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MED SURG TEST 2 Flashcards

1
Q

BP

A

the force exerted by the blood against the walls of the blood vessel

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2
Q

CO

A

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

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3
Q

Stroke Volume

A

the amount of blood pumped out of the left ventricle (70ml) multiplied by the HR for 1 minute

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4
Q

Hypertension

A 
Persistent elevation of :
Systolic blood pressure ≥140 mm Hg
»OR
Diastolic blood pressure ≥90 mm Hg 
»OR
Current use of antihypertensive medications
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5
Q

Prehypertension

A

Systolic BP: 120 to 139 mm Hg
»OR
Diastolic BP: 80 to 89 mm Hg

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6
Q

Isolated Systolic Hypertension (ISH)

A

oAverage SBP > 140 mm Hg & DBP < 90 mm Hg
or loss of elasticity from atherosclerosis
ISH is more common in older adults because of changes in BP patterns. SBP rises with aging, and DBP rises until approximately age 55 and then declines.

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7
Q

Pseudo Hypertension

A

Advanced atherosclerosis –don’t collapse
Sclerotic arteries do not collapse when the cuff is fully inflated. This results in much higher cuff pressures than are actually present within the vessels. Suspect pseudohypertension if arteries feel rigid, or when few retinal or cardiac signs are found relative to the pressures obtained by cuff.

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8
Q

Primary (essential or idiopathic) hypertension

A

Elevated BP without an identified cause

- 90% to 95% of all cases

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9
Q

Secondary Hypertension

A

Elevated BP with a specific cause
Contributing Factors
Coarctation of aorta (narrowing)
Renal disease (artery stenosis)
Endocrine disorders (Cushing syndrome, thyroid disease)
Neurologic disorders (brain tumors)
Cirrhosis
Sleep apnea
Cocaine
•Treatment of is aimed at eliminating the underlying cause
•Secondary hypertension is a contributing factor to hypertensive crisis

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10
Q

Risk Factors for Primary Hypertension

A 
•Age
•Alcohol
•Cigarette smoking
•Diabetes mellitus
•Elevated serum lipids
•Excess dietary sodium
•Gender
•Family history
•Obesity
•Ethnicity
•Sedentary lifestyle
•Socioeconomic status
Stress
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11
Q

Contributing Factors for Primary Hypertension

A

•Heredity
•Water and Na retention
oHigh sodium intake may activate a number of pressor mechanisms, resulting in water retention.
•Altered renin-angiotensin aldosterone mechanism
oContributes to the development of HTN
•Stress and increased SNS
oIncrease vasoconstriction, increased HR, renin release
•Insulin resistance
oHigh insulin concentration stimulates SNS activity, impairs nitric oxide

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12
Q

Hypertension Symptoms

A 
•Symptoms are often secondary to organ damage and can include 
oFatigue, reduced activity tolerance
oDizziness
oPalpitations, angina
oDyspnea
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13
Q

Diagnostic Studies of Hypertension

A

•History and physical examination
•Bilateral BP measurement
oUse arm with higher reading for subsequent measurements.
oBP is highest in early morning, lowest at night.
•Use a properly calibrated instrument.
•Patient should be seated quietly for 5 minutes in a chair, with feet on the floor and arms supported at heart level.
•Use appropriately sized cuff to ensure accurate readings.
•Obtain at least two measurements on two visits.
•“White coat” phenomenon may precipitate the need for ambulatory blood pressure monitoring (ABPM).
oNoninvasive, fully automated system that measures BP at preset intervals over 24-hour period
•Urinalysis, creatinine clearance
•BMP-Serum electrolytes, glucose, BUN and serum creatinine
•CBC
•Serum lipid profile
•ECG
•Echocardiogram
**These test are usually performed to rule out secondary HTN, or to determine damage caused by uncontrolled HTN

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14
Q

Complications of Hypertension

A

Damage occurs most frequently in the
oHeart
oBrain
oPeripheral vasculature
oKidney
oEyes
•Hypertensive heart disease
oCoronary artery disease
oLeft ventricular hypertrophy
oHeart failure
•Cerebrovascular disease
oStroke (risk 4x higher)
•Peripheral vascular disease
oIncreased development of atherosclerosis, aortic aneurysm, aortic dissection
•Nephrosclerosis
oHTN leading cause of ESRD (especially among African Americans)
•Retinal damage
oBlurred vision, retinal hemorrhage, loss of vision
•Hypertension is a major risk factor for cerebral atherosclerosis and stroke. Even in mildly hypertensive people, the risk of stroke is 4 times higher than in normotensive people.
•Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels, leading to the development of peripheral vascular disease, aortic aneurysm, and aortic dissection.
•Some degree of renal dysfunction is usually present in the hypertensive patient, even one with a minimally elevated BP. Renal dysfunction is the direct result of ischemia caused by the narrowed lumina of intrarenal blood vessels.
The appearance of the retina provides important information about the severity and duration of hypertension.

