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Med Surg 1 > Exam #3 Chapters 32,33,35,37,38 > Flashcards

Exam #3 Chapters 32,33,35,37,38 Flashcards

1
Q

Three Layers of the heart

A

Endocardium, Myocardium, Epicardium

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2
Q

Thin inner lining of the heart

A

Endocardium

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3
Q

Layer of muscle in the heart

A

Myocardium

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4
Q

Outer layer of the heart

A

Epicardium

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5
Q

Pericardium

A

Fibrous sac covering the heart

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6
Q

Purpose of the pericardial fluid (how much)

A

10-15 mL; Lubricated the space between the pericardial layers and prevents friction between the surfaces as the heart contracts

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7
Q

Is the interatrial or interventricular wall thicker?

A

Interventricular (2-3 times thicker)

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8
Q

Blood flow of the heart

A

Superior and Inferioir Vena cava-(tricupid vavle)-> R atrium-(pulmonary valve)-> R ventricle –> Pulmonary artery–> Lungs–> L atrium –> L ventricle –> aorta–> Rest of body

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9
Q

What is the only artery not carrying oxygenated blood

A

Pulmonary artery

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10
Q

Blood flow into the two major coronary arteries occurs primarily during…

A

Diastole

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11
Q

R coronary artery supplies blood to what in 90% of people? What can this cause?

A

AV node and bundle of His; for this reason, obstruction of this artery often causes serious defects in cardiac conduction

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12
Q

Systole

A

Contraction of myocardium, ejection of blood from the ventricles

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13
Q

Diastole

A

Relaxation of myocardium, filling of the ventricles

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14
Q

S1

A

Start of systole, “lub”, closure of tricuspid and mitral valves, radial or apical pulse

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15
Q

S2

A

Start of diastole, “dub”, closure of aortic and pulmonic valves

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16
Q

Cardiac Output

A

Amount of blood pumped by each ventricle in 1 min (norm. 4-8L/min)

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17
Q

Cardiac Index:

A

CO divided by body surface area, is adjusted for BSA and is a more precise measure of efficiency of the pumping action of the heart (Norm. 2.8-4.2 L/min/m^2)

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18
Q

When is CO increased

A

With high circulating volume

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19
Q

When is CO decreased

A

With low circulating vol. or decrease in strength of ventricular contraction

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20
Q

Stroke Volume

A

Volume of blood (in mL) ejected with each heartbeat (Norm. 50-100); determined by preload, afterload, and contractility

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21
Q

When is stroke vol decreased

A

Impaired cardiac contractility, valve dysfunction, CHF, beta blockers, MI

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22
Q

When is stroke vol increased

A

Volume overload, inotropy, hyperthermia, meds (ie. Digitalis, dopamine, dobutamine)

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23
Q

Preload

A

Stretch or filling pressure, determines the amount of stretch placed on myocardial fibers, vol of blood in the ventricles after diastole

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24
Q

Causes for increased preload

A

MI, aortic stenosis, and hypervolemia

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25
Q

Sign of left ventricular preload

A

PAWP= Pulmonary Artery Wedge Pressure

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26
Q

Signs of right ventricular preload

A

CVP= Central Venous Pressure

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27
Q

Afterload

A

Squeeze; pressure that fluid has to overcome to allow a forward flow, how hard the heart has to push; the more afterload, the less cardiac output

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28
Q

What affects afterload

A

Vasoconstriction, BP, heart valve resistance, and blood viscosity

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29
Q

Systemic Vascular Resistance (SVR)

A

Opposition encountered by left ventricle; force opposing movement of blood; created primarily in small arteries and arterioles

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30
Q

What increases SVR

A

Vasoconstrictors, low volume

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31
Q

What decreases SVR

A

Vasodilators, morphine, nitrates, high CO2

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32
Q

What does cardiac output r/t increased afterload eventually lead to

A

Ventricular hypertrophy- an enlargement of cardiac muscle tissue without an increase in CO or the size of the chambers

