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Sharlene and MB's PT party > Cardiovascular Disease (not PVD) and the medical/surgical management of CVD > Flashcards

Cardiovascular Disease (not PVD) and the medical/surgical management of CVD Flashcards

1
Q

Characteristics of atherosclerosis

A
  • lipid-laden plaques (lesions) affecting mod-lg size arteries
  • thickening and narrowing of the intimal layer of blood vessels
  • focal accumulation of lipids, platelets, monocytes, plaque, and other debris
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2
Q

Cardiovascular Disease: Risk factors- list of non-modifiable risk factors

A

age
family history
race
gender

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3
Q

Cardiovascular Disease: Risk factors- specific info on age

A

men > 45

women > 55

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4
Q

Cardiovascular Disease: Risk factors- specific info on family history

A
  • cardiac event in 1st degree male relative < 55 or 1st degree female relative < 65
  • risk increases further w/ younger age of onset, number of events, and how close genealogically the relative is
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5
Q

Cardiovascular Disease: Risk factors- specific info on race

A

African American

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6
Q

Cardiovascular Disease: Risk factors- specific info on gender

A

men > risk than pre-menopausal woman

after menopause risk is =

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7
Q

Cardiovascular Disease: Risk factors- list of modifiable risk factors

A 
cholesterol
diabetes
diet
hypertension
obesity
physical inactivity
tobacco
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8
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ cholesterol

A
  • Total cholesterol <200 mg/dL
  • LDL:<160mg/dL if at low risk for CVD, < 130 mg/dL if at mod risk for CVD, <100mg/dL if at high risk for CVD or have diabetes
  • HDL > 40 mg/dL for men, > 50 mg/dL for women
  • Triglycerides < 150 mg/dL
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9
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ diabetes

A

HgA1C < 7%

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10
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ hypertension

A

SBP <140 mmHg and DBP <90 mmHg

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11
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ diet

A

low fat diet w/ balance of veggies, fruits, grains, and meats

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12
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ obesity

A
  • BMI 18.5 - 24.9 kg/m2
  • waist for males < 40 in
  • waist for females <35 in
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13
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ physical inactivity

A

at least 30 min of activity 5-7 days/wk

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14
Q

Cardiovascular Disease: Risk factors- goals to reduce risk w/ tobacco

A

smoking cessation, regardless of time smoked, reduces risk

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15
Q

3 types of Acute Coronary Disease (ACD)

A 
Angina pectoris
Myocardial Infarction (MI) 
Heart Failure (HF)
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16
Q

General characteristics of ACD

A
  • spectrum of clinical entities from angina to MI to sudden cardiac death
  • imbalance of myocardial O2 supply and demand, causing ischemic chest pain
  • may have no symptoms (more likely with diabetic) but present new pathologic Q wave on ECG
  • subacute occlusions may have no symptoms
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17
Q

Angina Pectoris: What is Levine’s sign

A

pt. clutches fist over sternum

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18
Q

Angina Pectoris: general

A
  • chest pain or pressure due to ischemia, may have levine’s sign
  • imbalance in myocardial O2
  • vasospasm (symptoms may be silent at rest)
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19
Q

Angina Pectoris: causes of myocardial O2 imbalances

A 
exertion
emotional stress
smoking
extremes of temp, especially cold
overeating
tachyarrhythmias
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20
Q

Angina Pectoris: 3 major types

A

stable angina
unstable angina
variant angina

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21
Q

Angina Pectoris: info about stable angina

A
  • classic exertional angina occurring during exercise or activity
  • occurs at predictable rate-pressure product (RPP = HRxBP)
  • relieved w/ rest and/or nitroglycerin
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22
Q

Angina Pectoris: info about unstable angina pre-infarction, crescendo angina)

A
  • coronary insufficiency w/out any precipitating factors or exertion
  • chest pain increases w/ severity, frequency, and duration; refractory to treatment
  • increased risk for MI or lethal arrhythmia
  • pain is difficult to control
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23
Q

Angina Pectoris: inf about variant angina (Prinzmetal’s angina)

A
  • caused by vasospasm of coronary arteries in the absence of occlusive disease
  • responds well to nitroglycerin or calcium channel blocker long term
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24
Q

Angina Pectoris: symptoms in women

A
  • sensation of discomfort
  • crushing
  • pressing
  • bad ache
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25
Q

Angina Pectoris: general symptoms

A
  • SOB
  • fatigue
  • diaphoresis
  • weakness
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26
Q

Angina Pectoris: symptoms in older adults w/ atypical symptoms (absence of chest pain)

A
  • dyspnea
  • diaphoresis
  • nausa and vomitting
  • syncope
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27
Q

MI: what is it

A

prolonged ischemia , injury, and death of an area of the myocardium caused by occlusion of one or more coronary arteries

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28
Q

MI: precipitating factors

A
  • atheroscleroic heart disease w/ thrombs formation
  • coronary vasospasm
  • embolism
  • cocaine use
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29
Q

MI: 3 zones of infarction

A
  • zone of infarction
  • zone of injury
  • zone of ischemia
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30
Q

MI: info about zone of infarction

A

consists of necrotic, non-contratcile tissue
electrically inert
on ECG- pathological Q waves

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31
Q

MI: info about zone of injury

A

area immediately adjacent to central zone
tissue is non-contratcile
cells undergoing metabolic changes
electronically unstable
on ECG- elevated ST segments over injured area

32
Q

MI: info about zone of ischemia

A

outer area
cells undergoing metabolic changes
electronically unstable
on ECG- inverted T waves

33
Q

MI: Infarction sites

A

transmural

non-transmural

34
Q

MI: Infarction sites- transmural

A

full thickness of myocardium

often a ST elevated (STEMI) or Q wave MI

35
Q

MI: Infarction sites- non-transmural

A

sub-endocardial, sub-epicardial, intramural infarctions

Non-St elevated MI (NSTEMI) or non Q-wave MI

36
Q

MI: sites of coronary occlusion

A
  • Inferior MI, R ventricle infarction, disturbances in upper conduction system: R coronary artery
  • Lateral MI, ventricular ectopy: circumflex artery
  • Anterior MI, disturbances of lower conduction system: L anterior descending artery
37
Q

MI: what happens w/ impaired ventricular function

A
  • decreased stroke volume, cardiac output, and ejection fraction
  • increased end diastolic ventricular pressures
38
Q

MI: What happens when there is electrical instability

A

arrhythmias, present in injured or ischemic areas

39
Q

Heart Failure: general summary

A

clinical syndrome where heart is unable to maintain adequate circulation of blood to meet the metabolic needs of body

40
Q

Heart Failure: 3 types

A

L sided heart failure (CHF)
R sided HF
Biventricular HF

41
Q

Heart Failure: L sided heart failure (CHF)

A

characteriszed by:
-pulmonary congestion, edema, and low cardiac output due to back up of blood from L ventricle to L atrium
and lungs
-due to insult to L ventricle from myocardial disease
-excessive workload of heart ( HTN, valvular disease, and congenital defects)
- cardiac arrhythmias or heart damage
-

42
Q

Heart Failure: R sided HF

A

characterized by:

  • increased pressure load on R ventricle
  • mitral valve disease
  • chronic lung disease (cor pulmonale)
  • hallmark signs are jugular vein distention and peripheral edema
43
Q

Heart Failure: Biventricular HF

A
  • severe LV pathology producing back up into the lungs
  • Increased PA pressures
  • RV signs of HF
44
Q

Heart Failure: associated symptoms

A

muscle wasting
myopathies
osteoporosis

45
Q

Heart Failure: s/s of pulmonary congestion - L ventricle failure

A

dyspnea, dry cough
orthopnea
paroxysmal nocturnal dyspnea (PND)
pulmonary rales, wheezing

46
Q

Heart Failure: s/s of pulmonary congestion - R ventricle failure

A

dependent edema
weight gain
ascites
liver enlargement (hepatomegaly)

47
Q

Heart Failure: s/s of low cardiac output - L ventricle failure

A
  • hypotension
  • tachycardia
  • light headedness, dizziness
  • cerebral hypoxia- irritability, restlessness, confusion, impaired memory, sleep disturbances
  • fatigue, weakness
  • poor exercise tolerance
  • enlarged heart on x-ray
  • S3 heart sound, possibly S4
  • murmers of bi and/or tricuspid valve regurgitation
48
Q

Heart Failure: s/s of low cardiac output - R ventricle failure

A

-anorexia, nausea, bloating
-cyanosis (nail beds)
-R upper quadrant pain
-jugular vein distention
-R S3 heart sounds
murmers of pulmonary or tricuspid insufficiency

49
Q

Heart Failure: what is HF compensation and how is this done

A
  • heart returns to functional status w/ reduced CO and exercise tolerance
  • Physiologic compensatory mechanisms are SNS stimulation, LV hypertrophy, anaerobic metabolism, cardiac dilation, arterial vasoconstriction
  • medical therapy used to assist compensation
50
Q

Heart Failure: cause for sudden death

A

significant ischemia or ventricular arrhythmia

51
Q

Medications: list of medications used for management of CVD

A 
ACE inhibitors
Angiotension II receptor blockers
Nitrates
Beta-adrenergic blocking agents
Calcium channel blocking agents
Antiarrhythmics 
Digitalis
Diuretics
Aspirin
Tranquilizers
Hypolipidemic agents
52
Q

Medications: ACE inhibitors

A
  • inhibit conversion of Angiotension 1 to Angiotension 2
  • decreases sodium retention and peripheral vasoconstriction in order to decrease BP

EX: Captopril (Capoten), Enalopril (Vasotec), Lisinopril (Zestril)

53
Q

Medications: Angiotension II receptor blockers

A
  • blocks binder of angiotension 2 at the tissue/smooth muscle level, decreasing BP

Ex: Losatan (Cozaar)

54
Q

Medications: Nitrates

A
  • decrease preload through peripheral vasodilation
  • reduce myocardial O2 demand
  • dilate coronary arteries & improve coronary blood flow

Ex: Nitroglycerin

55
Q

Medications: Beta-adrenergic blocking agents

A
  • Reduce myocardial demand by reducing HR and contractility
  • control arrhythmias and chest pain
  • reduce BP

Ex: Atenolol (Tenormin), Metoprolol (Lopressor), Propranolol (Inderal)

56
Q

Medications: Calcium channel blocking agents

A
  • inhibit flow of calcium ions
  • decrease HR
  • decrease contractility
  • dilate coronary arteries
  • reduce BP
  • control arrhythmias and chest pain

Ex: Diltiazem ( Cardizem), Amlodipine (Norvasc)

57
Q

Medications: Antiarrhythmics

A
  • alter conductivity
  • restore normal heart rhythm
  • control arrhythmias
  • improve CO

Ex: Quinidine, Procainamide

58
Q

Medications: Digitalis

A
  • increases contractility and decreases HR
  • mainstay in the treatment of CHF

Ex: Digoxin

59
Q

Medications: Diuretics

A
  • decrease myocardial work (reduce preload and afterload)
  • control HTN

Ex: Furosemide (Lasix), Hydrochlorothiazide (Esidrix)

60
Q

Medications: Aspirin

A
  • decreases platelet aggregation

- may prevent MI

61
Q

Medications: Tranquilizers

A

decreases anxiety, sympathetic effects

62
Q

Medications: Hypolipidemic agents

A
  • reduce serum lipid levels when diet and weight reduction are not effective

Ex: Cholestyramine (Questran), Covastatin ( Mevacor), Simvastin (Zocor)

63
Q

Activity restrictions for acute MI

A
  • Activity can be increased once acute MI has stopped (peak in cardiac troponin levels)
  • Activity should be limited to 5 METs or 70% of age predicted HR max for 4-6 weeks following MI
64
Q

Activity restrictions for Acute HF

A
  • O2 demand should not be increased in pt.s in acute or decompensated HF
  • Once medically managed and no longer display signs of acute decompensation, activity may be increased while monitoring hemodynamic response to activity.
65
Q

List of surgeries for CVD

A
  • Percutaneous Transluminal Coronary Angioplasty (PTCA)
  • Intravascular Stents
  • Coronary Artery Bypass Graft (CABG)
  • Transplantation
  • Ventricular Assist Device
66
Q

What’s up with the Percutaneous Transluminal Coronary Angioplasty (PTCA)

A
  • Under fluoroscopy, surgical dilation of a blood vessel using a small balloon tipped catheter inflated inside the lumen
  • Relieves obstructed blood flow in acute angina or acute MI
  • Improves coronary blood flow, improves L ventricular function, and provide anginal relief
67
Q

Tell me about Intravascular Stents

A
  • an endoprosthesis (pliable wire mesh) implanted post-angioplasty to prevent re-stenosis and occlusion in coronary or peripheral arteries
  • often coated w/ medication to prevent thrombosis
68
Q

The what and why of the Coronary Artery Bypass Graft (CABG)

A
  • surgical circumvention of the obstruction in the coronary artery using an anastomosing graft (saphenous vein, intermal mammary artery)
  • multiple grafts may be necessary
  • Improves coronary blood flow, improves L ventricular function, and provide anginal relief
69
Q

Why resort to using Transplantation

A

used in end-stage myocardial disease such as cardiomyopathy, ischemic heart disease, and valvular heart disease

70
Q

3 types of transplantation

A

heteroptics
orthotopic
heart and lung transplantation

71
Q

What is heteroptic transplantation

A

involves leaving the natural heart and piggy- backing the donor heart

72
Q

What is orthotopic transplantation

A

involves removing the diseased heart and replacing it with a donor heart

73
Q

What is the heart and lung transplantation

A

involves removing both organs and replacing them with donor organs

74
Q

Major problems post-transplantation

A

rejection
infection
complications of immunosuppressive therapy

75
Q

Ventricular Assist Device. Go!

A
  • implanted device (accessory pump) that improves tissue perfusion and maintains cardiogenic circulation
  • used w/ severely involved patients such as cardiogenic shock unresponsive w/ meds, severe ventricular dysfunction
76
Q

What is thrombolytic therapy

A
  • given for acute MI
  • meds activate body’s fibrinolytic system, disolve clot, and restore coronary blood flow

Ex: streptokinase, TPA, urokinase

Sharlene and MB's PT party (35 decks)

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