Exam (elaborations)
CARDIAC ACP (1).
- Institution
- PMI Agile Certified Practitioner
Exam of 25 pages for the course PMI Agile Certified Practitioner at PMI Agile Certified Practitioner (CARDIAC ACP (1).)
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CARDIAC ACPACS spectrum - ANS-Unstable angina- Nstemi- STEMI- sudden cardiac death
acute vs chronic mitral valve regurgiation - ANS-´Acute:
´Example: Papillary muscle rupture
´No time for adaptation
´Presentation:
´Congestive heart failure
´Pulmonary edema
´Chronic:
´Example: Dilated left ventricle
´Time for compensation/adaptation
´Presentation:
´Fatigue, SOB
´Congestive heart failure
´Pulmonary edema
´Left atrial enlargement
´Holosystolic murmur at apex
Adenosine adverse effects - ANS-dyspnea, angina, nausea, impending doom, hypotension,
heartblock
Adenosine Diphosphate Receptor Antagonists MOA - ANS-•Irreversibly blocks the P2Y12
component of ADP receptors on the platelet surface, which prevents activation of the GP IIb/IIIa
receptor complex, thereby reducing platelet aggregation.
•Inhibition of platelet aggregation by clopidogrel is achieved through an active metabolite.
•Platelets are affected for the remainder of their lifespan (~7-10 days).
•Examples: Clopidogrel (Plavix), Ticagrelor.
Adenosine Indications and effects - ANS-▪Indications:
▪Treatment of re-entry circuit SVT/WPW
▪Diagnostic for SVT of unknown origin
▪Effects:
▪Decreases heart rate and reduces conduction velocity, especially at the AV node, which can
produce atrioventricular block
Adenosine MOA - ANS-Slows conduction through the AV node, interrupts Av nodal reentry
pathways and can restore normal sinus rhythm in PSVT via modulation of K currents and the
blunting of catecholamine repsonse
Amiodarone adverse effects - ANS-Pulmonary fibrosis
,hypothyroid
bradycardia(AV blaock
Hypotension
heart failure
resp failure
Amiodraone MOA - ANS-At therapeutic doses it has effect on NA, K and Ca effects as well a
alpha nad Beta clocking effects
Angiotension-Converting Enzyme (ACE) Inhibitors MOA - ANS-•ACE inhibitors produce
vasodilation by inhibiting the formation of angiotensin II
•Angiotensin II is a direct vasoconstrictor through the activation of AT1 receptors on vascular
smooth muscle.
•Angiotensin II facilitates the release of norepinephrine from sympathetic adrenergic nerves and
inhibits norepinephrine reuptake by these nerves. This effect of angiotensin II augments
sympathetic activity on the heart and blood vessels.
•Angiotensin II stimulates aldosterone secretion by the adrenal glands. Aldosterone stimulates
an increase in blood volume through sodium and water retention.
•ACE also breaks down bradykinin, a vasodilator substance, so inhibition of ACE increases
bradykinin levels and promotes vasodilation.
•Interestingly, bradykinins are thought to be responsible for many of the side effects of ACEi (dry
cough, angioedema).
aortic aneurysm - ANS-A weakness in the wall of the aorta that makes it susceptible to rupture.
Aortic aneurysm fusiform - ANS-circumfrential widening of the artery
aortic aneurysm risk factors - ANS-´Smoking (strongest risk factor)
´Hypertension
´Older age (peak incidence at age 70 to 80)
´Family history (in 15 to 25%)
´Race (more common in whites than in blacks)
´Male sex
Aortic aneurysm Saccular - ANS-localized, typically asymmetric outpouchings of the artery wall
Aortic dissection - ANS-´The surging of blood through a tear in the aortic intima with separation
of the intima and media and creation of a false lumen.
Aortic dissection presentation - ANS-´Excruciating chest and back pain
´Symptoms of malperfusion (stroke, myocardial infarction, intestinal infarction, renal
insufficiency, paraparesis, or paraplegia) due to interruption of the blood supply to a particular
vascular bed.
, ´Partial or complete deficits of major arterial pulses, which may wax and wane. Limb blood
pressures may differ, sometimes by > 30 mm Hg.
aortic regurgitation - ANS-•Blood flows from the aorta back into the left ventricle during
ventricular filling due to the incomplete closure of the aortic valve.
•Presentation:
•Fatigue
•Syncope
•SOB
•Palpitations
•Wide pulse pressure (increased SV and decreased SVR)
•Left ventricular dilatation
•Early diastolic murmur
•Causes:
•Widening or aneurysmal change of the aortic annulus (connective tissue disorders, tertiary
syphilis)
•Rheumatic heart disease
Aortic stenosis - ANS-•Narrowed opening between the leaflets of the aortic valve leads to
reduced blood flow from the left ventricle to the aorta. The reduction in forward blood flow also
results in a backing up of blood in the left ventricle.
•Presentation:
•Syncope
•Angina
•Dyspnea
•Pulsus paruus (weak) or tardus (delayed)
•Left ventricular hypertrophy
•Microangiopathic anemia
•Systolic ejection murmur
•Causes:
•Bicuspid aortic valve
•Age-related calcification (smoking, HTN, hyperlipidemia, diabetes)
Aspirin MOA - ANS-•Irreversibly inhibits formation of prostaglandin derivative, thromboxane A2,
via acetylation of platelet cyclooxygenase, thus inhibiting platelet aggregation.
•Irreversibly inhibits cyclooxygenase-1 and 2 enzymes, via acetylation, which results in
decreased formation of prostaglandin precursors.
•Has antipyretic, analgesic, and anti-inflammatory properties.
Assessment of VAD function - ANS-•Auscultate epigastrium/precordium for the hum of the pump
motor and check controller for audible alarm.
•Attempt to re-start controller if no hum or alarm is detected.
•Check that the batteries are not depleted or disconnected (plug into wall power supply if
uncertain).
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