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15
Q

Nursing Intervention for HTN

A

•Teach patients lifestyle modifications
oWeight reduction: Weight loss of 10 kg
(22 lb) may decrease SBP by approx. 5 to
20 mm Hg
oDASH eating plan
- Emphasizes vegetables, fruits, and fat-free or low-fat dairy products
- Includes whole grains, fish, poultry, beans, seeds, nuts, and vegetable oils
- Limits sodium, sweets, sugary beverages, and red meats
In terms of nutrition content, DASH is:
-Low in saturated and trans fats
- Rich in potassium, calcium, magnesium, fiber, and protein
- Dietary sodium reduction: <1500mg of sodium/day
oModeration of alcohol consumption:
§Men: No more than 2 drinks/day
§Women: No more than 1 drink/day
•When a person decreases caloric intake, sodium and fat intakes usually are also reduced. Although reducing the fat content of the diet has not been shown to produce sustained benefit for BP control, it may slow the progress of atherosclerosis and reduce overall CVD risk.

oPhysical activity: Regular physical (aerobic) activity, at least 30 minutes, most days of the week
oAvoidance of tobacco products
oPsychosocial risk factors
§Socioeconomic status, social isolation, lack of support, stress at work and family life, and depression

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16
Q

Medication Interventions for HTN

A

•Drug therapy: Classifications of common drugs used to treat hypertension
oDiuretics-Furosemide
oB-Adrenergic inhibitors -Metoprolol
oDirect vasodilators-Clonidine
oAngiotensin-converting enzyme inhibitors
§Lisinopril
oAngiotensin II receptor blockers-Valsartan
oCalcium channel blockers-Amlodipine

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17
Q

Side Effects of Cardiac Medications

A 
•Drug therapy and patient teaching
oIdentify, report, and minimize side effects.
§Orthostatic hypotension
§Sexual dysfunction
§Dry mouth
§Frequent urination
§Electrolyte imbalance (K, Mg)
§Some side effects may decrease over time
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18
Q

Nursing Diagnoses for HTN

A 
oIneffective health maintenance 
oAnxiety 
oSexual dysfunction 
oIneffective self-health management 
oDisturbed body image 
oIneffective tissue perfusion 
oRisk for falls
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19
Q

What Happens when HTN Occurs in Older Adults?

A
  • Isolated systolic hypertension (ISH): Most common form of hypertension in individuals age >50.
  • Older adults are more likely to have “white coat” hypertension.
  • Often a wide gap between the first Korotkoff sound and subsequent beats is called the ausculatory gap.
  • Failure to inflate the cuff high enough may result in serious underestimation of the SBP.
  • Older adults have varying degrees of impaired baroreceptor reflex mechanisms.
  • Consequently, orthostatic hypotension occurs often, especially in patients with ISH.
  • Altered metabolism of medications.
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20
Q

Hypertensive Emergency

A 
oSevere increase in BP (>220/140mm Hg)
oEvidence of acute organ damage, especially in the CNS
•Develops over hours to days
•Often occurs in patients with a history of HTN who have failed to comply with medications or who have been under medicated
•Secondary HTN is contributing cause
•Evidence of acute organ damage: 
oHypertensive encephalopathy, cerebral hemorrhage 
oAcute renal failure
oMyocardial infarction
oHeart failure with pulmonary edema
•Signs and symptoms of hypertensive encephalopathy: 
oSevere headache
oN/V
oSeizures, confusion 
oComa 
§Renal failure
§MI
§Pulmonary edema
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21
Q

Hypertensive Urgency

A

develops over days to weeks. This is a situation in which a patient’s BP is severely elevated (180/110mmHg), but no clinical evidence of target-organ damage is found.
May or may not require hospitalization
•Managed with oral medications
•Requires frequent follow up

