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PAT202 WINTER > W1 & 2 Cardiac > Flashcards

W1 & 2 Cardiac Flashcards

1
Q

what is coronary artery disease? (CAD)

A

narrowing or occlusion of the coronary arteries, usually as a result of atherosclerosis
-includes angina and myocardial infraction

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2
Q

what is myocardial ischemia?

A

lack of blood supply to the myocardium d/t a constriction or obstruction of a blood vessel

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3
Q

what is atherosclerosis?

A

presence of plaque w/in the walls of arteries

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4
Q

what is plaque?

A

is a fatty fibrous material that accumulates, thus producing varying degrees of intravascular narrowing- a situation that results in partial or total blockage of the blood vessels

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5
Q

what are the two main arteries of the myocardium the receive blood?

A

right and left coronary arteries

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6
Q

what is angina pectoris?

A

is chest pain, usually upon emotional distress or exertion. It is caused by the narrowing of coronary artery, which results in lack of sufficient oxygen to the heart muscles

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7
Q

what are the three types of anginas?

A
  • stabel angina
  • variant angina (Prinzemetal’s angina)
  • unstable angina
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8
Q

what is stable angina?

A
  • chest pain occurring intermittently over long period of time w/ the same pattern of onset, duration, intensity of symptoms (predictable)
  • caused by myocardial ischemia
  • stable angina may develop into unstable angina
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9
Q

what is variant/Prinzmetal’s angina?

A

occurs when the decreased myocardial blood flow is caused by spasms of the coronary arteries (w/ or w/out atherosclerosis)

  • If spasm persists long enough, infarction or serious dysrhythmias may occur but usually a benign condition
  • occurs at rest/nocturnal but is unpredictable
    (i. e sleep)
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10
Q

what is unstable angina?

A

associated w/ increase risk for myocardial infraction (MI)
-transient episodes of thrombotic vessels occlusion & vasoconstriction
-Unstable atherosclerotic plaque has ruptured
thrombus can form very quickly!
-Thrombus may break up → perfusion returns before significant myocardial necrosis occurs
reversible myocardial ischemia
but is sign of impending infarction!
pain DOES NOT resolve with the use of nitrates

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11
Q

what are the S/S of unstable angina?

A

increased dyspnea, diaphoresis, anxiety as angina worsens

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12
Q

what are the factors that have been shown to reduce the incidence of CAD?

A
  • limiting or abstaining from alcohol
  • eliminating foods that are high in cholesterol & saturated fat
  • treating HTN early
  • regular exercise and maintaining optimum weight
  • maintaining blood glucose levels w/in normal range
  • not using tobacco (smoking makes the heart work faster)
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13
Q

when the coronary arteries are significantly obstructed, what are the two most common interventions?

A

-percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) surgery

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14
Q

how does percutaneous transluminal coronary angioplasty (PTCA) or (PIC) work?

A
  • place a catheter, with a small inflatable ballon on the end in a section of a narrowed artery
  • the ballon will inflate and deflate which causes it to push toward against the narrowed wall of the artery
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15
Q

how does CABG work? (coronary bypass surgery)

A

-used for severe cases
-a small blood vessel from the leg or chest is used to create a bypass artery
-one end of the graft is sewn to the aorta and the other is sewn to the coronary artery
-blood from the aorta then flows through the new grafted vessel to the heart muscle “bypassing the blockage in the coronary artery
=reduce angina and risk for MI

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16
Q

what are the pharmacological goals for a client with angina?

A

-reduce the frequency of angina episodes & to terminate an incident of acute anginal pain

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17
Q

goals of pharmacological drugs for angina (4 different mechanisms)

A
  1. slowing the heart rate
  2. dilating veins so that the heart receives less blood (reducing preload)
  3. causing the heart to contract w/ less force (reduce contractility)
  4. dilating arterioles to lower BP= giving the heart less resistance when ejecting blood from its chambers (reducing afterload)
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18
Q

what is the first line of therapy for stable angina?

A

rapid-acting organic nitrates

  • relieve angina by dilating veins and coronary arteries
  • relaxes both arterial and venous smooth muscle
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19
Q

how does nitroglycerin work?

A

causes vasodilation making it easier for the heart to eject blood, resulting in decreased oxygen needs.
decreasing oxygen demands reduces pain caused by the heart muscle not receiving sufficient oxygen

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20
Q

when should nitroglycerin be taken?

