Exam #3 Chapters 32,33,35,37,38 Flashcards
1
Q
Three Layers of the heart
A
Endocardium, Myocardium, Epicardium
2
Q
Thin inner lining of the heart
A
Endocardium
3
Q
Layer of muscle in the heart
A
Myocardium
4
Q
Outer layer of the heart
A
Epicardium
5
Q
Pericardium
A
Fibrous sac covering the heart
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
7
Q
Is the interatrial or interventricular wall thicker?
A
Interventricular (2-3 times thicker)
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
9
Q
What is the only artery not carrying oxygenated blood
A
Pulmonary artery
10
Q
Blood flow into the two major coronary arteries occurs primarily during…
A
Diastole
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
12
Q
Systole
A
Contraction of myocardium, ejection of blood from the ventricles
13
Q
Diastole
A
Relaxation of myocardium, filling of the ventricles
14
Q
S1
A
Start of systole, “lub”, closure of tricuspid and mitral valves, radial or apical pulse
15
Q
S2
A
Start of diastole, “dub”, closure of aortic and pulmonic valves
16
Q
Cardiac Output
A
Amount of blood pumped by each ventricle in 1 min (norm. 4-8L/min)
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)
18
Q
When is CO increased
A
With high circulating volume
19
Q
When is CO decreased
A
With low circulating vol. or decrease in strength of ventricular contraction
20
Q
Stroke Volume
A
Volume of blood (in mL) ejected with each heartbeat (Norm. 50-100); determined by preload, afterload, and contractility
21
Q
When is stroke vol decreased
A
Impaired cardiac contractility, valve dysfunction, CHF, beta blockers, MI
22
Q
When is stroke vol increased
A
Volume overload, inotropy, hyperthermia, meds (ie. Digitalis, dopamine, dobutamine)
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
24
Q
Causes for increased preload
A
MI, aortic stenosis, and hypervolemia
25
Sign of left ventricular preload
PAWP= Pulmonary Artery Wedge Pressure
26
Signs of right ventricular preload
CVP= Central Venous Pressure
27
Afterload
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
28
What affects afterload
Vasoconstriction, BP, heart valve resistance, and blood viscosity
29
Systemic Vascular Resistance (SVR)
Opposition encountered by left ventricle; force opposing movement of blood; created primarily in small arteries and arterioles
30
What increases SVR
Vasoconstrictors, low volume
31
What decreases SVR
Vasodilators, morphine, nitrates, high CO2
32
What does cardiac output r/t increased afterload eventually lead to
Ventricular hypertrophy- an enlargement of cardiac muscle tissue without an increase in CO or the size of the chambers
33
Pulmonary Vascular Resistance (PVR)
Opposition encountered bt R ventricle
34
When is PVR increased
Pulmonary hypertension and hypoxia
35
When is PVR decreased
Meds (ie calcim channel blockers, aminophylline, isoproterenol, O2)
36
What increases afterload
HTN, hardened arteries, CAD, pulmonary HTN (rt HF), hypoxia, catecholemines
37
What decreases afterload
Vasodilators, acidosis, O2
38
Contractility
Strength of contraction; illustrate with old, flakey rubber band or balloon vs. new, stretchy rubber band or balloon
39
What increases Contractility
Meds (epinephrine, norepinephrine, isoproteneronol, dopamine, dobutamine, digitalis)
40
What decreases contractility
HF, alcohol, calcium channel blockers, acidosis
41
Positive inotropes
Meds that increase contractility
42
Negative Inotropes
Meds that decrease contractility
43
S/S that indicate Preload problems
JVD, lung sounds, and PWCP
44
S/S that indicate afterload problems
BP, skin temp, pulse pressure
45
S/S that indicate contractility problems
ejection fraction
46
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?
