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Care of Adult/Older patients > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

the most common type of cardiovascular disease and accounts for the majority of cardiovascular deaths.

A

CAD

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2
Q
  • Begins as soft deposits of fat that harden with age
  • Referred to as “hardening of arteries”
  • Can occur in any artery in the body
A

Atherosclerosis

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3
Q

Atheromas

A

(fatty deposits)

Preference for the coronary arteries

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4
Q

CAD Non-modifiable risk factors

A
  • Age
  • Gender
  • Ethnicity
  • Family history
  • Genetic predisposition
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5
Q

Modifiable risk factors

A
  • Elevated serum lipids (*LDL)
  • Hypertension
  • Tobacco use
  • Physical inactivity
  • Obesity
  • Diabetes
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6
Q

highest incidence of CAD & MI are in?

A

white middle aged men

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7
Q

Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are:

A) Obesity and smokeless tobacco use.
B) Hypertension and cigarette smoking.
C) Elevated serum lipids and diabetes mellitus.
D) Physical inactivity and elevated homocysteine levels.

A

Answer: B
Rationale: An elevated blood pressure and cigarette smoking (causes vasoconstriction) increase the rate of atherosclerosis. Atherosclerosis increases the workload of the heart and increases myocardial oxygen demand.

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8
Q

Diagnostic Tests for CAD

A
  • Cardiac catheterization
  • H& P
  • Chest X-ray
  • ECG
  • Lipid Profile
  • Percutaneous Cardiac Intervention
    - Angioplasty
    - Stenting - must be on antiplatelet therapy for as
    long as the stent is place
  • CT (Electronic Beam)
  • Calcium and plaque deposits
  • Stress Test: shows of blood flow through coronary artery
  • ECG
  • Echocardiogram: shows chambers an EF
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9
Q

Most definitive diagnostic test for CAD

A
  • Cardiac catheterization
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10
Q

Patient teaching for CAD

A
  • Health promoting behaviors
  • 30 minutes of physical activity >5 days/week
    • Weight training 2 days/week
  • Regular physical activity contributes to
    • Weight reduction
    • Reduction of >10% in systolic BP
    • Increase in HDL cholesterol
  • smoking cessation
  • stress reduction
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11
Q

Nutrition/Diet

A
  • Low fat
    • 30% of kcal
    • most from mono/polysaturated fats
  • low cholesterol
  • low sodium diet
  • increase complex carbs
    • whole grains
    • fruits/veggies
    • fiber
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12
Q

Sources of mono-unsaturated fats

A
  • fish oil
  • Oils (canol, peanut, olive)
  • Avocado
  • Nuts (almonds, peanuts, pecans)
  • Olives
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13
Q

Sources of poly-unsaturated fats

A
  • vegetable oils
  • nuts
  • seeds
  • margarine
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14
Q

Drugs that restrict lipoprotein production

A

Statins, niacin

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15
Q

Drugs that increase lipoprotein removal:

A

Questran (Cholestyramine)

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16
Q

Drugs that decrease cholesterol absorption:

A

Ezetimibe (Zetia)

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17
Q

Drugs that decrease triglycerides:

A

Omega-3 fatty acids

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18
Q

Why would a patient with CAD need antiplatelet therapy?

A
  • decrease risk factors

- prevent clotting

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19
Q

Unless contraindicated, this medication is recommended for most people at risk for CAD.

A

low-dose aspirin

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20
Q

Medication of choice or patients with a stent and why?

