College of Pharmacy

ASSIGNMENT 2: ANGINA, ARRHYTHMIA& HEART FAILURE

Questions:

1. What are the different types of angina?

Angina stable - The most typical type of angina is stable angina. Exertion usually
triggers it, and it normally subsides with rest or angina medicine. Angina, for
instance, may cause pain while you're walking uphill or in chilly weather.

Discomfort from stable angina is predictable and frequently comparable to chest

pain from earlier bouts. The average duration of the chest pain is five minutes or
less. erratic angina (a medical emergency).

Unstable angina (a medical emergency) - Unpredictable and happening at rest is

unstable angina. Alternatively, the pain from angina is getting worse and requires
less exertion. The typical duration is 20 minutes or more, and it is usually severe and
lasts longer than stable angina. Rest and the typical angina drugs don't seem to help
the pain. The heart will become oxygen-starved and suffer a heart attack if the blood
flow doesn't improve. An emergent medical intervention is necessary for unstable
angina.

Variant angina (Prinzmetal angina) - Prinzmetal angina, another name for variant
angina, doesn't result from coronary artery disease. It is brought on by a spasm in
the arteries of the heart, which momentarily lowers blood flow. The primary
symptom of variant angina is severe chest discomfort. It usually happens in cycles,
usually while you're sleeping or at rest. Medication for angina may be able to reduce
the pain.

Refractory angina. Angina episodes are frequent despite a combination of

medications and lifestyle changes.

2. Discuss the significance of atherosclerosis in the development of angina.

Arteriosclerosis is the buildup of lipids, cholesterol, and other substances in and

on the artery walls. Plaque is the term used to describe this accumulation. The
 plaque may cause arteries to narrow, obstructing blood flow. Additionally, the
plaque could rupture and cause a blood clot. Symptoms of atherosclerosis normally
do not appear until an artery has become so constricted or clogged that it cannot
provide enough blood to organs and tissues. A blood clot can entirely stop blood
flow. The clot may rupture, resulting in a heart attack or stroke.

When atherosclerosis narrows the arteries near your heart, it can lead to coronary
artery disease, which can cause chest pain (angina), a heart attack, or heart failure.

3. Should we administer beta blockers and calcium channel blockers simultaneously

to treat angina? Why or why not?

According to Sage Journal the combination of calcium channel blockers and beta
blockers is more successful than beta blocker monotherapy in the treatment of
exercise-induced angina pectoris. Because ischemia in exercise-induced angina is
essentially preceded by an increase in heart rate, calcium channel blockers with
negative chronotropic properties may outperform nonchronotropic drugs in this
regard.

In the past, B-blockers were used in conjunction with short-acting CCBs to minimize
the tachycardia caused by these medicines. The issue of increased heart rate has
been significantly reduced with the development of long-acting nifedipine and
felodipine; a faster heart rate does not occur with the use of amlodipine.5 In
addition to improvements in heart rate, -blockers and DHP CCBs combine to produce
BP reductions that are greater than when either agent is used alone. Because CCBs
are metabolically neutral, they are preferred for the initial therapy of hypertension
in severely hypertensive patients who have or are at risk for metabolic problems.

4. Discuss the phases of action potential.

Phases of action potential

Depolarization, also known as the rising phase, occurs when positively charged
sodium ions (Na+) flow into a neuron through open voltage-gated sodium channels.
As more sodium rushes in, the membrane potential reverses its polarity. During this
polarity transition, the membrane develops a positive value for a moment (+40
millivolts).
Repolarization or falling phase is induced by the delayed shutting of sodium
channels and the activation of voltage-gated potassium channels. As a result, the
membrane's sodium permeability returns to normal. As sodium ion entrance
 decreases, sluggish voltage-gated potassium channels open and potassium ions rush
out of the cell. This expulsion helps to restore the cell's localized negative membrane
potential.

Hyperpolarization is a condition in which some potassium channels remain open

while sodium channels are reset. Excessive potassium efflux occurs during a time of
elevated potassium permeability before the potassium channels close. This causes
hyperpolarization, as evidenced by a brief dip following the spike.

5. Why are inotropics important in the management of CHF?

Patients with chronic heart failure who are waiting for a heart transplant are
candidates for intravenous inotropic assistance until a donor heart becomes
available. This aids in maintaining hemodynamic stability and optimizing fluid status
and pulmonary pressures prior to surgery. Inotropic drugs, on the other hand, can
be used as palliative therapy in patients with severe heart failure who are not
candidates for advanced heart failure therapies such as transplant or mechanical
circulatory support. Inotropes can assist these individuals limit their hospitalizations
and relieve their symptoms.

REFERENCE/s:

Tariq, S., & Aronow, W. S. (2015). Use of Inotropic Agents in Treatment of Systolic
Heart Failure. International journal of molecular sciences, 16(12), 29060–29068.
https://doi.org/10.3390/ijms161226147

Tiffany R. Richards, Sheldon W. Tobe,

Combining Other Antihypertensive Drugs With β-Blockers in Hypertension: A Focus
on Safety and Tolerability, Canadian Journal of Cardiology retrieved September 19,
2022 from: https://www.sciencedirect.com/science/article/pii/S0828282X13013676

Mayo Clinic (nd), Arteriosclerosis / atherosclerosis

https://www.mayoclinic.org/diseases-conditions/arteriosclerosis-
atherosclerosis/symptoms-causes/syc-20350569

Libretext Medicine (2020) The Action Potential and Propagation retrieved from:
https://med.libretexts.org/Bookshelves/Anatomy_and_Physiology/Book%3A_Anato
my_and_Physiology_(Boundless)/10%3A_Overview_of_the_Nervous_System/10.5%
3A_Neurophysiology/10.5E%3A_The_Action_Potential_and_Propagation

Felson, S (2021), Atherosclerosis, WebMD retrieved September 19, 2020 from:

https://www.webmd.com/heart-disease/what-is-atherosclerosis