Blood Pressure; afterload is affected by the size of the ventricle, wall tension and areterial blood pressure
47
Autonomic Nervous system- how does it affect the HR
Can increase the HR up to 180 bpm for short time without untoward effects
48
How does the SNS Affect the HR
release of epinephrine/norepinephrine and speeds everything up (ie HR, AV node, force of contractions), also causes vasoconstriction
49
How does the PSNS affect the HR
Slows everything down (ie HR, SA node rate) causes vasodilation; vagus nerve
50
How do Baroreceptors affect the HR
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)
51
How do Chemoreceptors affect the HR
Sense changes in CO2 and O2 and can cause increased HR and BP
52
Factors affecting HR
ANS, SNS, PSNS, Baroreceptors, and chemoreceptors
53
What does mean arterial pressure tell us
If organs are being perfused
54
Arterial BP
A measure of the pressure exerted by blood against the walls of the arterial system
55
Systolic BP
Peak pressure exerted against the arteries when the heart contracts
56
Diastolic BP
Residual pressure in the arterial system during ventricular relaxation (or filling)
57
What are the two main factors influencing BP
CO and SVR
58
Pulse pressure
Difference between systolic and diastolic; normally 1/3 of the systolic
59
When might there be an increased pule pressure
During exercise or in individuals with atherosclerosis of the larger arteries as the result of increased systolic
60
When might there be a decreased pulse pressure
HF or hypovolemia
61
Mean Arterial Pressure (MAP)
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
62
What MAP is needed to adequately perfuse and sustain vital organs of an average person
60 mm HG
63
What happens when the MAP falls below 60 mm HG
Vital organs are under-perfused and will become ischemic
64
What is one of the greatest risk factors for cardiovascular disease
Age; leading cause of death in >85 uears of age
65
What is the most common CV problem (geri)
Coronary artery disease secondary to atheroscleorsis
66
CV changes result from...
Aging, disease, environmental factors, and lifetime behaviors
67
HR changes in GERI
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
68
What is hard to distinguish in GERI regarding arteries
Normal aging vs. atherosclerosis
69
BP changes in GERI
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
70
Postprandial hypotension
Decrease in BP of at least 20 mm Hg that occurs withing 75 minutes after eating
71
Heart sound changes in GERI
Murmur from regurgitation/narrowing of mitral and aortic valves
72
ECG changes in GERI
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)
73
Medication response changes in GERI
Less sensitive to beta blockers, increased sensitivity to vasopressin (ADH)
74
Physical changes in GERI
Dependent edema due to incompetent venous valves
75
Subjective data needed for cardiac assessment
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)
76
Health hx needed for cardiac assessment
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
77
Risk factors for CV problems
Increased serum lipids, HTN, smoking, sedentary lifestyle, obesity, stress, DM
78
Familial disorders to be concerned about
Heart disease before age 55, intermittent claudication, varicose veins; other disorders that affect CV- asthma, renal disease, liver disease, obesity
79
Exercise intolerance concerns
Chest pain, SOB, claudication (cramping in the lower legs when walking or exercising)
80
Sleep concerns (subjective data)
Paroxysmal nocturnal dyspnea, orthopnea, sleep apnea- need to sleep upright or with pillows, sleep spnea increases risk of dysrhythmias
81
Highlighted sub. data
Allergies to iodine, familial disorders, constipation, exercise intolerance, PND, orthopnea, sleep apnea, sexual problems
82
Sexual problems with CV
Fear of sudden death during intercourse, ED, HRT, or BCPs can increase risk for blood clots (asp. if they are a smoker)
83
VS for CV ob. assessment
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
Inspect extremities for...
Edema, dependent rubor, clubbing, variscosities, and lesions (such as stasis ulcers)
85
What can be an indicator for R-sided HF
Jugular vein distension
86
What would be felt if pt. has suspected valvular disorder
Abnormal pulsations or thrills on chest wall at 5 spots
87
What is expected when the PMI is below the 5th ICS and left of the mid-clavicular line
Heart may be enlarged
88
Asses what with pulse deficit
Auscultate apical pulse while palpating radial pulse, if different have one person count each one for a full minute, r/t dysrhythmias
89
S3
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
S4
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
Pericardial friction rubs
High-pitches, scratchy sounds, usu. heard best at apex when sitting or leaning forward; r/t pericarditis
92
Risk predictors: C-Reactive protein
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
Risk predictors: Homocysteine
Elevated levels increased risk for CAD, peripheral vascular disease (PVD), and stroke; Hcy is an amino acid that is produced during protien catabolism
94
Diagnostic studies of CV system
Triglycerides (60 is low risk, LDL=
95