A

at the first indication of chest pain

  • DO NOT WAIT UNTIL PAIN BECOMES SEVERE
  • can be taken in 5 min interval for up to 3 doses
  • if pain does not subside after 2 doses, 911 should be called
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21
Q

what are the side effects of nitroglycerin?

A

orthostatic hypotension (common)
headache (should decrease over time)- can take acetaminophen if needed
-dizziness, and flushing
-vasodilation causes increased intraocular pressure
-*reflex tachycardia

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22
Q

when should the nurse assess when a pt takes nitroglycerin?

A
  • BP- most likely to reflect the adverse effects of this drug
  • should check client’s BP ONE hour AFTER ADMINISTERING NITROGLYCERIN OINTMENT
  • if 20mg HG below - remove the ointment and report to physical immediately
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23
Q

_ is prohibited with nitrates?

A

alcohol (bc it enhances the effects of alcohol)

severe cases cause cardiovascular collapse

24
Q

negative chronotropic effect is

A

slowing the heart rate

25
Q

negative inotropic effect is

A

reducing contractility

26
Q

why should clients be advised against abruptly stopping beta blocker therapy?

A

may result in sudden increase in cardiac workload and worsen angina

27
Q

beta blockers are to be used with caution in clients w/?

A

w/ asthma, COPD, or impaired renal function

28
Q

what are some important education regarding beta blockers?

A
  • change positions slowly-report dizziness/lightheadedness
  • do not take OTC meds or herbal products w/out discussing them w/ HCP
  • do not discontinue meds abruptly
  • if pulse falls below 50beats/min, notify HCP (sometimes 60 BPM in different agencies)
  • alternate periods of activity w/ periods of rest to avoid fatigue
29
Q

beta blockers have a direction interaction with_

A

insulin-potential increase of hypoglycaemic effects

-monitor blood glucose levels

30
Q

what is the effect of a beta blocker?

A

decrease heart rate, contractility, and after load=decrease in blood pressure

  • reduce myocardial oxygen demand
  • slow impulse conduction through the heart= suppressing dysrhythmias
  • reduces morality when given 8 hrs of MI onset
31
Q

what is the first line of therapy for variant angina?

A

calcium channel blockers

32
Q

how do calcium channel blockers work?

A

by relieving angina by dilating the coronary vessels and reducing the workload of the heart

33
Q

what is the primary cause of MI?

A

advanced coronary artery disease

-plaque build-up can severely narrow one or more branches of the coronary arteries

34
Q

what are the pharmacological treatment goals for acute MI?

A
  • restore blood supply (perfusion) to the damaged myocardium as quickly as possible using thrombolytics
  • reduce myocardial oxygen demands w/ nitrates and beta blockers to prevent further MIs
  • control/prevent associated dysrhythmias w/ beta blockers or other antidysrhythmics
  • reduce post MI mortality with ASA (aspirin) and (ACE) inhibitors
  • control MI pain with narcotics (morphine)
35
Q

thrombolytics and MI

A

if given w/ hours (20 mins-12 hours) after an onset of MI, thrombolytic agents can dissolve clots and restore perfusion to affected regions of the myocardium
-after that it is ineffective

36
Q

what is the primary risk associated with thrombolytics?

A

-excessive bleeding from interference w/ the normal clotting process

37
Q

when is thrombolytic therapy contraindicated ?

A
  • recent trauma
  • surgery
  • internal bleeding
  • active peptic ulcers
  • postpartum w/in 10 days
  • history of intracranial hemorrhage
  • suspected ischemic stroke w/in the past 3 months
  • bleeding disorder, severe liver disease, or thrombocytopenia
38
Q

what do you give as soon as MI is suspected?

A

-160 to 35mg of ASA

ASA in the weeks following an acute MI dramatically reduces morality d/t antiplatelet action

39
Q

why is heparin given following an MI?

A

an anticoagulant to prevent additional thrombi from forming

-after 3 days, clients are switched to warfarin

40
Q

what is the first line of therapy for chronic angina?

A

beta-adrenergic blockers

41
Q

beta blockers can improve survival of myocardial infraction if given _?