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22
Q

Nursing Interventions HTN Emergency

A

•Requires Hospitalization
oIV drug therapy: Titrated to decrease no more than MAP 25% in first hour (110-115mm Hg
oMonitor cardiac and renal function
oNeurologic checks
oDetermine cause
oEducation to avoid future crises
•When hypertensive emergencies are managed, mean arterial pressure (MAP) is often used instead of systolic and diastolic BP readings to guide and evaluate drug therapy.
•The initial treatment goal is to decrease MAP by no more than 25% within minutes to 1 hour. If the patient is stable, the goal for BP is 160/100 to 110 mm Hg over the next 2 to 6 hours.

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23
Q

MAP

A

(SBP+2DBP)/3

§MAP at least 60, normally between 70-110

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24
Q

WBC

A

5,000 - 10,000/mm3

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25
Hbg
Male: 14-17.4 g/dL Female: 12-16 g/dL
26
Hct
Male: 42-52% Female: 36-48%
27
Plt
140-400
28
BUN
6-20mg/dL | Elderly: 8-23mg/dL
29
Creatinine
Female: 0.4-1mg/dL Male: 0.6 -1.2 mg/dL
30
BNP
<100pg/mL
31
PTT
60-70 sec
32
PT
11-13 sec (therapy > 1.5-2 times control)
33
INR
0.8-1.2
34
What is the most common type of cardiovascular disease and accounts for the majority of these deaths?
Coronary artery disease
35
Patients with CAD can have two outcomes, what are they?
Asymptomatic or chronic stable angina
36
Atherosclerosis
Type of blood vessel disorder-major cause of CAD oBegins as soft deposits of fat that harden with age oReferred to as “hardening of arteries” oCan occur in any artery in the body oAtheromas (fatty deposits) §Preference for the coronary arteries
37
Nonmodifiable Risk Factors for CAD and ACS
``` •Age •Gender •Ethnicity •Family history •Genetic predisposition Vietnam Vets – Exposed to Agent Orange ext ```
38
Modifiable Risk Factors for CAD and ACS
* Elevated serum lipids (*LDL) * Hypertension * Tobacco use * Physical inactivity * Obesity * Diabetes * The incidence of CAD and MI is highest among white, middle-aged men. * After age 65, the incidence in men and women equalizes, although cardiovascular disease causes more deaths in women than in men. * Additionally, CAD is present in African American women at rates higher than in their white counterparts.
39
Diagnostics Tests for CAD and ACS
``` •H&P •Chest Xray •ECG •Lipid Profile •Cardiac catheterization •Percutaneous Cardiac Intervention oAngioplasty oStenting-must be on o antiplatelet therapy •CT (Electronic Beam) oCalcium and plaque deposits •Stress Test oImpact of blood flow •ECG •Echocardiogram ```
40
Nursing Interventions for CAD
•Teach patients health-promoting behaviors oLow fat, low cholesterol, low sodium diet o30 minutes of physical on most days/week oRegular physical activity contributes to §Weight reduction §Reduction of >10% in systolic BP §Increase in HDL cholesterol
41
Medications for CAD
``` •β-Adrenergic Blockers-Preferred drug oDecrease myocardial contractility, HR, SVR, BP •Calcium Channel Blockers oVasodilation, decreased SVR, myocardial contractility •Ace Inhibitors oDecrease risk for cardiac events (MI) •Antiplatelet therapy oASA-recommended for most people at risk oClopidogrel (Plavix) ```
42
Gerontologic Considerations for CAD
•Strategies to reduce risk factors are effective but often under prescribed and under utilized •Necessary to modify guidelines for physical activity (walking)-start slowly oTwo points when elderly may consider lifestyle change(s): §When hospitalized §When symptoms result from CAD and not from normal aging
43
Chronic Stable Angina
•Myocardial Ischemia oDemand for myocardial O2 exceeds the ability of the coronary arteries to supply •Angina oChest pain caused by reversible myocardial ischemia •Chronic Stable Angina oCP that occurs intermittently over a long period of time with the same pattern of onset, duration, and intensity of symptoms
44
Diagnostic Tests for Chronic Stable Angina
* H&P * CXR * ECG * Cardiac markers * Lipid Panel * Cardiac catheterization-Most Specific * Stress Test * Echocardiogram
