exam 2 medsurg Flashcards
1
Q
pH definition
A
strength of hydrogen ions in a solution
2
Q
normal blood pH
A
7.35-7.45
3
Q
acidic pH
A
has more H+
4
Q
base pH
A
has more OH- hydroxyl ions
5
Q
pH resulting in death
A
7 or less and 7.8 or more
6
Q
the most common acid
A
carbonic acid H2CO3
7
Q
regulates CO2
A
lungs
8
Q
waste products of carb, fat, protein metabolism
A
acids
9
Q
most common base
A
bicarbonate HCO3
10
Q
regulate bicarbonate in ECF
A
kidneys
11
Q
waste product of glucose
A
CO2
12
Q
carbonic acid
A
the form in which CO2 is transported in the blood
13
Q
first line of defense, takes seconds
A
chemical. The bicarbonate buffer system is includes bicarbonate (HCO3) and carbonic acid (H2CO3) are constantly regulated by the respiratory and urinary system. These two components increase and decrease depending on the need of the body.
Protein buffer system: hemoglobin promotes movement of chloride across the RBC in exchange for bicarbonate.
14
Q
second line of defense, takes minutes
A
respiratory. breathing rids body of CO2. Co2 is carried in the body in the form of carbonic acid and bicarbonate. During body metabolism, CO2 is produced which reacts with H2O to form carbonic acid resulting in decreasing pH (as acidity increases). Where as in the lungs, carbonic acid breaks into CO2 and H2O and increased exhalation of CO2 results in increasing pH (acidity decreases)
15
Q
third line of defense, takes 24-48 hours
A
renal, strongest mechanism. When there high levels of hydrogen ions in the body, the kidneys (a) secrete hydrogen ions and reabsorb sodium ions; (b) ammonia a by product of protein metabolism combines with hydrogen ions to form ammonium ions (NH4+) which is excreted in the urine in exchange of sodium reabsorption into blood. When there are low levels of hydrogen ions in the body, kidneys retain hydrogen ions to form bicarbonate.
16
Q
pH high
A
alkalosis
17
Q
pH low
A
acidosis
18
Q
metabolic acidosis
A
ph <7.35. bicarb <22 mEq/L. often renal failure
19
Q
metabolic acidosis clinical manifestations
A
headache, confusion, hypotension, dysrhythmia, increased respirations.
20
Q
metabolic acidosis treatment
A
underlying cause, bicarbonate
21
Q
metabolic alkalosis
A
ph >7.45. bicarb >26mEq/L. often with hypokalemia
22
Q
metabolic alkalosis clinical manifestations
A
tachycardia, hypokalemia, respiratory depression
23
Q
metabolic alkalosis treatment
A
underlying cause, IV NACL to restore fluid volume and allow excretion of excess bicarb
24
Q
respiratory acidosis
A
ph< 7.35. PaCO2 > 42 mm/Hg. Due to inability to excrete CO2.
25
respiratory acidosis clinical manifestations
sudden increased pulse and RR, HTN, LOC change
26
respiratory acidosis treatment
improve ventilation
27
respiratory alkalosis
pH >7.45. PaCO2 <35 mm/Hg. due to hyperventilation
28
respiratory alkalosis clinical manifestations
lightheadedness, parathesias, loss of consciousness
29
respiratory alkalosis treatment
cause of hyperventilation, paper bag breathing.
30
acidosis
too muc H+ ions in body. too much CO2 in the body results in acidosis.
31
alkalosis
too much bicarbonate. the body has lost CO2 or the pt hyperventilated so much they lost too much CO2
32
cardiac valves
tricuspid, mitral, pulmonic, aortic
33
Mean arterial pressure
must be at lease 60 mm/Hg to maintain adequate blood flow through coronary arteries and perfuse major organs (brain)
34
cardiac output
amount of blood pumped from the left ventricle per minute. heart rate x stroke volume.