A
  • Clopidogrel (Plavix)

- keeps platelets “slippery” to prevent sticking to the stent

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21
Q

β-Adrenergic Blockers actions

A
  • Decrease
    • myocardial contractility
    • HR
    • CO
    • BP
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22
Q

Calcium Channel Blocker actions

A
  • Vasodilation
  • decreases
    • myocardial contractility
    • blood pressure
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23
Q

Ace Inhibitors actions

A
  • decreases blood pressure by causing vasodilation

- decrease risk for cardiac events (MI)

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24
Q

Demand for myocardial O2 exceeds the ability of the coronary arteries to supply

A

Myocardial Ischemia

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25
Q

Chest pain caused by reversible myocardial ischemia

A

Angina

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26
Q

chest pain that occurs intermittently over a long period of time with the same pattern of onset, duration, and intensity of symptoms

A

Chronic Stable Angina

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27
Q

diagnostics for Chronic Stable Angina

A
  • H&P
  • Chest Xray
  • ECG
  • Cardiac markers: myocardial injuries
  • Lipid Panel
  • Cardiac catheterization-Most Specific
  • Stress Test
    • Visualize blockage (diagnostic)
    • Open blockages (interventional)
  • Echocardiogram
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28
Q

Nitrate action

A
  • vasodilation
  • decreases pre & afterload
  • decreases cardio O2 demand
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29
Q

Tx for chronic stable angin

A
  • nitrate
  • β-Adrenergic blockers
  • Calcium channel blockers
  • Ace Inhibitors (patients with an EF of <40%)
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30
Q

Nitrate A/E

A
  • orthostatic hypo-tension
  • dizziness
  • HA
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31
Q

ischemic discomfort resulting from plaque accumulation and/or rupture leading to thrombus formation

A

Acute Coronary Syndrome (ACS)

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32
Q

Types of Acute Coronary Syndrome (ACS)

A
  • Unstable angina (UA)
  • Non-ST segment elevation myocardial infarction (NSTEMI)
  • ST segment elevation myocardial infarction (STEMI)
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33
Q
  • chest pain that is new in onset
  • occurs at rest or with increasing frequency, duration, or with less effort.
  • pain typically lasts 10 minutes or more.
  • must be treated immediately
A

Unstable Angina

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34
Q

occurs because of abrupt stoppage of blood flow through a coronary artery from a thrombus caused by platelet aggregation.

A

Myocardial Infarction

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35
Q

Types of MI

A
  • ST elevation (STEMI)

- Non-ST elevation (NSTEMI)

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36
Q

In order to limit the infarct size during a STEMI, the artery must be opened……..

A
  • within 90 minutes of presentation.
  • By:
    • PCI (preffered)
    • thrombolytic or fibrinolytic therapy
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37
Q

The acute MI process evolves over time. The earliest tissue to become ischemic is?

A

the subendocardium (the innermost layer of tissue in the heart muscle).

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38
Q

If ischemia persists during an MI, it takes approximately how long for the entire thickness of the heart muscle to become necrosed.

A

4 to 6 hours

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39
Q

an inferior wall and/or posterior wall MI results from?

A

Blockage of the right coronary artery

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40
Q

an anterior wall infarction results from?

A

blockages in the left anterior descending artery

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41
Q

LV wall MIs result from?

A

blockages in the left circumflex artery

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42
Q

Why would a younger person have a more serious first MI than an older person with the same degree of blockage?

A

the older person may have good COLLATERAL CIRCULATION, resulting from a long hx of CAD

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43
Q

MI clinical manifestations (typical)

A

Chest Pain that is

  • Severe
  • not relieved by rest, position change, or nitrate administration
  • described as heaviness, pressure, tightness, burning, constriction, crushing
  • located substernal or epigastric
  • May radiate to neck, lower jaw, arms, back
  • Often occurs in early morning
  • usually lasts > 20 min
  • Atypical in women, elderly
  • No pain if cardiac neuropathy (diabetes)
44
Q

MI clinical manifestations (atypical)

A
  • discomfort instead of pain
  • weakness
  • nausea
  • indigestion
  • shortness of breath.
45
Q

MI symptoms, some women may experience?

A
  • Fatigue/weakness
  • sleep disturbances
  • SOB
  • nausea
  • anxiety
  • dizziness
  • cold sweats
46
Q

MI symptoms in patients with diabetes?

A
  • may experience silent (asymptomatic) MIs because of cardiac neuropathy
  • SOB
  • fatigue/weakness, -
  • abdominal pain (instead of chest pain)
  • n/v
  • diaphoresis
47
Q

MI symptoms in older patients?

A
  • may experience a change in mental status (e.g., confusion)
  • fatigue/weakness
  • abd pain
  • diaphoresis
  • shortness of breath
  • pulmonary edema
  • dizziness
  • dysrrhythmia
48
Q

early warning signs of a heart attack?

A
  • pressure in center of chest
  • pain in shoulder, neck or arms
  • chest discomfort with fainting, sweating, or nausea
49
Q

diagnostic testing for an MI?

A
  • H&P
  • Characteristics of CP
  • Serum cardiac markers (troponin, myoglobin)
    • Released into the blood from necrotic heart muscle
  • ECG
  • Stress test (ONLY if cardiac markers are negative)
  • Cardiac Catheterization
50
Q

Initial Tx for Acute Coronary Syndrome (ACS)

A
  • Assess ABC’s
  • Position upright, -
  • administer O2
  • Vitals and pox
  • Listen to heart and lungs
  • 12 lead ECG-continuous monitoring
  • Establish IV (2)
  • Assess pain
  • Medicate for pain (nitro, morphine)
  • Sublingual NTG q 5min X 3 (hold SBP <90)
  • Baseline blood work
  • Chest Xray
  • Assess for CI for antiplatelet, anticoagulation, or thrombolytic therapy-PCI
  • Administer ASA
  • Administer antidysrhythmics
51
Q

Ongoing Tx: Angina wiith negative cardiac markers

A
  • Antiplatelet/anticoag
    • ASA and/or Heparin
  • Coronary angiography
  • PCI (percutaneous Intervention)
    • angioplasty/stenting
52
Q

Ongoing Tx: STEMI or NON-STEMI with positive cardiac markers

A
  • Thrombolytic therapy
  • PCI
  • Surgical revascularization
    • CABG
53
Q

Nursing assessments post PCI

A
  • Frequent vitals
  • Evaluation of puncture site for bleeding
  • Maintain bed rest
54
Q

Scar tissue replaces necrotic tissue how long after MI?

A

6 weeks

55
Q

Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle

A

Ventricular remodeling

56
Q

MI Complications

A
  • dysrhytmias (80% of pt)
  • HF
  • Cardiogenic shock
57
Q

S/S of Cardiogenic shock

A
  • Occurs when there is decreased CO
  • S/S similar to HF
    • Tachycardic,
    • hypotensive,
    • tachypneic
    • crackles
    • S/S of hypo-perfusion
58
Q

S/S of hypo-perfusion

A
  • Cyanosis
  • pallor
  • diaphoresis
  • weak peripheral pulses
  • cool
  • clammy skin
  • delayed Cap Refill
  • decreased renal blood flow = decreased urine output
59
Q

indications for Coronary Surgical Revascularization

A
  • Failed medical management
  • Presence of left main coronary artery or three-vessel disease
  • Not a candidate for PCI (e.g., lesions are long or difficult to access)
  • Failed PCI with ongoing chest pain
  • Diabetes
  • Long term benefits
60
Q

How long do CABG pts stay in the ICU?

A

24-36 hrs

61
Q

Risk factors for Sudden Cardiac Death

A
  • LV hypertrophy
  • myocarditis
  • hypertrophic cardiomyopathy
62
Q

the total blood flow through the systemic or pulmonary circulation per minute

A

cardiac output

63
Q

amount of blood pumped out of the left ventricle =____mL

A

70

64
Q

Pre-HTN values

A
  • Systolic BP: 120 - 139
    OR
  • Diastolic BP: 80 - 89
65
Q

Subtypes of HTN

A
  • Isolated systolic hypertension (ISH)

- Pseudo hypertension

66
Q

Isolated systolic hypertension (ISH)

A
  • Average SBP > 140 & DBP < 90 mm Hg
  • due to loss of elasticity from atherosclerosis
  • more common in older pts
67
Q

Pseudo hypertension

A
  • occurs with advanced atherosclerosis
  • sclerotic arteries do not collapse when the cuff is fully inflated, cause higher cuff pressures than are actually present within the vessels.
  • Suspect if arteries feel rigid, or when few retinal or cardiac signs are found relative to the pressures obtained by cuff.
68
Q

Risk factors or Primary HTN

A
  • Age
  • Alcohol
  • Cigarette smoking
  • Diabetes mellitus
  • Elevated serum lipids
  • Excess dietary sodium
  • Gender (more in men)
  • Family history
  • Obesity
  • Ethnicity (more in AA men)
  • Sedentary lifestyle
  • Socioeconomic status
  • Stress
69
Q

action of nitric oxide

A

causes vaso-relaxation/dilation

70
Q

BP is highest during which part of the day?

A

early morning

71
Q

How long should pts be seat prior to a BP reading?

A

5 min

72
Q

Hypertension Diagnostic Studies

A
  • Urinalysis
  • creatinine clearance
  • Serum electrolytes -
  • glucose
  • BUN
  • serum creatinine
  • Serum lipid profile
  • ECG
  • Echocardiogram
73
Q

Hypertension Complications

A
  • speeds up atherosclorosis development
  • Coronary artery disease
  • LV hypertrophy
  • HF
  • Peripheral Artery Disease
  • aortic aneurysm
  • aortic dissection
  • Cerebro Vascular Disease (stroke risk x4 higher)
  • Nephrosclorosis
    • ESRD (leading cause)
  • Retinal damage
    • blurred vision
    • hemorrhage
    • loss of vision
74
Q

Lifestyle modifications needed for patients with HTN?

A
  • Weight reduction
  • DASH eating plan
  • Dietary sodium reduction: Normal is <2300 mg of sodium/day
  • AA, DB, CKD <1500mg of sodium/day
  • Physical activity
  • Moderation of alcohol consumption:
    • Men: 2 drinks/day
    • Women: < 1 drink/day
75
Q

AVG sodium intake should be?

A

< 2300 mg/day

76
Q

Effects of weight loss on HTN?

A
  • Weight loss of 10 kg (22 lb) may decrease SBP by approx. 5-20 mm Hg
77
Q

DASH diet?

A
  • Dietary Approaches to Stop HTN
  • emphasizes:
    • fruits/veggies
    • fat free or low fat dairy
    • whole grains
    • fish/poultry
    • beans, nuts, seeds
78
Q

Physical activity recommendations for pts with HTN?

A
  • Regular physical (aerobic) activity, at least 30 minutes, most days of the week
  • Vigorous aerobic activity at least 20 minutes x3 days/week
  • Muscle strengthening x2 days/week
  • Flexibility and balance exercises x2 days/week
79
Q

Physchosocial Risk Factors for HTN?

A
  • Socioeconomic status
  • social isolation
  • lack of support
  • stress at work and family life
  • depression
80
Q

Smoking cessation reduces risk factors for HTN within?

A

1 yr

81
Q

Metoprolol mechanism of action, class and generic name?

A
  • Selective B1-Adrenergic inhibitor
  • Anti HTN/anginal
  • Loressor
82
Q

Metoprolol therapeutic affects?

A
  • slows hr
  • decrease CO
  • decreases BP
83
Q

Clonidine mechanism of actions and class?

A
  • adrenergic antagonist

- antihypertensive

84
Q

Clonidine therapeutic affects?

A
  • vasodilation
  • decreases BP
  • decrease HR
  • produces analgesia in epidural
85
Q

Furosemide mechanism of action, class and generic name?

A
  • increases excretion of Na, Cl, K at the ascending loop of henle
  • Diuretics
  • Lasix
86
Q

Furosemide uses?