45
Chronic Angina Drug Therapy
•Drug therapy: Nitrates (short and long acting) §preload and afterload §myocardial O2 demand •Administration: oSublingual or spray: Quick, short acting oNitroglycerin ointment oTransdermal controlled-release nitroglycerin •Side effects oOrthostatic hypotension, dizziness, HA
46
Teaching for Chronic Stable Angina
``` •Medications •Identify factors the precipitate angina oWeather, large meals •Low NA, low fat, low cholesterol diet •Ideal body weight •Physical activity o30 min a day (most days) •NTG use •Smoking cessation ``` •A Antiplatelet/anticoagulant/antianginal •B B blocker/blood pressure control •C Cigarette smoking cessation, cholesterol management, calcium channel blockers, cardiac rehab •D Diet, diabetes management, depression •E Education, exercise F Flu vaccine
47
What is PQRST used for and what does it stand for?
``` It is used to asses chest pain P - Precipitating Events Q - Quality of the pain R - Radiation of pain S - Severity of Pain T - Timing ```
48
What do ABCDEF stand for in Chronic Stable Angina teaching?
A - Antiplatelet/anticoagulant/antianginal B - B blocker/ blood pressure control C - Cigarette smoking cessation, cholesterol management, calcium channel blockers, cardiac rehab D - Diet, diabetes management, depression E - Education, exercise F- Flu vaccine
49
What is Acoronary Syndrome (ACS)
Ischemic discomfort resulting from plaque accumulation and/or rupture leading to thrombus formation
50
What kind of chest pain occurs in an unstable angina?
New, occurs at rest, or has worsening pattern. It's unpredictable and emergent
51
What are early warning signs of a heart attack?
Pressure in center of chest Pain in shoulders, neck or arms Chest discomfort with fainting, sweating or nausea
52
What are clinical manifestations of a MI?
Left chest pain, pressure, burning with or without radiation to left arm or jaw ( NOT releived by positioning, rest, or nitrates) Diaphoresis, ashen, clammy, cool to touch BP and HR elevated initially BP and HR drops as CO is decreased N/V Fever- may increase in 1t 24 hrs Crackles, JVD, hepatic engorgement, edema-may occur hours to days later
53
What are some atypical signs and symptoms of an MI in Women, Elderly, diabetics?
Women - fatigue, SOB, weakness, sleep disturbances, nausea, anxiety, dizziness, cold sweats Elderly - Fatigue, weakness, abdominal pain, diaphoresis, n/v, dizziness, AMS Diabetics - SOB, fatigue, weakness, abdominal pain, n/v, diaphoresis
54
Diagnostic tests for MI
•H&P •Characteristics of CP •Serum cardiac markers oReleased into the blood from necrotic heart muscle •ECG •Stress test (ONLY if cardiac markers are negative) •Cardiac Catheterization
55
Initial Treatment for an MI includes
``` •Assess ABC’s •Position upright, administer O2 •Obtain vs and pox •Listen to heart and lungs •Obtain 12 lead ECG-continuous monitoring •Establish IV (2) •Assess pain •Medicate for pain (nitro, morphine) oSublingual NTG q 5min X 3 (hold SBP <90) •Baseline blood work •Chest Xray •Assess for contraindications for antiplatelet, anticoagulation, or thrombolytic therapy-PCI •Administer ASA Administer antidysrhythmics ```
56
Ongoing treatment for an MI includes:
``` Angina with – Cardiac Markers •Antiplatelet/anticoag oASA and/or Heparin •Coronary angiography •PCI (percutaneous Intervention)-angioplasty/stenting STEMI or NSTEMI with + Cardiac Markers •Thrombolytic therapy •PCI •Surgical revascularization oCABG ```
57
When is a patient a candidate for Coronary Surgical Revascularization?
oFail medical management oPresence of left main coronary artery or three-vessel disease oNot a candidate for PCI (e.g., lesions are long or difficult to access) oFailed PCI with ongoing chest pain oDiabetes
58
What are some surgical intervention complications for Coronary Revascularization?
``` oCardiac arrhythmias-atrial fibrillation oStroke oBleeding and anemia (incision site/chest tube) oHypothermia oF/E imbalances oRespiratory changes oIncision site infections oConstipation oCognitive dysfunction oSelf-concept changes ```