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33
Q

Pulmonary Vascular Resistance (PVR)

A

Opposition encountered bt R ventricle

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34
Q

When is PVR increased

A

Pulmonary hypertension and hypoxia

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35
Q

When is PVR decreased

A

Meds (ie calcim channel blockers, aminophylline, isoproterenol, O2)

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36
Q

What increases afterload

A

HTN, hardened arteries, CAD, pulmonary HTN (rt HF), hypoxia, catecholemines

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37
Q

What decreases afterload

A

Vasodilators, acidosis, O2

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38
Q

Contractility

A

Strength of contraction; illustrate with old, flakey rubber band or balloon vs. new, stretchy rubber band or balloon

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39
Q

What increases Contractility

A

Meds (epinephrine, norepinephrine, isoproteneronol, dopamine, dobutamine, digitalis)

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40
Q

What decreases contractility

A

HF, alcohol, calcium channel blockers, acidosis

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41
Q

Positive inotropes

A

Meds that increase contractility

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42
Q

Negative Inotropes

A

Meds that decrease contractility

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43
Q

S/S that indicate Preload problems

A

JVD, lung sounds, and PWCP

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44
Q

S/S that indicate afterload problems

A

BP, skin temp, pulse pressure

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45
Q

S/S that indicate contractility problems

A

ejection fraction

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46
Q

A patient is receiving a drug that decreases afterload. To evaluate the patient’s response to this drug, what is most important for the nurse to assess?

A

Blood Pressure; afterload is affected by the size of the ventricle, wall tension and areterial blood pressure

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47
Q

Autonomic Nervous system- how does it affect the HR

A

Can increase the HR up to 180 bpm for short time without untoward effects

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48
Q

How does the SNS Affect the HR

A

release of epinephrine/norepinephrine and speeds everything up (ie HR, AV node, force of contractions), also causes vasoconstriction

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49
Q

How does the PSNS affect the HR

A

Slows everything down (ie HR, SA node rate) causes vasodilation; vagus nerve

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50
Q

How do Baroreceptors affect the HR

A

If pressure or stretch is increased in the arterial system (ie. volume overload) the baroreceptors will inhibit the SNS and enhance the PSNS, causing decreased HR and peripheral vasodilation (decreased arterial pressure causes opposite)

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51
Q

How do Chemoreceptors affect the HR

A

Sense changes in CO2 and O2 and can cause increased HR and BP

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52
Q

Factors affecting HR

A

ANS, SNS, PSNS, Baroreceptors, and chemoreceptors

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53
Q

What does mean arterial pressure tell us

A

If organs are being perfused

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54
Q

Arterial BP

A

A measure of the pressure exerted by blood against the walls of the arterial system

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55
Q

Systolic BP

A

Peak pressure exerted against the arteries when the heart contracts

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56
Q

Diastolic BP

A

Residual pressure in the arterial system during ventricular relaxation (or filling)

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57
Q

What are the two main factors influencing BP

A

CO and SVR

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58
Q

Pulse pressure

A

Difference between systolic and diastolic; normally 1/3 of the systolic

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59
Q

When might there be an increased pule pressure

A

During exercise or in individuals with atherosclerosis of the larger arteries as the result of increased systolic

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60
Q

When might there be a decreased pulse pressure

A

HF or hypovolemia

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61
Q

Mean Arterial Pressure (MAP)

A

The average pressure within the arterial system that is felt by organs int he body; not the average of the diastolic and systolic because the length of diastole exceeds that of systole at normal HR

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62
Q

What MAP is needed to adequately perfuse and sustain vital organs of an average person

A

60 mm HG

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63
Q

What happens when the MAP falls below 60 mm HG

A

Vital organs are under-perfused and will become ischemic

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64
Q

What is one of the greatest risk factors for cardiovascular disease

A

Age; leading cause of death in >85 uears of age

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65
Q

What is the most common CV problem (geri)

