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FAQ's

How long does the VIVIT dissection last?

The post mortem experience is 5 hours long, split into 2 parts.

How many people can participate in one VIVIT dissection?

There is 150 tickets available for each session. This is a comfortable number that can engage with the experience given the AV equipment installed.

Is the anatomy human?

No. The anatomy is of swine origin. Identical in size and structure -once harvested the samples are moved into VIVIT. VIVIT is a life size synthetic cadaver which is dissected for the audience to teach the structure and function of the human body.

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Common drugs to reduce blood pressure


In our previous blog post we mentioned some medications that are used in heart failure. These drugs are very common and are used to treat various cardiovascular conditions.

MISTIME is a common way to look at drugs, this encourages you to look at all different aspects of the pharmacology as well as how it affects the patient.

M – mechanism of action

I – indications

S – side effects

T – therapeutic effects

I – interactions and contraindications

M – monitoring

E – education


ACE inhibitors e.g. Ramipril

M – Within the body there is a system called the Renin angiotensin system, which controls blood pressure. When the kidneys detect a low blood pressure they release renin which produces angiotensin I. Angiotensin I is converted to angiotensin II by an enzyme called ACE. Angiotensin II causes the constriction of blood vessels causing an increase in blood pressure. ACE inhibitors stop the ACE enzyme from working and therefore reduce the amount of angiotensin II being produced therefore lowering blood pressure.

I – controlling acute and chronic high blood pressure, treating heart failure, preventing strokes, preventing and treating kidney disease in people with hypertension or diabetes.

S – dry cough is the most common side effect, increase in levels of potassium, low blood pressure, dizziness, headache, weakness, sun sensitivity, chest pain, kidney failure, allergic reactions, pancreatitis.

T – reduce blood pressure and help prevent side effects of high blood pressure, eg strokes.

I – shouldn’t be used with other antihypertensive drugs such as ARBs due to the risk of hypotension. NSAIDs can decrease the antihypertensive effects. Potassium sparing diuretics due to the risk of hyperkalaemia. Contraindications include hypersensitivity, pregnancy, breastfeeding. Relative contraindications include aortic stenosis, renal dysfunction (eGFR<60), bilateral renal artery stenosis

M – blood pressure, potassium and creatinine need to be monitored when starting ACE inhibitors.

E – patient should be warned about side effects especially hypotension and how to deal with this if it occurs, to try and prevent falls.

Beta-blockers e.g. Bisoprolol

M – as the name suggests these block beta receptors, beta-adrenergic receptors, these receptors are normal stimulated by adrenaline and noradrenaline. These come in various different types. Bisoprolol and atenolol beta-blockers are cardioselective meaning that they block beta-1 receptors that are found in the heart. Blocking of these receptors causes a decrease in the heart rate and decreased cardiac contractility, slows the conduction through the atrioventricular node decreasing the cardiac workload. There are other beta blockers that are less selective to the beta-1 receptor, such as propranolol, which inhibits all beta receptors. There are beta-2 receptors within the smooth muscle of the airways lungs and blockage of these receptors can cause bronchial constriction.

I – hypertension, coronary artery disease, angina, heart failure, antiarrhythmic agents. Propranolol can be used in essential tremor, migraine prophylaxis and hyperthyroidism

S – As the purpose of these drugs is to slow down the heart, bradycardia can be a side effect where the heart rate is decreased below what is desired. They can also cause bradyarrhythmia’s, an tachyarrhythmia such as torsades de pointes, orthostatic hypotension, drowsiness, fatigue, in some cases can cause depression and hallucinations. Beta blockers that aren’t cardiacselective can result in bronchoconstriction which is especially a problem in asthmatic patients. The non-selective can also cause peripheral vasoconstriction by blocking the beta-3 receptors which can result in erectile dysfunction and raynaud’s phenomenon.

T – decrease of heart rate, control of palpitations

I – Non-selective shouldn’t be given to asthmatic patients due to the bronchoconstriction described above. Shouldn’t be prescribed with calcium channel blockers as this can result in precipitate atrioventricular block.

M – blood pressure and heart rate

E – patients should be warned that stopping beta blockers suddenly can result in withdrawal, causing tachycardia, hypertension, can cause acute coronary syndrome. Due to this the dose should be tapered down over 7-10 days if coming off beta blockers.

Calcium channel blockers e.g. amlodipine

M – these bind and block L type calcium channels. These are predominantly the type of calcium channel that is found in the myocardium and the vascular smooth muscles. Blocking these channels causes peripheral arterial vasodilation and myocardial depression leading to a drop in blood pressure as well as a decreasing in the heart rate and force of contraction of the heart. Different types of calcium channel blocks have more effects on vasodilation or myocardial depression. For example amlodipine has a greater vasodilating effect with minimal myocardial depression, where as verapamil doesn’t cause a great deal of vasodilation but is a potent myocardial depressor. When the calcium channel blocker binds to the L type calcium channel it causes failure of the calcium channel to open in response to depolarization of the cell membrane, therefore there is a decrease in the transmembrane calcium current which leads to vascular smooth muscle relaxation and therefore vasodilation occurs. Also this decrease in transmembrane calcium current within the myocardium causes a decrease in cardiac muscle contractility, decreasing cardiac output and therefore blood pressure. It also decreases the sinoatrial node rate resulting in bradycardia, and the atrioventricular node conduction therefore terminating any supraventricular arrhythmias.

I – hypertension, angina and supraventricular tachycardias

S – depending on the main function of the calcium channel blocker; those that cause increased vasodilation can result in peripheral oedema (especially amlodipine), headaches, dizziness, facial flushing. Those that have a greater effect on the myocardium can result in reduced contractility/bradyarrhythmia’s and drug induced atrioventricular block, constipation is also a side effect of these.

T – relief of symptoms

I – Interactions depend on the type of calcium channel blocker, for example verapamil reduced the elimation and therefore increases the blood levels of carbamazepine and some statins, which can lead to toxicity from these drugs. Contraindications include symptomatic hypotension, acute coronary syndromes

M – blood pressure

E – educate about side effects

Look out for next week’s blog on types of diuretics and kidney anatomy and physiology.


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