59
What are some ACS Medications?
``` oNitroglycerin oMorphine Sulfate oAspirin oβ-Adrenergic Blockers oAce Inhibitor oAntidysrhythmic drugs oCholesterol lowering drugs oStool softeners ```
60
ACs Teaching
•Same as chronic stable angina •S/S of MI, when to call for help •Resumption of work, physical activity, sexual activity •Measures to promote health and recovery oS/S of infection/complication of MI/surgery
61
ACS complications
oDysrhythmias(80% of patients) oHeart failure (HF) oCardiogenic shock §Occurs when there is decreased CO §S/S similar to HF »Tachycardic, hypotensive, tachypneic, crackles §Signs and symptoms of hypo-perfusion »Cyanosis, pallor, diaphoresis, weak peripheral pulses, cool, clammy skin, delayed CRT »Decreased renal blood flow-decreased urine output
62
What is Ineffective Endocarditis
Infection of the inner layer of the heart that usually affects the cardiac valves •Was almost always a fatal condition until development of penicillin •Occurs when blood turbulence within heart allows causative agent to infect previously damaged valves or other endothelial surfaces •Most commonly ostaphylococcus aureus and streptococcus viridans •Vegetation's cause embolizations oFibrin, platelets adhere to valve surface •Rheumatic Heart disease
63
Principle Risk Factors For Ineffective Endocarditis
``` oCardiac conditions Prior endocarditis Prosthetic valves Valve disease Cardiac lesions Congenital heart disease Pacemakers Marfan’s syndrome Cardiomyopathy ``` ``` •Noncardiac -Hospital acquired bacteremia -IV drug abuse •Procedure-Associated risks -Intravascular devices -Dental procedures -Respiratory procedures -GI and GU procedures ```
64
Clinical Manifestations of Ineffective Endocarditis
``` oLow grade fever (90%), Chills oWeakness, malaise, fatigue oAnorexia, weight loss oArthralgias, myalgias, back pain oVascular Manifestations oembolism-organ infarction ```
65
Vascular Manifestations of Ineffective Endocarditis
a) Splinter hemorrhages in nail beds b) Petechiae c) Osler’s nodes on fingers or toes d) Janeway’s lesions on palms or soles e) Roth’s spots
66
Tests Performed to Diagnose Ineffective Endocarditis
•Definitive diagnosis if 2 major criteria: oPositive blood cultures (2 drawn 30 min apart) oNew or changed murmur oEchocardiogram shows intracardiac mass or vegetation •Chest X-ray and ECG can provide more information on extent of disease •WBS •ESR
67
Medications for Ineffective Endocarditis
``` •IV Antibiotic administration (4-6 wks) oMonitor antibiotic serum levels (e.g., peak and trough) oSubsequent blood cultures oMonitor renal function •Fungal and prosthetic valve endocarditis oRespond poorly to antibiotics oMay need valve replacement •Acetaminophen or Ibuprofen ``` •Teach Prophylactic Treatment oAntibiotics before dental or invasive procedures
68
Nursing Interventions for Ineffective Endocarditis
``` •Increase activity slowly •TEDS •C&DB •Observe for complications or worsening disease •Teach oRisk reduction §Avoid sick people §Good nutrition oGood oral hygiene §Antibiotics oNotify HCP prior to invasive procedures for antibiotics ```
69
Complications of Ineffective Endocarditis
•Dysrhythmias •Valve dysfunction •Heart failure Sepsis
70
Manifestations of Stenosis in the Mitral Valve
``` oExertional Dyspnea-reduced lung compliance oFatigue and palpations-A-fib oMurmur •Less common oHoarseness-atrial enlargement on laryngeal nerve oHemoptysis-Pulmonary HTN oCP-decreased co oSeizure-embolism oStroke-embolism ```
71
Causes of Regurgitation
MI, Rheumatic heart disease, Mitral valve prolapse
72
Manifestations of Regurgitation
``` oAcute §New systolic murmur §Pulmonary edema oChronic §Asymptomatic for years §Weak, fatigued §Dyspnea §palpitations §Audible S3 §murmur ```
73
Mitral Valve Prolapse complications
oMitral valve regurgitation oInfective endocarditis oSudden death oCerebral ischemia
74
Mitral Valve Prolapse Clinical Manifestations
``` oDyspnea oFatigue oPalpitations oDizziness and syncope oTachycardia oAtypical chest pain oMurmur §Systolic §Clicks ```