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
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
Electrocardiogram
Resting ECG (12 lead); Ambulatory ECG monitoring (telemetry); Event monitor or loop recorder; Exercise or stress testing
97
What is an event monitor used for
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
Echocardiogram
Ultrasound of heart; provides information regarding structures and motion of heart; measures ejection fraction (50% is normal)
99
Echocardiogram provides information about what abnormalities
Valvular structures and motion, cardiac chamber size and contents, ventricular and septal motion and thickness, pericardial sac, and ascending aorta
100
Stress Echocardiography
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
Nuclear Cardiology (MUGA)
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
MRI
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
CT
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
Cardiac Catheterization
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
Cardiac Cath for right
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
Cardiac Cath for Left
Use femoral or brachial artery, to aorta, across aortic valve, into L ventricle
107
Angiography
Done with a L sided heart cath, inject dye into coronary arteries (makes pt. feel flushed) to look for lesions
108
Cardiac Cath procedure
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
Post Cardiac cath care
Neuro checks q 15 min x 1 hr; compression device over injection site; close monitoring of VS and ECG
110
Complications of Cardiac cath
Bleeding/hematoma, allergic reaction, infection, clot, aortic dissection, dysrhythmias, MI, stroke, puncture ventricles of lung
111
Regulation of BP (SNS)
Increases HR and contractility; vasoconstriction; release of renin from the kidneys
112
Regulation of BP (Baroreceptors)
Send inhibitory impulses to the sympathetic vasomotor center in the brainstem
113
Regulation of BP (Renal System)
Controls sodium excretion and ECF volume increasing venous return and SV, inc. CO & BP; Renin-angiotensin-aldosterone system (RAAS)
114
Regulation of BP (Endocrine System)
Epinephrine increases HR and contractility; Increases blood sodium osmolarity stimulating release of ADH (increases ECF volume)
115
Regulation of BP (Renin-angiotensin-aldosterone system- RAAS)`
Vasoconstriction; increases SVR; causes sodium and water retention by the kidneys increasing blood volume and CO
116
Definition: HTN
Persistent systolic >140, diastolic >90
117
Definition: PreHTN
Systolic 120-139 or diastolic 80-89
118
Isolated systolic HTN (ISH)
Sys >140 with dias.
119
Pseudohypertension
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
Causes of primary HTN
95% of those with HTN; no identified cause
121
Causes of secondary HTN
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
Risk factors for HTN
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
S/S of HTN
"Silent Killer"; no s/s until organ disease occurs, fatigue, activity intolerance, dizziness, palpitations, angina, dyspnea
124
Complications of HTN: hypertensive heart diasease
CAD, L ventricular hypertrophy, HF
125
Complications of HTN: cerebrovascular disease
Atherosclerosis, stroke, HTN encephalopathy
126
Complications of HTN: Peripheral Vascular Disease (PVD)
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
Complications of HTN: Nephrosclerosis
End-stage renal disease, renal dysfunction; nocturia is common symptom
128
Complications of HTN: Retinal Damage
Blurred vision, retinal hemorrhage, blindness; tells us the severity and duration of HTN
129
Diagnostic studies for HTN
Not much to be done since most have no cause; UA, BUN, creatinine, electrolytes, blood glucose, lipid profile, uric acid, ECG, Echocardiogram
130
Lifestyle modifications for HTN
Weight reduction, exercise 30 min/day, DASH eating plan, Na+ reduction, limit alcohol, regular physical activity, avoid tobacco, stress management
131
DASH eating plan
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
Sodium restriction diet with HTN
133
Treatment goal of HTN
BP
134
Treatment HTN
Make decisions based on overall CVD risk; lifestyle modifications should be the foundation of tx; most need at least one med
135
Diuretics with HTN
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
Diuretic SE
Low potassium (except for spironalactone), low magnesium, dehydration (remember if K+ low, digoxin toxicity is a higher risk)
137
Beta Blockers with HTN
"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
Beta Blocker SE
Fatigue, impotence, wheezing or SOB (why we don't use in asthmatics)
139
ACE inhibitors with HTN
"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
ACE SE
Dry cough, low BP, high K+, angioedema (swelling of the lips and face - must stop the drug if this occurs)
141
Angiotensin ll Receptor Blockers (ARB) with HTN
"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
Angiotensin ll Receptor Blockers (ARB) SE
High K+, decreased kidney function
143
Calcium Channel Blockers with HTN
"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
Calcium Channel Blockers SE
Bradycardia, low BP, headache, dizziness, nausea
145
Alpha adrenergic blockers with HTN