A

Coronary artery disease secondary to atheroscleorsis

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66
Q

CV changes result from…

A

Aging, disease, environmental factors, and lifetime behaviors

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67
Q

HR changes in GERI

A

No change in resting supine; decreased HR, CO, SV in response to stress or exercise due to lack of elastin in the heard and decreased contractility

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68
Q

What is hard to distinguish in GERI regarding arteries

A

Normal aging vs. atherosclerosis

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69
Q

BP changes in GERI

A

HTN is NOT expected, increased systolic (decrease or no change in diastolic;arteries less elastic but more sensitive to vasopressin (ADH) leading to inc. sys.); Increased pulse pressure, orthostatic hypotension, postprandial hypotension

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70
Q

Postprandial hypotension

A

Decrease in BP of at least 20 mm Hg that occurs withing 75 minutes after eating

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71
Q

Heart sound changes in GERI

A

Murmur from regurgitation/narrowing of mitral and aortic valves

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72
Q

ECG changes in GERI

A

Sinus (dec. pacemaker cells) & atrial (dec. conductions cells) dysrhythmias; heart block (bradycardia caused by electrical conduction probs.); abnormal resting ECG in 50% (increasing all intervals)

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73
Q

Medication response changes in GERI

A

Less sensitive to beta blockers, increased sensitivity to vasopressin (ADH)

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74
Q

Physical changes in GERI

A

Dependent edema due to incompetent venous valves

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75
Q

Subjective data needed for cardiac assessment

A

History of present illness, past health history, past and current medications, surgery or other treatments (note whether an ECG or chest x-ray has been done for baseline data)

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76
Q

Health hx needed for cardiac assessment

A

Chest pain, SOB, fatigue, alcohol/tobacco use, anemia, rheumatic fever, strep. throat infection, CHD, stroke, palpitation, dizziness with position changes, syncope, HTN, thrombophlebitis, intermittent claudication, varicosities, and edema

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77
Q

Risk factors for CV problems

A

Increased serum lipids, HTN, smoking, sedentary lifestyle, obesity, stress, DM

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78
Q

Familial disorders to be concerned about

A

Heart disease before age 55, intermittent claudication, varicose veins; other disorders that affect CV- asthma, renal disease, liver disease, obesity

79
Q

Exercise intolerance concerns

A

Chest pain, SOB, claudication (cramping in the lower legs when walking or exercising)

80
Q

Sleep concerns (subjective data)

A

Paroxysmal nocturnal dyspnea, orthopnea, sleep apnea- need to sleep upright or with pillows, sleep spnea increases risk of dysrhythmias

81
Q

Highlighted sub. data

A

Allergies to iodine, familial disorders, constipation, exercise intolerance, PND, orthopnea, sleep apnea, sexual problems

82
Q

Sexual problems with CV

A

Fear of sudden death during intercourse, ED, HRT, or BCPs can increase risk for blood clots (asp. if they are a smoker)

83
Q

VS for CV ob. assessment

A

Measure BP bilaterally, orthostatic BP (lying, sitting, standing); Sys. should not increase more than 20 mm Hg from supine to standing; HR should not increase more that 20 bpm from supine to standing

84
Q

Inspect extremities for…

A

Edema, dependent rubor, clubbing, variscosities, and lesions (such as stasis ulcers)

85
Q

What can be an indicator for R-sided HF

A

Jugular vein distension

86
Q

What would be felt if pt. has suspected valvular disorder

A

Abnormal pulsations or thrills on chest wall at 5 spots

87
Q

What is expected when the PMI is below the 5th ICS and left of the mid-clavicular line

A

Heart may be enlarged

88
Q

Asses what with pulse deficit

A

Auscultate apical pulse while palpating radial pulse, if different have one person count each one for a full minute, r/t dysrhythmias

89
Q

S3

A

Ventricular; heard closely after S2, ventricular gallop, “Kentucky”; can be normal in young adults nut usu. a sign of left ventricular failure or mitral valve regurgitation (decreased compliance of ventricles during filling)