75
Manifestations of Aortic Valve Stenosis
``` oAngina oSyncope, exertional dyspnea oNormal to soft S1, Diminished or absent S2 oMurmur oLoud S4 oPoor Prognosis ```
76
Aortic Valve Regurgitation Manifestations
``` •Acute Manifestations oCP, HF •Chronic Manifestations oRemains asymptomatic for years oExertional dyspnea oOrthopnea oParoxysmal nocturnal dyspnea oMurmur-diastolic ```
77
Diagnostic Tests to Determine Valvular Heart Disease
* H&P * Echocardiogram-valve structure, function and chamber size * ECG-rhythm and ischemia * Chest Xray-size of heart * Cardiac Cath-measure the pressures in the valve and the size of the valve opening * CBC Labs (infection)
78
Valvular Heart Disease Findings
``` •Cardiovascular oAbnormal heart sounds oTachycardia, Dysrhythmias oHypotension •Respiratory: oCrackles, wheezes, hoarseness •Gastrointestinal oAscites oHepatomegaly •Integumentary: oDiaphoresis oPeripheral edema oTemperature oClubbing ```
79
Treatment of Valvular Heart Disease
``` •Focus on preventing oExacerbations of heart failure oAcute pulmonary edema oThromboembolism oRecurrent endocarditis •Drug therapy oDigitalis oDiuretics oAntiarrhythmics oβ-Blockers oAnticoagulants oAntibiotics ```
80
Patient Teaching for Valvular Heart Disease
* Anticoagulant * Prophylactic antibiotic * Low-sodium diet * Activity modifications * Oxygen therapy * Avoid infectious people * Avoid stress and fatigue * Rest * Hygiene * Signs and symptoms of infection * Stress follow-up care * Same as previous cardiac teaching
81
What is the mechanical valve goal for INR?
2.5- 3.5
82
Nursing Diagnoses for Valve Disease
oExcess fluid volume oDecreased cardiac output oActivity intolerance oKnowledge Deficit
83
What happens in Dilated Cardiomyopathy? Who does it effect most often?
The heart enlarges and becomes weaker. It's most common in middle-aged African American and men
84
What is Hypertrophic Cardiomyopathy?
Massive ventricular hypertrophy, rapid, forceful contraction of the L ventricle, impaired relaxation, obstruction of aortic outflow
85
Causes of Dilated Cardiomyopathy
Cardio-toxic agents (alcohol, cocaine), CAD, Genetic, HTN
86
Causes of Hypertrophic Cardiomyopathy
Aortic Stenosis, Genetic, HTN
87
What are the manifestations of Dilated and Hypertrophic CardMeg?
D - fatigue, weakness, palpitations, dyspnes, HF symptoms H - Exertional dyspnea, fatigue, angina, syncope, palpitations
88
What are the diagnostic test of Dilated and Hypertrophic CardMeg?
D - Echo, Chest XRay, ECG, BNP, Cardiac Cath H - Echo, ECG, Cardiac Cath, Stress Test
89
What medications do you give to treat Cardiomyopathy?
``` oNitrates (except in hypertrophic causes worsening chest pain) oB-adrenergic blockers oAntidysrhythmics oACE inhibitors oDiuretics oDigoxin (except in hypertrophic) oAnticoagulants (if indicated) ```
90
What invasive treatments are possible with Cardiomyopathy? D and H
``` •Dilated oVentricular Assist device oCardiac Transplant oCardiac resynchronization oImplantable cardioverter-defibrillator oTransplant •Hypertrophic oCardiac resynchronization oImplantable cardioverter-defibrillator oSurgical correction (removing a portion of the ventricular muscle) ```
91
What is important patient teaching in Cardiomyopathy? D and H
•All previous cardiac education •Medication teaching •Low Fat, Chol, and Na diet •6-8 glasses of H2O (unless contraindicated) •Maintain reasonable weight, avoid large meals •Avoid alcohol, caffeine, OTC meds •Reduce stress •S/S of HF oMay focus on end of life care oSuggest caregiver learn CPR •Avoid strenuous activity •Any activity that causes in increase in systemic vascular resistance is dangerous and should be avoided •Rest and elevation of the feet to improve venous return
92
What can cause sinus bradycardia? What is it? What are some sings and symptoms? How can you treat it?
slower than normal hr cauased by a disruption of the electrical impulses. This can occur during sleep, in athletes, with a carotid massage, a valsalva maneuver, administration of beta blockers or ace S/S pale, cool skin, hypotension, weakness, angina, dizziness, syncope, confusion, SOB Treatment Atropine, pacemaker, adjust or hold medications