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
Alpha adrenergic blockers SE
Dry mouth, sedation, fatigue, impotence, low BP
147
Vasodilators with HTN
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
Nursing Implications with vasodilators
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
Vasodilators SE
Headache, low BP, dizziness
150
HTN drug therapy SE
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
Nursing Interventions with HTN
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
Proper BP measurement
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
GERI considerations r/t HTN
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
Hypertensive Crisis
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
Hypertensive Crisis S/S
Severe headache, n/v, seizures, confusion, coma, papilledema, tremors, decreased urine output
156
Complications of hypertensive crisis
Angina, MI, pulmonary edema (chest pain, dyspnea), aortic dissection (sudden, excruciating chest/back pain, reduced/absent pulses in the extremities), stroke
157
Hypertensive Crisis tx
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
Definition of HF
Abnormal cardiac function involving impaired cardiac pumping and/or filling; associated with HTN, CAD, MI; older adults; high morbidity and mortality
159
Risk factors for HF
CAD, age, HTN (primary factors); diabetes, smoking, obesity, high cholesterol; African Americans have higher incidence, develop earlier, higher mortality
160
Patho of sys. HF
Problem with pumping; caused by MI, HTN, cardiomyopathy, valve disease
161
S/S of sys. HF
left ventricular hypertrophy, decreased EF (b/c L ventricle can't generate enough pressure to eject blood into the aorta)
162
Patho of dia. HF
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
S/S of dia. HF
Pulmonary congestion, pulm. HTN, ventricular hypertrophy, normal EF
164
Patho mixed HF
Very low EF (
165
Compensatory Mechanism w/ HF: SNS activation
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
Compensatory mechanism w/ HF: Neurohormonal responses
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
Compensatory Mechanism w/ HF: Ventricular Dilation
Way to cope with increased vol.
168
Compensatory Mechanism w/ HF: Ventricular Hypertrophy
Increase in muscle mass and wall thickness; requires more O2 to work
169
Counter Regulatory Mechanisms
Production of ANP, BNP, and NO; Causes vasodilation and diuresis; blocks the effects of the RAAS; inhibit the development of hypertrophy
170
Atrial Natriuretic Peptide (ANP)
Released when the heart senses high blood volume; reduces water and sodium through diuresis, thus reducing BP
171
Brain or B-type Natriuretic Peptide (BNP)
Released when the heart senses stretching of the ventricles, acts like ANP does
172
Nitric Oxide (NO)
Causes vasodilation; decreases afterload
173
Left-sided HF
Most common; caused by L ventricular dysfunction and blood backing up into the pulmonary veins leading to pulmonary edema; pulmonary congestion and edema
174
Right-sided HF
Causes backup of blood into systemic circulation causing JVD, hepatomegaly, splenomegaly, peripheral edema; caused by L-sided
175
Acute Decompensated HF (ADHF)
Pulmonary Edema; Anxious, pale, cyanotic, cold and clammy, severe dyspnea, tachypnea, orthopnea, frothy blood-tinged sputum, inc. HR, crackles/wheezes/ronchi
176
S/S of Chronic HF
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
S/S R-sided HF
Murmurs, heaves, JVD, edema, weight gain, ascites, hepatomegaly, fatigue, nausea, anorexia/GI bloating
178
S/S L-sided HF
S3, S4, heaves, PMI displaced, hypoxia, crackles/ pleural effusion, dyspnea, restlessness, confusion, fatigue, PND, orthopnea, cough, frothy/pink-tinged sputum
179
Complications with HF
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
Diagnostic goal
Determine cause
181
Diagnostic EF
Ejection fraction; distinguishes between sys. and dia. HF; Echo or nuclear imaging (MUGA); normal is 60-75%
182
Diagnostic: BNP
Differentiate whether dyspnea is from HF; inc. w/ ventricular dysfunction
183
ADHF treatment
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
ADF treatment- Drugs
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
How do we know if the drugs worked with ADHF
Decreased SOB
186
Chronic HF treatment
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
Chronic HF treatment- Drugs
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
Drugs to use CAUTIOUSLY in chronic HF treatment
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
Nutrition with HF
Sodium restrict (if 3lbs over 2 days); 3 day diet hx
190
Nursing Interventions: HF Health prmotion
Aggresively identify and treat rx factors; flu and pneumonia vaccine, educate about diet/meds/exercise; slowing progression
191
Nursing interventions: Acute HF
Conserve energy, decrease anxiety, may need salt and fluid restrictions, need support system
192
Nursing interventions: HF Ambulation/Home care
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
FACES
Fatigue, Activity limitation, Chest congestion/cought, Edema. Short of breath
194
When to call Dr. with HF
Weight gain, difficulty breathing, PND, dry/hacking cough, fatigue, swelling, dizziness, FACES
