Arterial blood pressure is regulated by cardiac output and systemic vascular resistance (Lilley, Rainforth Collins, Snyder, 2014). Cardiac output is the amount of blood that comes from the left ventricle and is measured L per minute (Lilley, et al., 2014). SVR is the resistance of blood flow based off of the diameter of the blood vessel and vascular (Lilley, et al., 2014). One can calculate this by blood pressure divided by cardiac (Lilley, et al., 2014). Many factors interact to regulate these two major variables in order to keep the blood pressure within normal limits (Lilley, et al., 2014).
The renin-angiotensin-aldosterone system is used as a potent vasoconstrictor and it induces aldosterone secretion from the adrenal gland (Lilley, et al., 2014). While aldosterone stimulates sodium and water reabsorption in order to raise blood pressure (Lilley, et al., 2014). But when the system is put together as a whole it ultimately inhibits this process, causing blood pressure to be lowered (Lilley, et al., 2014).
Classic angina is also known as chronic stable angina and effort angina (Lilley, et al., 2014). Classic angina’s triggers can be stress or exertion (Lilley, et al., 2014). Classic angina can be exacerbated by nicotine, coffee, alcohol, and other drugs that stimulate the sympathetic nervous system (Lilley, et al., 2014). Pain associated with classic angina is severe but subsides within fifteen minutes of rest or antianginal drug therapy (Lilley, et al., 2014). Unstable angina is also known as preinfarction angina and crescendo angina (Lilley, et al., 2014). Unstable angina occurs usually in the early stages of progressive coronary artery disease (Lilley, et al., 2014). Often the end result is a MI in the years to follow (Lilley, et al., 2014). The pain associated with unstable angina increases in severity along with the frequency of attacks (Lilley, et al., 2014). While in increasing years this pain can/will appear when a person is at risk (Lilley, et al., 2014). Prinzmental angina is also known as vasospastic angina and/or variant angina (Lilley, et al., 2014). Prinzmental angina is the result of spasms in the smooth muscular layer surrounding atherosclerotic coronary arteries (Lilley, et al., 2014). The pain associate with this type of angina occurs at rest without and cause associated with it (Lilley, et al., 2014). Prinzmental angina seems to follow a regular pattern occurring at the same time of the day (Lilley, et al., 2014). ECG changes and dysrhythmia changes accompany all of these different types of angina (Lilley, et al., 2014).
The standard protocol for the use of sublingual nitrates associate with angina pain is used to treat acute angina attacks (Lilley, et al., 2014). The reasons for using this route is because the tongue and cheeks are highly vascular which bloodstream and also avoids the first pass effect (Lilley, et al., 2014). If the patient has orders (prescription) for these meds then the RN/provider must go over all of the following: meds must be taken at first sign of chest pain, patient must sit or lie down to take one tablet, if not relieved in five minutes call 911 (Lilley, et al., 2014). The patient must take another dose while waiting and a third five minutes later, but cannot exceed three tablets. Patient needs to avoid swallowing until the tablet is dissolved (Lilley, et al., 2014). The patient will also need education on medication storage such, as keeping it away from moisture, light, heat, and cotton filler material (Lilley, et al., 2014).Keep medications in original bottle in order to not lose potency (Lilley, et al., 2014).This medication is only potent for three to six months(Lilley, et al., 2014). Education is a must about adverse side effects such as flushing of the face, dizziness, fainting, brief throbbing headache, increased heart rate, and light headedness (Lilley, et al., 2014).
The key teaching points for a patient starting digoxin (Lanoxin) are that their blood levels need to