NUR 239 Lecture Notes - Lecture 18: Myocardial Infarction, Ventricular Fibrillation, Angiotensin
21 May 2018
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Key Terms:
1. Catecholamines- animes like epinephrine, norepinephrine, and dopamine that affect the
cardiovascular system
2. Decompensation- inability of the heart to adequately circulate oxygenated blood to the
body’s organs
3. Digitalis Toxicity- accumulation of digoxin in the body which leads to nausea, vomiting,
atrial/ventricular tachydysrhythmias, ventricular fibrillation, sinoatrial block,
atrioventricular shock and visual disturbances
4. Digitalization- administration of loading doses of digoxin to achieve therapeutic blood
levels faster
5. Ejection Fraction- % of the total amount of blood in the LV that is ejected with each
beat
6. Endothelin- a peptide that raises BP; contributes to onset of HF
7. Inotropic- related to or influences the force of myocardial contractility
8. Phosphene- intermittent brightness in a limited area of the visual field
9. Renin- enzyme produced in the kidneys that converts angiotensinogen to angiotensin I
and then to angiotensin II
10. Therapeutic Index- margin between a drug being effective versus toxic
11. Maintenance Dose-a dose administered on a routine basis to produce a therapeutic
effect and control symptoms
12. Ventricular Remodeling- dilation and hypertrophy of ventricles in the initial phases of
HF
Key Learning Objectives - Answer the follow questions (Chapter 30 – Drug Therapy for
Heart Failure):
● In this chapter, what type of heart failure is the focus?
○ Left Ventricular Heart Failure
● List the common health conditions that may result in heart failure
○ Hypertension, cardiomyopathy, and acute myocardial infarction
● Describe the compensatory measures in place to prevent hypotension. How does
this affect preload and afterload?
○ Neurohormonal- baroreceptors of the aortic arch and carotid sinus are blunted in
those experiencing heart failure
■ This results in high levels of catecholamines which cause flight or fight
responses and increase the force of myocardial contractility
○ Renin-Angiotensin-Aldosterone System- influence cardiac output and systemic
blood pressure
■ Angiotensin II is a powerful vasoconstrictor and triggers a cascade of
effects aimed at restoring blood flow to vital organs
○ Both mechanisms worsen the fluid overload or preload and increase afterload
● Explain the normal pathway of the RAA system.
○ Renin acts on angiotensinogen to convert it to angiotensin I which then
stimulates the production of angiotensin II
● Describe the clinical manifestations of heart failure. What causes the symptoms?
○ Dyspnea and fatigue which can then lead to exercise intolerance and fluid
retention.
■ Fluid retention results in the development of pulmonary congestion and
peripheral edema
■ Orthopnea or pulmonary edema may occur at night because fluid has
shifted into the interstitial space d
● If the patient has compensated heart failure, what symptoms might be reported?
○ No symptoms at rest and no edema
○ Fatigue and dyspnea only occur when activities that require moderate to high
exertion are performed
● Explain the signs, symptoms, and causes of left-sided heart failure and right-sided
heart failure. Use Figure 30.1 (p. 580) to help you compare and contrast the clinical
manifestations for each side.
○ Left Sided
■ Results in: the decrease of cardiac output
■ Causes: myocardial infarction or cardiomyopathy; drugs can cause or
exacerbate heart failure by leading to myocardial toxicity
○ Right Sided
■ Causes:stenosis or regurgitation of pulmonic or tricuspid valves, right
sided ventricular infarction, cardiomyopathy. Or recurrent left sided HF
■ Results in: an increase in the right atrial, right ventricular, end diastolic
and systemic venous pressures
● Which type of heart failure is more common (right-sided or left-sided)?
○ Left sided
● Does right-sided HF lead to Left-sided HF or does Left-sided HF lead to
Right-sided HF?
○ Left sided heart failure typically leads to right sided failure
Drug Class
Cardiac Glycosides
Beta-adrenergic Blockers
Generic name
Digoxin
Propranolol
PK
Oral and parenteral options available
Action
-Produces a cardiotonic effect that improves the
contractility and pumping ability of the heart
-Increases the force of myocardial contractility
-Blocks stimulation of beta (myocardial) and beta2
(pulmonary, vascular, and uterine) adrenergic
receptor sites
Use
-Management of mild to moderate heart failure
in adults and children
-Used to control the ventricular response rate in
adults with chronic atrial fibrillation
-Decreased heart rate and BP
-Suppression of arrhythmias
-Prevention of MI
Document Summary
Inotropic - related to or influences the force of myocardial contractility. Key learning objectives - answer the follow questions (chapter 30 drug therapy for. List the common health conditions that may result in heart failure. Describe the compensatory measures in place to prevent hypotension. Neurohormonal- baroreceptors of the aortic arch and carotid sinus are blunted in those experiencing heart failure. This results in high levels of catecholamines which cause flight or fight responses and increase the force of myocardial contractility. Renin-angiotensin-aldosterone system- influence cardiac output and systemic blood pressure. Angiotensin ii is a powerful vasoconstrictor and triggers a cascade of effects aimed at restoring blood flow to vital organs. Both mechanisms worsen the fluid overload or preload and increase afterload. Explain the normal pathway of the raa system. Renin acts on angiotensinogen to convert it to angiotensin i which then stimulates the production of angiotensin ii. Describe the clinical manifestations of heart failure.