90
Q

S4

A

Heard before S1, atrial gallop, “Mississippi”; can be normal in older adults if no heart disease, but usu. a sign of CAD, cardiomyopathy, left ventricular hypertrophy, aortic stenosis

91
Q

Pericardial friction rubs

A

High-pitches, scratchy sounds, usu. heard best at apex when sitting or leaning forward; r/t pericarditis

92
Q

Risk predictors: C-Reactive protein

A

Marker for inflammation, Risk factor for coronary artery disease; CRP is a protein produced by the liver during periods of acute inflammation; the level may also predict the risk for future cardiac events in patients with unstable angina and MI

93
Q

Risk predictors: Homocysteine

A

Elevated levels increased risk for CAD, peripheral vascular disease (PVD), and stroke; Hcy is an amino acid that is produced during protien catabolism

94
Q

Diagnostic studies of CV system

A

Triglycerides (60 is low risk, LDL=

95
Q

A patient arrives at an urgent care center after experiencing unrelenting substernal and epigastric pain and pressure for about 12 hours. The nurse reviews laboratory results with the understanding that at this point in time, a myocardial infarction would by indicated by peak levels of

A

Troponin; this is the biomarker of choice in the diagnosis of MI; myocardial muscle protein released into the circulation after injury; levels peak at 10-24 hours

96
Q

Electrocardiogram

A

Resting ECG (12 lead); Ambulatory ECG monitoring (telemetry); Event monitor or loop recorder; Exercise or stress testing

97
Q

What is an event monitor used for

A

To document less frequent ECG events; portable unit that uses electrodes to store ECG data once triggered by pt.; disadvantage is if symptoms occur for short period of time, they may be over before put on pt

98
Q

Echocardiogram

A

Ultrasound of heart; provides information regarding structures and motion of heart; measures ejection fraction (50% is normal)

99
Q

Echocardiogram provides information about what abnormalities

A

Valvular structures and motion, cardiac chamber size and contents, ventricular and septal motion and thickness, pericardial sac, and ascending aorta

100
Q

Stress Echocardiography

A

Combo of treadmill test and US images, evaluate wall montion abnormalities; for indiv. unable to exercise, IV drug is used to produce stress on heart while pt. is at rest

101
Q

Nuclear Cardiology (MUGA)

A

IV injection of radioactive isotope, lay still for 20 min with arms up, may have repeat scans (within few minutes to hours after injection);Very common; provides structural info and EF, can also do perfusion imaging to dx CAD

102
Q

MRI

A

CAn find even a small MI, assist with assessment of EF, can’t dx CAD, help predict recovery after MI; noninvasive (but must lie still); can’t do if they have pacemaker or ICD

103
Q

CT

A

Visualizes heart anatomy , circulation, and big vessels; may or may not use IV contrast; coronary CTA can be done faster and with less risk than a cardiac cath but can’t place stents or do angioplasty if needed; calcium can be seen in therosclerotic plaques; no IV, no sedation, no NPO, rapid, low risk

104
Q

Cardiac Catheterization

A

Invasive; angiography involves injection of dye (shows coronary lesions); intracoronary ultrasound done with angio (shows vessel walls/plaques); Fractional flow reserve measures pressure/flow (determines need for angioplasty)

105
Q

Cardiac Cath for right

A

Use basillic or cephalic vein or femoral vein, to vena cava, to R atrium, to R ventricle, then pulmonary artery (to assess fxn of left side of heart too)

106
Q

Cardiac Cath for Left

A

Use femoral or brachial artery, to aorta, across aortic valve, into L ventricle

107
Q

Angiography

A

Done with a L sided heart cath, inject dye into coronary arteries (makes pt. feel flushed) to look for lesions

108
Q

Cardiac Cath procedure

A

NPO for 6 hrs before; requires sedation; check iodine sensitivity; may be asked to cough or take a deep breath during dye injection; may have to stop antidysrhythmic meds if having EPS

109
Q

Post Cardiac cath care

A

Neuro checks q 15 min x 1 hr; compression device over injection site; close monitoring of VS and ECG