A

w/in 24 hour

42
Q

what is troponin I (Tnl)

A

a serum protein whose measurement is used as a sensitive and specific diagnostic test to help identify myocardial schema during acute coronary syndrome

43
Q

adipokines and cardiovascular risk

A 
decrease adiponection (hypoadiponectinemia) in obese individuals have been linked to an increase risk in cardiovascular disease 
-antiatherogenic effects include anti-inflammatory, insulin-sensitizing, enhancement of nitric oxide, reduced vascular smooth muscle cell proliferation
44
Q

how does chronic kidney disease affect

coronary artery disease

A

pt w/ chronic kidney disease are at an increase risk for coronary artery disease and risk increases as glomerular filtration rate declines
-in chronic kidney disease, dsylipidemia, endothelial dysfunction, vascular calcification and elevated levels of growth factors, and toxic oxygen radicals all contribute to atherogenesis and coronary artery disease

45
Q

how dose air pollution and ionizing radiation contribute to coronary artery disease?

A

exposure to air pollution is strongly correlated w/ coronary risk
-toxins in pollution contribute to macrophage activation, oxidation of LDL, autonomic imbalance, thrombosis, and inflammation of the vessel walls

46
Q

what medication has an increase risk of coronary artery disease?

A

NSAIDS

47
Q

what is a stable plaque?

A

gradually increase in size and may partially occlude the vessel lumina=limiting coronary flow and causing schema esp during exercise

48
Q

what causes unstable plaque?

A

occur when fissuring or superficial erosion of the plaque leads to transient episode of thrombotic vessel occlusion and vasoconstriction at the site of plaque damage. this thrombus occludes the vessel for no more than 10-20 mins, w/ return of perfusion before significant myocardial necrosis occurs
-are prone to ulceration or rupture even if there has been no significant impairment of coronary blood flow before the event

-when this ulceration or rupture occurs, underlying tissues of the vessel wall are exposed, resulting in platelet adhesion and thrombus formation. Thrombus formation can suddenly cut off blood supply to the heart muscle, resulting in acute myocardial ischemia, and if the vessel obstruction cannot be reversed rapidly, ischemia will progress to infarction.

49
Q

how does myocardial ischemia develop?

A

-if the supply of coronary blood cannot meet the demand of the myocardium for oxygen and nutrients

50
Q

what causes stable angina?

A

by gradual luminal narrowing and hardening of the arterial walls. so affected vessels cannot dilate in response to increased myocardial demand associated w/ physical exertion or emotional stress
-with rest, blood flow is restored and no necrosis of myocardial cells result
pain is caused by the buildup of lactic acid or abnormal stretching of the ischemic myocardium that irritates mycardial nerve fibres

51
Q

what are s/s of stable angina?

A

pain may radiate to the neck, lower jaw, left arm, and left shoulder
-occasionally pain to the back or down the right arm
-pallor, diaphoresis and dyspnea
women s/s- atypical chest pain, palpitations, sense of unease, and severe fatigue

52
Q

what are s/s of stable angina?

A

pain may radiate to the neck, lower jaw, left arm, and left shoulder
-occasionally pain to the back or down the right arm
-pallor, diaphoresis and dyspnea (SOB)
women s/s- atypical chest pain, palpitations, sense of unease, and severe fatigue

53
Q

what causes variant angina?

A
  • from decrease vagal activity, hyperactivity of the sympathetic nervous system, and decrease nitric oxide activity
  • could also be caused by altered calcium channel function in arterial smooth muscle and endothelial dysfunction w/ release of inflammatory mediators such as serotonin, histamine, endothelia or thromboxane
54
Q

what is silent ischemia and mental stress (induced ischemia)

A

myocardial ischemia does not always cause angina and may be associated only w/ nonspecific symptoms such as fatigue, dyspnea, or feelings of unease

  • may occur during mental stress and anger- mental stress results in the release of catecholamines and an increase in heart rate, BP, and vascular resistance, and electrical instability
  • linked to increase levels of hs-CRP, decrease activity of vasodilator (nitric oxide)
55
Q

myocardial infraction (MI) results when

A

prolonged ischemia causes irreversible damage to the heart muscle
-can be non-ST-elevation (non-STEMI) and ST -elevation MI (STEMI)

56
Q

what is positive inotropic agents?

A

meds that increase contractility

PAT202 WINTER (16 decks)

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