93
What is sinus tachycardia? When does it occur? What are some sings and symptoms? How can you treat it?
Faster than normal d/t abnormal electrical impulses. This can occur with exercise, fever, pain, anxiety, increased caffeine, hypovolemia, anemia, hypoxia, MI, HF, administration of meds (atropine, epinephrine, Sudafed, theophyline) S/S decreased cardiac output, dizziness, dyspnes, and hypotension can present as CP or cause an MI Treatment -treat cause, vagal maneuvers, beta blockers
94
What are the signs of an atrial flutter?
saw toothed flutter waves, atrial rate of 200-350 bpm, and ventricular rates that vary with conduction ratio, decreased cardiac output.
95
When can an atrial flutter occur?
oCAD, HTN, mitral valve disorders, COPD
96
What are complications of an atrial flutter?
oHF, Thrombi formation (CVA, PE)
97
What kinds of treatment options are available for atrial flutters?
goal to decrease ventricular rate oB Blockers, antidysrhythmics, CC Blockers oCatheter ablation (treatment of choice), Cardioversion if hemodynamically unstable oLong term use of coumadin if Aflutter continues
98
What is an atrial fib? When can it occur?
``` •Atrial rate 350-600 bpm •Controlled ventricular rate 60-100 •Uncontrolled ventricular rate > 100 •Most common dysrhythmia •Prevalence increases with age •Can occur with: oCAD, HTN, HF, valvular heart disease, alcohol intoxication, electrolyte disturbances, pericarditis ```
99
What are s/s of atrial fib? What are complications?
•S/S oDecreased cardiac output •Complications: oThrombi formation (CVA, PE)
100
What are treatment options for Atrial fibrillation?
oCC blockers, B-Blockers, Cardioversion (1st choice) Catheter ablation or Maze procedure(2nd choice) §Long term use of coumadin if Afib continues
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What are premature Ventricular Contractions?
* Wide distorted QRS – rate is irregular * Ventricular bigeminy * Ventricular trigeminy * Couplet
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When do ventricular contractions occur?
oStimulants (caffeine, alcohol, nicotine) digoxin, aminophylline, fever, hypoxia, exercise, emotional stress, MI, HF, CAD, electrolyte imbalance (K, Mg)
103
What are signs and symptoms, complications, and treatments of ventricular contractions?
``` S/S Can be benign oReduced cardiac output, CP, HF, pulse deficit •Complication oVentricular Tachycardia – 3 or more PVCs together •Treatment oTreat cause oB Blockers ```
104
What is ventricular Tachycardia? When Does it Occur?
Ventricular rate 150-250 bpm- regular or irregular •Sustained VT - >30 seconds •Nonsustained VT - <30 seconds •Can be lethal •Can occur with oMI, CAD, significant electrolyte imbalance (K, Mg) oPossible in patients without evidence of heart disease
105
What are signs and symptoms of Ventricular Tachycardia?
oSevere decreased cardiac output | §Hypotension, pulmonary edema, decreased cerebral blood flow, cardio-pulmonary arrest
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What are complications of Vent Tachy?
•Complications | oVentricular fibrillation/ Death
107
What are treatment options for Vent Tachy?
B Blockers, antidysrhythmics, cardioversion/defib
108
What is Ventricular Fibrilation? S/s? Complications? Treatment?
``` •The ventricle is quivering, no contraction, no cardiac output •Heart rate is not measureable-no pulse •Can occur with oMI, HF, sustained Vtach, hyperkalemia •S/S oUnresponsive, pulseless, apneic •Complications oDeath •Treatment Immediate CPR and ACLS, defibrillation ```
109
What is Asystole? S/S? Complications? Treatment?
Asystole •Represents total absence of ventricular electrical activity •No ventricular contraction occurs because depolarization does not occur. •Can occur with oAdvanced cardiac disease such as end stage HF •S/S oUnresponsive, pulseless, and apneic state •Complication oDeath •Treatment CPR and ACLS
110
What causes most sudden cardiac deaths?