110
Q

Complications of Cardiac cath

A

Bleeding/hematoma, allergic reaction, infection, clot, aortic dissection, dysrhythmias, MI, stroke, puncture ventricles of lung

111
Q

Regulation of BP (SNS)

A

Increases HR and contractility; vasoconstriction; release of renin from the kidneys

112
Q

Regulation of BP (Baroreceptors)

A

Send inhibitory impulses to the sympathetic vasomotor center in the brainstem

113
Q

Regulation of BP (Renal System)

A

Controls sodium excretion and ECF volume increasing venous return and SV, inc. CO & BP; Renin-angiotensin-aldosterone system (RAAS)

114
Q

Regulation of BP (Endocrine System)

A

Epinephrine increases HR and contractility; Increases blood sodium osmolarity stimulating release of ADH (increases ECF volume)

115
Q

Regulation of BP (Renin-angiotensin-aldosterone system- RAAS)`

A

Vasoconstriction; increases SVR; causes sodium and water retention by the kidneys increasing blood volume and CO

116
Q

Definition: HTN

A

Persistent systolic >140, diastolic >90

117
Q

Definition: PreHTN

A

Systolic 120-139 or diastolic 80-89

118
Q

Isolated systolic HTN (ISH)

A

Sys >140 with dias.

119
Q

Pseudohypertension

A

False HTN ,that occurs when a person has severe atherosclerosis; hardened arteries don’t collapse with cuff inflated (BP falsely elevated); only way to know that arteries feel rigid and no other organ changes; arterial line only way to get proper reading

120
Q

Causes of primary HTN

A

95% of those with HTN; no identified cause

121
Q

Causes of secondary HTN

A

5% of those with HTN; caused by something specific that can be identified and treated, suspect if >age 50 and suddenly develops high BP; include endocrine and kidney problems, diabetic retinopathy, sleep apnea, preg., meds

122
Q

Risk factors for HTN

A

Age (>50); alcohol (>1oz/day); Smoking, DM, High serum lipids, high dietary Na+; Gender (men 55); family history, obesity (central abdominal), ethnicity (African Americans), sedentary lifestyle, socioeconomic stats, stress

123
Q

S/S of HTN

A

“Silent Killer”; no s/s until organ disease occurs, fatigue, activity intolerance, dizziness, palpitations, angina, dyspnea

124
Q

Complications of HTN: hypertensive heart diasease

A

CAD, L ventricular hypertrophy, HF

125
Q

Complications of HTN: cerebrovascular disease

A

Atherosclerosis, stroke, HTN encephalopathy

126
Q

Complications of HTN: Peripheral Vascular Disease (PVD)

A

Aortic aneurysm, aortic dissection; intermittent claudication is common symptoms (pain with walking/exercise, subsides with rest- c/b too little blood flow during exercise)

127
Q

Complications of HTN: Nephrosclerosis

A

End-stage renal disease, renal dysfunction; nocturia is common symptom

128
Q

Complications of HTN: Retinal Damage

A

Blurred vision, retinal hemorrhage, blindness; tells us the severity and duration of HTN

129
Q

Diagnostic studies for HTN

A

Not much to be done since most have no cause; UA, BUN, creatinine, electrolytes, blood glucose, lipid profile, uric acid, ECG, Echocardiogram

130
Q

Lifestyle modifications for HTN

A

Weight reduction, exercise 30 min/day, DASH eating plan, Na+ reduction, limit alcohol, regular physical activity, avoid tobacco, stress management

131
Q

DASH eating plan

A

Emphasizes fruits, veggies, fat-free or low-fat milk, whole grains, fish, poultry, beans, seeds, nuts
Decreased red meat, salt, sweets, added sugars, sugared bev.
No rest. on caffeine or protein

132
Q

Sodium restriction diet with HTN

A
133
Q

Treatment goal of HTN

A

BP

134
Q

Treatment HTN

A

Make decisions based on overall CVD risk; lifestyle modifications should be the foundation of tx; most need at least one med

