrived at the Emergency setting of this NYC hospital. As important medical background the patient has a previous diagnosis of Chronic Arterial Hypertension of 5 years in treatment with Losartan and Insulin resistance syndrome in treatment with diet and exercise. On the third day under mechanical ventilation and invasive hemodynamic monitoring the patient starts with hemodynamic signs of myocarditis with acute cardiac failure and cardiogenic shock.

If the patient started with Low blood pressure and is managed with an INTRAVENOUS infusion of crystalloid solutions (Hartmann IV solution), explain the physiological mechanisms that would get activated, include the order (sympathetic, parasympathetic, baroreceptors, Bainbridge reflex, frank starling).

Answer 1

Ans) Baroreceptors are stretch receptors and respond to the pressure induced stretching of the blood vessel in which they are found. Baroreflex induced changes in blood pressure are mediated by both branches of the autonomic nervous system: the parasympathetic and sympathetic nerves.

- Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one’s foot from the break and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require sympathetic stimulation.

- The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors (Cardiac Receptors) located in both sides of atria at the venoatrial junctions.

- The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant.