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NR567 Final Exam Study Guide
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NR567 Final Exam Study Guide
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NR567 FinalExam Study
Guide
, NR567 Final Exam Study Guide
Therapeutic dosing and monitoring of warfarin (Coumadin)
Treatment with warfarin should be initiated with standard doses of 5–10 mg. The initial adjustment of the
prothrombin time takes about 1 week, which usually results in a maintenance dosage of 5–7 mg/d. The prothrombin
time (PT) should be increased to a level representing a reduction of prothrombin activity to 25% of normal and
maintained there for long-term therapy. When the activity is less than 20%, the warfarin dosage should be reduced
or omitted until the activity rises above 20%. Inherited polymorphisms
in 2CYP2C9 and VKORC1 have significant effects on warfarin dosing; however, algorithms incorporating genomic
information to predict initial warfarin dosing were no better than standard clinical algorithms in two of three large
randomized trials examining this issue. The recommended INR for prophylaxis and treatment of thrombotic disease is
2–3. Patients with some types of artificial heart valves (eg, tilting disk) or other medical conditions increasing
thrombotic risk have a recommended range of 2.5–3.5.
Types of anticoagulants- mechanisms of action and indications for use
• Vitamin K antagonists.
• Direct Oral Anticoagulants (DOACs)
• Low molecular weight heparins (LMWH)
What is the mechanism of action for anticoagulants?
• Anticoagulants achieve their effect by suppressing the synthesis or function of various clotting factors that are
normally present in the blood. Such drugs are often used to prevent the formation of blood clots (thrombi) in
the veins or arteries or the enlargement of a clot that is circulating in the bloodstream.
What are the indications for anticoagulants?
• Anticoagulation is an important component of the management strategy for several common medical
conditions. It is indicated for the prevention of recurrent thrombosis in patients with venous thromboembolism
(VTE), which includes deep venous thrombosis and pulmonary embolism, and ischemic stroke.
Understand Starling’s law
The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume
increases due to the myocyte stretch causing a more forceful systolic contraction. This assumes that other factors
remain constant.
The Frank–Starling law of the heart (also known as Starling's law and the Frank–Starling mechanism) represents the
relationship between stroke volume and end diastolic volume.[1] The law states that the stroke volume of the heart
increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic
volume), when all other factors remain constant.
[1]
As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an
increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with
the venous return, arterial blood supply and humoral length,[2] without depending upon external regulation to make
alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output
equality.
Medications which increase and decrease preload and afterload
For heart failure, ACE inhibitors and ARBs reduce workload on the myocardium by reducing both preload and afterload.
, Preload: When some measure of left ventricular performance such as stroke volume or stroke work is plotted as a
function of left ventricular filling pressure or end-diastolic fiber length, the resulting curve is termed the left ventricular
function curve (Figure 13–4). The ascending limb (<15 mm Hg filling pressure) represents the classic Frank-Starling
relation described in physiology texts. Beyond approximately 15 mm Hg, there is a plateau of performance. Preloads
greater than 20–25 mm Hg result in pulmonary congestion. As noted above, preload is usually increased in heart
failure because of increased blood volume and venous tone. Because the function curve of the failing heart is lower,
the plateau is reached at much lower values of stroke work or output. Increased fiber length or filling pressure
increases oxygen demand in the myocardium, as described in Chapter 12. Reduction of high filling pressure is the goal
of salt restriction and diuretic therapy in heart failure. Venodilator drugs (eg, nitroglycerin) also reduce preload by
redistributing blood away from the chest into peripheral veins.
Afterload: Afterload is the resistance against which the heart must pump blood and is represented by aortic impedance
and systemic vascular resistance. As noted in Figure 13–2, as cardiac output falls in chronic failure, a reflex increase in
systemic vascular resistance occurs, mediated in part by increased sympathetic outflow and circulating catecholamines
and in part by activation of the renin- angiotensin system. Endothelin, a potent vasoconstrictor peptide, is also involved.
This sets the stage for the use of drugs that reduce arteriolar tone in heart failure.
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Antidote therapies for benzodiazepines
Flumazenil is approved for use in reversing the CNS depressant effects of benzodiazepine overdose and to hasten
recovery following use of these drugs in anesthetic and diagnostic procedures. Although the drug reverses the
sedative effects of benzodiazepines, antagonism of benzodiazepine-induced respiratory depression is less predictable.
When given intravenously, flumazenil acts rapidly but has a short half-life (0.7–1.3 hours) due to rapid hepatic
clearance. Because all benzodiazepines have a longer duration of action
than flumazenil, sedation commonly recurs, requiring repeated administration of the antagonist.
Adverse effects of flumazenil include agitation, confusion, dizziness, and nausea. Flumazenil may cause a
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