35
heart rate
the number of times the ventricles contract in one minute
36
cardiac index
cardiac output / body surface area
37
Cardiac index normal range
2.7-3.2 L/min/m
38
Cardiac index normal range
2.7-3.2 L/min/m
39
cardiovascular system assessment
patient history, nutritional history, family history and genetic risk, current health problems (pain, discomfort, dyspnea, DOE, orthopnea, PND, fatigue, palpitations, edema, syncope, extremity pain)
40
2.2 LB
1 KG= 1 L of H2O
41
cardiovascular system physical assessment
general appearance, skin, extremities, blood pressure
42
precordium
assessment- inspect, palpate, percuss, auscultation- normal heart sounds, paradoxical splitting, gallops and murmurs, pericardial friction rub
43
serum markers of myocardial damage
troponin- T and I, creatinin kinase (CK), myoglobin, serum lipids (total cholesterol <200 mg/DL, triglyceride <150 mg/DL, HDL >40 mg/DL, LDL <70 mg/DL), homocysteine, highly sensitive C-reactive protein
44
the leading cause of death in US for men and women of all racial and ethnic groups
coronary artery disease
45
the most prevalent cardiovascular disease in adults
coronary artery disease
46
coronary artery disease
broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium.
47
coronary artery disease
broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium.
48
ischemia
blood flow is partially blocked. insufficient oxygen is supplied to meet the requirements of the myocardium. usually followed by infarction.
49
infarction
follows ischemia. necrosis or tissue death of myocardium. irreversible damage.
50
infarction
follows ischemia. necrosis or tissue death of myocardium. irreversible damage.
51
blockages
narrowing of the coronary vessels reduce blood flow to the myocardium
52
CAD contributing factors
high LDL and total cholesterol. Low HDL. triglycerides >150. hypertension. elevated C-reactive protein and fibrinogen level. metabolic syndrome- insulin resistance, central obesity
53
CAD prevention
control cholesterol abnormalities (diet, physical activity, medication), smoking cessation, manage hypertension, control diabetes.
54
angina
chest pain that results from the imbalance between oxygen supply and demand
55
2 types of angina
stable and unstable
56
chronic stable angina
chest discomfort that occurs with moderate to prolonged exertion in a pattern that is familiar to the patient. can occur over several months.
57
chronic stable angina results in
slight limitation of activity and is usually associated with a thickened fixed atherosclerotic plaque.
58
chronic stable angina relieved by
nitroglycerine or rest and is often managed with drug therapy. rarely does CSA require aggressive treatment.
59
angina clinical manifestations
tightness, choking, or heavy sedation, substernal :radiates to neck, jaw, shoulders, back or arms (usually left), anxiety, dyspnea, SOB, dizziness, N/V, pain less than 15 minutes.
60
unstable angina
characterized by increased frequency and severity and is not relieved by rest and NTG. requires medical intervention.
61
angina treatment
decrease myocardial oxygen demand and increase oxygen supply, oxygen, reduce and control risk factors (lipids), monitor for heart failure, Chart 40-1
62
angina medications
nitroglycerine, beta-adrenergic blocking agents, calcium channel blocking agents, antiplatelet and anticoagulant meds (aspirin, heparin
63
garlic supplements
small effect on reduction
64
nitro
a nitrate often produces collateral blood flow to the heart and dilates the coronary artieries. It decreases the oxygen demand of the mycocardium by causes peripheral vasodilation (hence fall in BP).
Pain relief should begin in 1-2 mins and clearly evident in 3- 5 mins. If the patient’s systolic BP drops below 100 or 25 mmHg than norm, lower the head of the bed.
65
aspirin
inhibits platelet aggregation and decreases the likelihood of thrombosis
66
glyco
prevents fibrinogen to attach to activated platelets at the site of the thrombus
67
congestive heart failure
the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. indicates myocardial disease- a problem with the contraction of the heart of filling of the heart.
68
causes of left sided heart failure
hypertension, CAD, vascular disease (mitral or aortic), indicates LHF: poor cardiac output and pulmonary congestion.