135
Q

Diuretics with HTN

A

Usually given as first line treatment; Fluid overload; decreased preload by decreasing fluid buildup; take in the morning (so they aren’t up all night peeing)

136
Q

Diuretic SE

A

Low potassium (except for spironalactone), low magnesium, dehydration (remember if K+ low, digoxin toxicity is a higher risk)

137
Q

Beta Blockers with HTN

A

“lols”; used fro HTN, angina, dysrhythmias, post-MI (prevents another); not recommended for HF or asthmatics; blocks epinephrine, decreases HR, BP, contractility, CO, and vasodilates

138
Q

Beta Blocker SE

A

Fatigue, impotence, wheezing or SOB (why we don’t use in asthmatics)

139
Q

ACE inhibitors with HTN

A

“prils”; HTN, HF, DM (protect kidneys); can prevent heart attack and stroke; lowers lvl of angiotensin ll, lowers bp,and vasodilates (decreases afterload); don’t take with ASA or NSAIDs; need diuretic

140
Q

ACE SE

A

Dry cough, low BP, high K+, angioedema (swelling of the lips and face - must stop the drug if this occurs)

141
Q

Angiotensin ll Receptor Blockers (ARB) with HTN

A

“sartans”; used in HTN, HF; give if unable to tolerate an ACE; Blocks angiotensin ll from having any effect, lowers BP, vasodilates (decreases afterload); can take awhile to work (so not first line); can be used to help with those on ACE bothered by dry cough

142
Q

Angiotensin ll Receptor Blockers (ARB) SE

A

High K+, decreased kidney function

143
Q

Calcium Channel Blockers with HTN

A

“dip”, “pine”, also Diltiazem, Verapamil; used for angina, HTN, dysrhythmias; do not use after MI or with HF; not used as first line; do not give grapefruit juice; interrupts the movement of calcium into the cells of the heart, vasodilates (decrease afterload), decrease contractility (pumping strength)

144
Q

Calcium Channel Blockers SE

A

Bradycardia, low BP, headache, dizziness, nausea

145
Q

Alpha adrenergic blockers with HTN

A

Clonidine, Hytrin, Cardura; used for HTN, BPH, vasodilates, lowers BP, lowers CO; don’t take with alcohol or sedatives, may need to take at bed time; often used for prostate issues

146
Q

Alpha adrenergic blockers SE

A

Dry mouth, sedation, fatigue, impotence, low BP

147
Q

Vasodilators with HTN

A

Nitrates; used for angina, HTN (those who can’t take ACE), MI, HF; vasodilates (increases afterload), decreases preload; rarely used as primary tx for HTN, usually angina

148
Q

Nursing Implications with vasodilators

A

Must monitor BP (needs to be above 100 to give), repeat every 5 minutes for 3 times; keep in dark area; must ask if the have taken any ED drugs prior to giving

149
Q

Vasodilators SE

A

Headache, low BP, dizziness

150
Q

HTN drug therapy SE

A

Can be severe enough pts won’t take; orthostatic hypotension (check HR (>50) and BP (>100) before giving); Sexual dysfunction; Potassium (most make it low except ACE and ARB); Dry mouth(too irritating wiyh ACE, d/c with beta); nocturia

151
Q

Nursing Interventions with HTN

A

Health promotion (lifestyle modifications); Home- home BP monitoring, pt compliance, need to be seen monthly until BP is stable and then see q 3-6 mo.

