Question

1.Suppose a patient in a hospital was given an overdose of CA+2 via an intravenous injection.

A= What would be the effect on the heart?
B= Construct a treatment plan (based on the frog heart experiment) as to what drug or ion could be prescribed to counteract the situation and explain how this would work.
C= Describe how drugs like calcium channel blockers are used to treat patients?

2. Martin is a 67-Year old, obese, smoker that enters the emergency room complaining of palpitations, dizziness, and shortness of breath. After a few minutes of waiting for attention, he collapses to the floor and the physicians determine that he is in cardiac arrest. Epinephrine is chosen as the drug of choice to treat Martin.

A= Briefly describe cardiac arrest and investigate how epinephrine works to resolve this condition in the patient.
B= Based on the experiment (frog heart experiment), do you think Atropine could be beneficial in treating a patient in cardiac arrest and/or Bradycardia? explain why either way.
C= Investigate how this drug relates to vagal nerve stimulation and how this would be beneficial to a patient in cardiac arrest.

Answer 1

1. a) Calcium channel blockers (CCB) target on the L-type voltage-gated calcium channels in the heart. CCBs has three main subclasses, with each subclass having different effect on the cardiac tissues and vascular smooth muscles. The three classes are Phenylalkylamines (Verapamil), Benzothiazepines (Diltizaem), and Dihydropyridines (Nifedipine, Amlodipine, Felodipine, Nicardipine, Nimodipine).  Verapamil has a strong affinity for both myocardium and vascular smooth muscle. It suppresses cardiac contractility, SA nodal automaticity, AV nodal conduction, and causes potent vasodilation. Diltiazem has a similar range of effects as Verapamil with less vasodilation; its effect is more potent on chronotropic action. Dihydropyridines are very effective vasodilators but exert less influence on cardiac pacemakers and myocardial contractility. Both Verapamil and Diltiazem causes significant bradycardia, hypotension, conduction disturbances, and escape rhythms. Nifedipine triggers hypotension and reflex sinus tachycardia. All subclasses reduce pancreatic insulin secretion and induce end-organ insulin resistance causing hyperglycemia. Additionally, CCBs interfere with calcium-stimulated mitochondrial action and glucose catabolism; which result in lactate production and ATP hydrolysis contributing to acidosis.

b) Treatment: Stabilization of airway as necessary, IV boluses of isotonic crystalloid, IV Calcium salts, IV Glucagon, IV high-dose of insulin and glucose, IV vasopressors, and IV lipid emulsion therapy. IV calcium salts such as Calcium gluconate, Calcium chloride are used to overcome the cardiovascular effects of CCBs. Glcucagon increases the intracellular levels of cyclic adenosine monophosphate and increase the heart rate. Vassopressors help to improve hypotension. Patients with profound CCB toxicity might require higher doses of vasopressors. Initiation of high dose of insulin therapy has positive inotropic effects. Invasive treatment modalities including Extracorporeal membrane oxygentation (ECOM) can be performed based on the severity of the symptoms.

c) Calcium channel blockers are medications that relax blood vessels and increase the supply of blood, oxygen to heart and also helps in reducing the heart workload. It is used tot treat high blood pressure, coronary artery disease, coronary spasm, angina, abnormal heart rhythms, hypertrophic cardiomyopathy, diastolic heart failure, pulmonary hypertension.

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