69
causes of right sided heart failure
left ventricle failure, right ventricular myocardial infarction, pulmonary hypertension
70
causes of high output failure
increased metabolic needs, septicemia, high fever, anemia, hyperthyroidism
71
left sided failure clinical manifestations
LV can not pump blood effectively, decreased cardiac output and elevated pulmonary venous pressure. weakness, low oxygen, confusion, pulmonary congestion, breathlessness, oliguria, tachycardia, palpitations, weak peripheral pulses, cool extremities
72
right sided failure clinical manifestations
RV cannot eject sufficient amounts of blood. fluid is retained and pressure builds up in the venous system. peripheral edema, jugular vein distention, swollen hands and feet, anorexia, nausea, weight gain, polyuria at night, advanced stage- ascites and increased abd girth.
73
CHF diagnostics
CXR (hazy lung fields, cardiomegaly), echocardiogram (heart enlargement, ineffective ventricular contraction), BUN, elevated creatinine (from renal dysfunction), lipid panel, increased liver enzymes.
74
CHF treatment
bedrest to decrease work of heart, frequent rest periods, elevated HOB (high fowlers), oxygen, diet (may restrict fluids, Na+), diuretics, anticoagulants (ASA, coumadin), vasodilators (nitrates, calcium channel blockers).
75
valvular disorders
mitral valve prolapse, mitral regurgitation, mitral stenosis, aortic regurgitation, aortic stenosis
76
stenosis
narrowing of valve opening
77
insufficiency
inability of valve to close compleltely
78
mitral valve prolapse characteristics
one or both leaflets enlarge and protrude into LA during systole. usually benign (but may progress to mitral insufficiency. cause unknown. more common in young women. may have anxiety problems.
79
mitral valve prolapse clinical manifestations
chest pain (different from angina, not with exertion, is prolonged and not easily relieved), palpitations, dizziness, fatigue, anxiety (like panic attack).
80
mitral valve prolapse treatment
medications-antibiotics, anticoagulants, antianxiety, antiarrhythmic. avoid caffeine. relaxation techniques. for chest pain0 lie flat with legs elevated against wall for 3-5 mins.
81
mitral stenosis
mitral valve leaflets become thickened and fibrotic. commissure if formed. affects women 20-40 years old. caused primarily by rheumatic fever.
82
mitral stenosis clinical manifestations
dyspnea, fatigue, cough, chest pain, activity intolerance.
Late: pulmonary edema
Extremely loud S1.
heart murmur- described as sounding like rumbling underground train.
83
mitral valve treatment
similar to CHF
medications : anticoagulants, antibiotics, antiarrhythmics.
surgery: mitral commissurotamy, mitral valve replacement, balloon valvuloplasty.
84
mitral insufficiency
often occompanies mitral stenosis. LA and LV enlarged as result of backflow of blood. LV enlarges in attempt to maintain cardiac output. Left side of heart fails and S/S of mitral stenosis develop.
High pitched murmur.
85
mitral insufficiency treatment
medications: vasodilators to decrease afterload and regurgitation, digitalis, diuretics, prophylactic antibiotics.
decreased activity
surgery: annuloplasty, mitral valve replacement
86
aortic stenosis
flow of oxygenated blood through aortic valve is impeded, causing enlarged LV, powerful LA contraction.
87
aortic stenosis risk factors
aortic valve is most commonly diseased in the elderly, esp. men.
rheumatic fever
longer lifespan
drug abuse
88
aortic stenosis clinical manifestations
```
no s/s until valve opening decreases to 1/3 normal size.
exertional dyspnea
angina, syncope
displaced PMI- to the left
late: fatigue, orthopnea
```
89
aortic stenosis treatment
prophylactic antibiotics for dental and invasive procedures.
for heart failure: digoxin, diuretics, low Na+ diet, activity restriction
surgery: balloon valvuloplasty, aortic valve replacement
90
aortic insufficiency patho
regurgitation of blood into LV causes LV to hypertrophy. LV failure and myocardial ischemia occur. Eventually, right sided failure.