Ventricular dysrhythmias (tachycardia and Fib, though fib is most common)
111
Risk factors for Heart Failure
``` oCoronary artery disease (CAD) oHypertension oMyocardial infarction oAdvancing age oDiabetes oCigarette smoking oObesity oHigh serum cholesterol ```
112
What is a normal ejections fracture?
55-60%
113
When would you see a mixed systolic and diastolic heart failure?
Dialated cardiomyopathy, high pulmonary pressures, biventricular failure
114
What happens with right side heart failure?
``` oHepatomegaly oSplenomegaly oCongestion of the GI tract oJugular vein distention (JVD) oPeripheral edema ```
115
Manifestations of Chronic Heart Failure
* Fatigue * Dyspnea * Paroyxsmal nocturnal dyspnea * Tachycardia * Edema * Nocturia * Skin changes * Behavioral changes * Chest pain * Weight changes
116
What are some diagnostic studies used to determine Chronic Heart Failure?
``` •History, physical examination •Chest x-ray •Electrocardiogram (ECG) •Stress testing •Laboratory data oCardiac enzymes, b-type natriuretic peptide [BNP], basic metabolic panel, liver function studies, complete blood count •Echocardiogram •Cardiac catheterization •Endomyocardial biopsy (new unexplained HF) •B type Natriuretic Peptide Assay (BNP) oBNP is excreted from cardiac membranes in response to ventricular volume expansion and pressure overload in HF o>100pg/ml – predictor of HF ```
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Chronic Heart Failure Assessment Findings
``` Expected assessment findings •Resp oCrackle lung sounds, cough, pulse ox •CV oIrregular heart rhythm, rate, and sounds, murmur, edema, decreased perfusion •GI oEdema, enlarged liver and spleen, appetite •GU oDecreased urine output ``` ``` •Skin oEdema, temp, color •MS oDecreased activity tolerance, adl’s •Mental Status oOrientation oLOC oBehavioral change •Psych/soc oCoping, depression ```
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Nursing Interventions for Chronic Heart Failure
``` •High fowlers position •Oxygen therapy •Vital signs and ECG monitoring oMonitor laboratory values (H/H, BNP, MG, K, BUN, Cr) •Intake/output •Daily weights •Administer medications •Patient teaching •Cardiac resynchronization therapy (if uncontrolled Afib occurs) ```
119
Drug Therapy for Chronic Heart Failure
•Diuretics-mobilize fluid, reduce pulmonary venous pressure, reduce preload-risk for electrolyte imbalance. •Angiotensin-converting enzyme (ACE) inhibitors are the primary drug of choice in chronic HF patients with systolic dysfunction. •Vasodilator-improving EF through improved ventricular contraction. •Angiotensin II receptor blockers (ARB)- may be used in patients who are ACE inhibitor intolerant. •β-Adrenergic blockers in combination with ACE inhibitors and diuretics have improved survival of patients with HF. •Digitalis glycosides-risk for digoxin toxicity. •Morphine-decrease anxiety, preload and afterload •Antidysrhythmics-prevent and treat dysrhythmias •Anticoagulants-prevent thromobembolism oRecommended for all patients with EF<20% and /or Afib
120
Patient Education for CHF
Diet Education and Weight Management •Diet education and weight management are critical to the patient’s control of chronic HF. oDietary restriction of sodium. (2000mg NA) oIn moderate to severe HF fluid is restricted to < 2000ml daily oDaily weight §Contact primary care provider for a weight gain of 3 lb over 2 days, or 3 to 5 lb over a week.
121
CKMB lab
myocardial tissue injury
122
Troponin
released following an MI
123
Myoglobin
Myocardial injury
124
C-reactive protein
Inflammation can predict cardiac disease and events
125
BNP > 100
Diagnostic for HF
126
Cholesterol
Elevated = risk for atherosclerotic HD
127
Triglycerides
Elevated is associated with CV disease and diabetes
128
ECG
Can detect heart rhythms, presence of injury, or MI
129
Echo
can detect congenital defect, wall motion, and EJF
130
Cardiac Cath
Measures pressures within heart chambers and EJF.
131
Stress Test
Assess extent of cardiovascular disease

MED SURG TEST 2 (1 decks)

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