152
Q

Proper BP measurement

A

Arm at level of heart; Initially measure in both arms and use arm with higher reading for future; do not smoke, exercise, or drink caffeine 30 min before; BP higher in morning, lowest at night; feet flat on floor; single value not as important as a series of values

153
Q

GERI considerations r/t HTN

A

Higher ISH and white coat HTN; be aware of auscultatory gap; more sensitive to slight BP changes; resistant to ACE and ARB; orthostatic hypotn common; postprandial hypotn is more common

154
Q

Hypertensive Crisis

A

Can develop over hrs or days; rate of rise, not actual BP, is most important (MAP more important than BP); most common is failure to take routine BP meds; cocaine/crack use can cause

155
Q

Hypertensive Crisis S/S

A

Severe headache, n/v, seizures, confusion, coma, papilledema, tremors, decreased urine output

156
Q

Complications of hypertensive crisis

A

Angina, MI, pulmonary edema (chest pain, dyspnea), aortic dissection (sudden, excruciating chest/back pain, reduced/absent pulses in the extremities), stroke

157
Q

Hypertensive Crisis tx

A

Goal= slowly love BP (decrease MAP by 25% in 1 hour); IV sodium nitropress along with oral BP meds; check BP q 2-3 min; monitor ECG dysrhythmias; hourly urine output; bedrest’ frequent neuro checks; vaso., adren. inh., ACE

158
Q

Definition of HF

A

Abnormal cardiac function involving impaired cardiac pumping and/or filling; associated with HTN, CAD, MI; older adults; high morbidity and mortality

159
Q

Risk factors for HF

A

CAD, age, HTN (primary factors); diabetes, smoking, obesity, high cholesterol; African Americans have higher incidence, develop earlier, higher mortality

160
Q

Patho of sys. HF

A

Problem with pumping; caused by MI, HTN, cardiomyopathy, valve disease

161
Q

S/S of sys. HF

A

left ventricular hypertrophy, decreased EF (b/c L ventricle can’t generate enough pressure to eject blood into the aorta)

162
Q

Patho of dia. HF

A

Problem with filling (ventricles can’t relax; decreased SV and CO); caused by stiff ventricles, L ventricular hypertrophy from HTN, aortic stenosis, hypertrophic cardiomyopathy, majority have no identifiable heart disease

163
Q

S/S of dia. HF

A

Pulmonary congestion, pulm. HTN, ventricular hypertrophy, normal EF

164
Q

Patho mixed HF

A

Very low EF (

165
Q

Compensatory Mechanism w/ HF: SNS activation

A

Release Epi/norepi; first to be activated when CO is low, but is the least effective; works for short term but increases the workload of a falling heart over time

166
Q

Compensatory mechanism w/ HF: Neurohormonal responses

A

RAAS cascade (activated when blood flow to the kidneys decreases), ADH release (when blood flow is decreased to the brain), endothelin release (causes vasoconstriction which leads to hypertrophy), inflammatory response

167
Q

Compensatory Mechanism w/ HF: Ventricular Dilation

A

Way to cope with increased vol.

168
Q

Compensatory Mechanism w/ HF: Ventricular Hypertrophy

A

Increase in muscle mass and wall thickness; requires more O2 to work

169
Q

Counter Regulatory Mechanisms

A

Production of ANP, BNP, and NO; Causes vasodilation and diuresis; blocks the effects of the RAAS; inhibit the development of hypertrophy

170
Q

Atrial Natriuretic Peptide (ANP)

A

Released when the heart senses high blood volume; reduces water and sodium through diuresis, thus reducing BP

171
Q

Brain or B-type Natriuretic Peptide (BNP)

A

Released when the heart senses stretching of the ventricles, acts like ANP does

172
Q

Nitric Oxide (NO)

A

Causes vasodilation; decreases afterload

173
Q

Left-sided HF

A

Most common; caused by L ventricular dysfunction and blood backing up into the pulmonary veins leading to pulmonary edema; pulmonary congestion and edema

174
Q

Right-sided HF

A

Causes backup of blood into systemic circulation causing JVD, hepatomegaly, splenomegaly, peripheral edema; caused by L-sided

175
Q

Acute Decompensated HF (ADHF)

A

Pulmonary Edema; Anxious, pale, cyanotic, cold and clammy, severe dyspnea, tachypnea, orthopnea, frothy blood-tinged sputum, inc. HR, crackles/wheezes/ronchi