91
aortic insufficiency causes
rheumatic fever, infections (syphilis, endocarditis), chronic hypertension, calcification, blunt chest trauma
92
aortic insufficiency clinical manifestations
may be asymptomatic
early s/s: signs of CHF, chest pain
widening pulse pressure
93
aortic insufficiency treatment
medications: prophylactic antibiotics, digoxin, diuretics
| aortic valve replacement
94
mechanical valves
do not deteriorate or become infected as easily, but are thrombogenic and require life-long anticoagulant therapy.
95
tissue (biologic) valves
xenograft (heterograph): pig or cow valve.
homograft (allograft): human valve
autograph: pt's own valve
96
infectious diseases of the heart
Any of the layers of the heart may be affected by an infectious process.
Diseases are named by the layer of the heart that is affected.
Diagnosis is made by patient symptoms and echocardiogram.
Blood cultures may be used to identify the infectious agent and to monitor therapy.
Treatment is with appropriate antimicrobial therapy. Patients require teaching to complete the course of appropriate antimicrobial therapy, and require teaching for infection prevention and health promotion.
97
pericarditis
inflammation of sac surrounding heart. may be acute (virus, fungi, bacteria, chemotherapy, MI, chest trauma or surgery)
may be chronic (TB, radiation, metastasis, connective tissue disorders
98
pericarditis clinical manifestations
precordial chest pain is hallmark symptom. aggrevated moving and deep breathing. dyspnea, fever, chills, pericardial friction rub, heart sounds: difficult to hear, if effusion present.
99
pericarditis diagnostics
elevated wbc, ST segment ^ on EKG, echocardiogram- wide gap between epicardium and pericardium. CXR- enlarged heart.
100
pericarditis treatment
rest, pericardiocentesis, pericardial window, meds (analgesics, antipyretics, NSAIDS), manage pain.
101
thrombophlebitis
AKA phlebitis, thrombophlebitis, deep vein thrombosis
102
thrombophlebitis veins most affected
superficial- saphenous
| deep- femoral, poplital, small calf veins
103
thrombophlebitis risk factors
bedrest, general surgery for those over 40, leg trauma, obesity, previous venous insufficiency, oral contraceptives, malignancy and chemotherapy
104
thrombophlebitis clinical manifestations
positive homan's sign, calf pain, inflammation (warm, tender, swollen) as result of congestion distal to clot, others (may vary).
105
thrombophlebitis diagnosis
H & P, venogram (use of dye), doppler ultrasound
106
thrombophlebitis treatment
bedrest, elevate extremity, warm, moist soaks, ted hose, thrombocytic therapy, anticoagulants (Heparin first (PTT), then coumadin (PT)), never massage or rub, watch for signs of bleeding, prevent recurrence.
107
vascular system assessment
```
characteristics of arterial and venous insufficiency,
chest pain,
changes in skin and appearance,
pulses,
aging changes
```
108
atherosclerosis
formation of plaque within arterial walls.
wall stiffens, thickens and decreases in diameter.
lipids, calcium, thrombi adhere to damaged wall.
over time, fat and fibrin harden.
decreased blood flow.
causes hypertension, impaired tissue perfusion and aneurysms.
109
atherosclerosis risk factors
diabetes mellitus, smoking, hypertension, sedentary lifestyle, african american or hispanic, low HDL and high LDL
110
atherosclerosis clinical manifestations
hypertension, extremities cold/cool with diminished or absent pulses, prolonged capillary filing/ bruit of large arteries, decreased intensity and audibility of a pulse
111
atherosclerosis diagnostics
total serum cholesterol levels, HDL-LDL, triglycerides, homocysteine
112
atherosclerosis treatment
diet therapy, smoking cessation, exercise, drug therapy, gene therapy
113
PVD and PAD risk factors
tobacco use, hyperlipidemia, HTN, DM, obesity, stress, sedentary lifestyle, age, gender, genetics,
PVD: Virchow's triad, hip surgery
114
PVD clinical manifestations
classic: calf/ groin tenderness, unilateral leg swelling.