A
  • edema associate with HF and renal/liver disease
  • acute pulmonary edema
  • HTN
87
Q

Lisinopril mechanism of action and class?

A
  • prevents conversion of angiotensin I into angiotensin II (dilation)
  • ACE Inhibitor/anti HTN
88
Q

Valsartan mechanism of action & class?

A
  • Angiotensin II Receptor Blocker (ARB)

- Anti HTN

89
Q

Valsartan Therepeutic affects?

A
  • vasodilation
  • decrease peripheral resistance
  • decrease BP
90
Q

Amlodipine mechanism of action & class?

A
  • inhibits movement of calcium across cardiac and smooth muscle cell membranes
  • Anti anginal/HTN
91
Q

Amlodipine therapeutic affects?

A
  • vasodilation of the coronary arteries and peripheral arteries/arterioles
  • decreases BP by reducing peripheral resistance
92
Q

Most common AEs with cardiac meds?

A
  • Orthostatic hypotension
  • Sexual dysfunction
  • Dry mouth
  • Frequent urination
  • Electrolyte imbalance (K, Mg)
  • Some side effects may decrease over time
93
Q

ausculatory gap

A
  • a wide gap between the first Korotkoff sound and subsequent beats.
  • caused by under inflation of the BP cuff, use 2 step method
94
Q

How to assess for orthostatic hypotension?

A
  • BP and HR supine, sitting, and standing
  • Measure within 1 to 2 minutes of position change
  • Positive if:
    • ↓ of 20 mm Hg or more in SBP
    • ↓10 mm Hg or more in DBP,
    • ↑ 20 beats/minute or more in heart rate
95
Q

Contributing factors to secondary HTN?

A
  • Coarctation of aorta (narrowing)
  • Renal disease (artery stenosis)
  • Endocrine disorders
  • Neurologic disorders (brain tumors)
  • Cirrhosis
  • Sleep apnea
  • Cocaine
96
Q

Tx of secondary HTN?

A

tx is aimed at the cause

97
Q

2 types of hypertensive crisis?

A
  • Hypertensive emergency

- Hypertensive urgency

98
Q

Hypertensive emergency

A
  • develops over hrs to days
  • Severe increase in BP (>220/140mm Hg)
  • Evidence of acute organ damage
  • Usually hospitalized
  • secondary HTN is a contributing cause
99
Q

Hypertensive urgency

A
  • develops over days to weeks
  • Severely elevated BP
  • NO evidence of organ damage
  • May NOT require hospitalization
100
Q

hypertensive encephalopathy

A
  • a syndrome in which a sudden rise in BP is associated with:
    • severe headache,
    • N/V
    • seizures
    • confusion
    • coma.
101
Q

A hypertensive emergency is often manifested as?

A

hypertensive encephalopathy

102
Q

Evidence of acute organ damage in pts in hypertensive emergency?

A 
- Hypertensive encephalopathy
 cerebral hemorrhage 
- Acute renal failure
- Myocardial infarction
- Heart failure with pulmonary edema
103
Q

S/S of Hypertensive Encephalopathy?

A
  • Severe headache
  • N/V
  • Seizures
  • confusion
  • Coma
  • Renal failure
  • MI
  • Pulmonary edema
104
Q

Nursing Interventions for Hypertensive Emergency

A
  • Requires Hospitalization
  • IV drug therapy: Titrated to decrease no more than 25% of the MAP in first hour
  • If stable, the goal is 160/100 to 110 mm Hg over the next 2 to 6 hours.
  • Monitor cardiac and renal function
  • Neurologic checks
  • Determine cause
  • Education to avoid future crises
105
Q

Nursing Interventions for Hypertensive Urgency?

A
  • May or may not require hospitalization
  • Managed with oral medications
  • Requires frequent follow up until BP is controlled
106
Q

Normal Mean Arterial Pressure (MAP) range?

A
  • 70-110

- need > 60 for normal cardiac function

Care of Adult/Older patients (5 decks)

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