176
Q

S/S of Chronic HF

A

FACES; Fatigue, Activity limitation, Cough (dry, nonproductive; may be 1st clinical symp.), Edema, Short of breath; Paroxysmal nocturnal dyspnea, tachycardia (may not occur w/ beta blocker), nocturia, weight gain

177
Q

S/S R-sided HF

A

Murmurs, heaves, JVD, edema, weight gain, ascites, hepatomegaly, fatigue, nausea, anorexia/GI bloating

178
Q

S/S L-sided HF

A

S3, S4, heaves, PMI displaced, hypoxia, crackles/ pleural effusion, dyspnea, restlessness, confusion, fatigue, PND, orthopnea, cough, frothy/pink-tinged sputum

179
Q

Complications with HF

A

Pleural effusion (inc. pressure in pleural cap). Dysrhythmias (a fib promoting clot formation in atria and can inc. rx for stroke), L ventricular thrombus (inc. rx stroke), Hepatomegaly (liver congest. with ven. blood & lead to cirrhosis), Renal failure (from dec. perfus. to kidneys)

180
Q

Diagnostic goal

A

Determine cause

181
Q

Diagnostic EF

A

Ejection fraction; distinguishes between sys. and dia. HF; Echo or nuclear imaging (MUGA); normal is 60-75%

182
Q

Diagnostic: BNP

A

Differentiate whether dyspnea is from HF; inc. w/ ventricular dysfunction

183
Q

ADHF treatment

A

High Fowler’s w/ feet horizontal or dangle; O2; ECG, O2 stat monitoring; VS, urine output hourly; Hemodynamic monitoring; Ultrafiltration for vol. overload; Circulatory assist devices (inc. blood flow but dec. heart’s workload); Treat depression

184
Q

ADF treatment- Drugs

A

Morphine (red. pre- and afterload, dec. O2 demand, GIVE FIRST), Diuretics (Lasix), vasodilators (IV nitro; must titrate to prevent hypotension-monitor BP q 5-10 min); Positive inotropes (only if nothing else works, digitalis; improves contractility; short term only)

185
Q

How do we know if the drugs worked with ADHF

A

Decreased SOB

186
Q

Chronic HF treatment

A

O2 (dec. fatigue and dysp.); Physical/Emotional rest (rehab; help dec. need for O2); Biventricular pacing or CRT; may also have implanted cardioverter-defib (ICD; helps improve L ventricular function and CO); circulatory assist devices

187
Q

Chronic HF treatment- Drugs

A

Diuretics (thiazide 1st choice); ACE (prim. of choice; dec. BP and inc. CO and tissue perfusion) or ARBs(if intolerant to ACE); Aldosterone antagonists (spirinolactone; monitor K+); BiDil (only for African Americans)

188
Q

Drugs to use CAUTIOUSLY in chronic HF treatment

A

Beta Blockers (carvedilol; must stat slowly over 2 weeks b/c they cause SOB at first) and Positive Inotropes (Digoxin; used when other treat. fail; “slaps the heart”; watch for dig. tox.)

189
Q

Nutrition with HF

A

Sodium restrict (if 3lbs over 2 days); 3 day diet hx

190
Q

Nursing Interventions: HF Health prmotion

A

Aggresively identify and treat rx factors; flu and pneumonia vaccine, educate about diet/meds/exercise; slowing progression

191
Q

Nursing interventions: Acute HF

A

Conserve energy, decrease anxiety, may need salt and fluid restrictions, need support system

192
Q

Nursing interventions: HF Ambulation/Home care

A

Take meds (even when feeling well), treat anxiety and depression, teach to take pulse (digitalix and beta), energy conservation, know s/s of worsening HF (FACES)

193
Q

FACES

A

Fatigue, Activity limitation, Chest congestion/cought, Edema. Short of breath

194
Q

When to call Dr. with HF

A

Weight gain, difficulty breathing, PND, dry/hacking cough, fatigue, swelling, dizziness, FACES

Med Surg 1 (1 decks)

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