aching, cramping pain in LE at rest, pulses present but hard to palpate, edema and calf thickness, induration- warmth, purplr/blue color extremity, thick rough skin
115
PAD clinical manifestations
intermittent claudication, sharp, constant pain, diminished or absent pulses, dependent rubor, extremities pale when elevated, dry shiny skin, cool temp, hair loss, thick nails
116
PVD diagnostics
D-dimer, MRI, impedance plethysmography, venous duplex ultrasonography, CT scan
117
PAD diagnostics
arteriography, plethysmography, C-reactive protein (CRP- inflammatory marker), D-dimer, homocysteine level (protein indicating thrombin formation)
118
PVD treatment
prevention- weight loss, smoking cessation, regular exercise, compression stockings, pneumatic compression devices, leg exercises, alternate up and down of LE, anticoagulant therapy-heparin, surgical management
119
PAD treatment
prevention- foot care, exercise program, medications (pentoxifylline [trental], cilostazol [pletal]), use of antiplatelet agents, avoid cold temps, avoid prolonged dependency of LE, surgical management (angioplasty, atherectomy, bypass)
120
Buerger's Disease
Recurring inflammatory process of the small and intermediate vessels of the LE, probably an autoimmune disorder.
Most often occurs in men ages 20-35.
Risk or aggravating factor:tobacco.
Progressive occlusion of vessels results in pain, ischemic changes, ulcerations, gangrene
121
Raynaud's disease
intermittent arterial vasoocclusion, usually of fingertips or toes.
associated with other underlying conditions such as scleroderma.
manifestations: sudden vasoconstriction resulting in color changes, numbness, tingling or burning pain.
episodes are usually brought on by a trigger such as cold or stress.
occurs most frequently in young women.
protect from cold/ other triggers. Avoid injury to hand/fingers.
122
Most common CV problem in US
hypertension
123
hypertension risk age
30-50, complications increase after age 50
124
hypertension nationality risk
2x as many african american's as whites
125
hypertension
persistent systolic elevation >140 and diastolic >90.
| severity defined according to diastolic B/P.
126
hypertension (primary or essential) risk factors
age>60, alcoholic, salt, caffeine, obesity, hyperlipidemia, smoking, stress, ethnicity.
95% of hypertension is this type
127
secondary hypertension caused by
underlying factors such as: kidney disease, arterial disease, pregnancy, drugs- estrogen, glucocorticoids, cyclosporines, erythropoietin
128
hypertension complications
MI, PVD, Chronic renal failure, CVA
129
hypertension clinical manifestations
```
may be none
headaches
lightheaded/dizzy
abd. bruits, tachycardia
sweating, pallor
epistaxis
```
130
hypertension diagnostics
initally B/P in both arms in standing, sitting and lying position- BP above 140/90 on 2 or more occasions.
test to check for complications
131
hypertension treatment
```
lifestyle modifications is the first step
weight reduction
smoking cessation
sodium restriction
exercise
relaxation techniques
modified alcohol intake
drug therapy
```
132
hypertension medication
diuretics, beta blockers, Ca++ channel blockers, angiotensin converting enzyme (ACE) inhibitors, alpha adrenergic blockers, central adrenergic blockers, rauwolfia derivatives, vasodilators
133
hydrochlorothiazide (diuril), Lasix, Bumex
Diuretics
134
Propranalol (Inderal)
Beta adrenergic blocker
135
Nifedipine (procardia), Verapanil (Calan)
Ca++ channel blocker
136
Captopril (Capoten)
Angiotensin converting enzyme (ACE) inhibitor
137
Prazosin (Minipress)
Alpha adrenergic blocker
138
Methyldopa (Aldomet)
central adrenergic blockers
139
Reserpine (Serpasil)
Rauwolfia derivatives
140
Hydralazine (Apresoline)
vasodilator
141
hypertension teaching
Monitor B/P regularly
Encourage patients to take medications and keep appointments even when feeling well
Consult doctor or pharmacist about OTC drugs
If orthostatic hypotension
rise slowly
avoid prolonged standing
avoid hot baths/showers
Do not stop abruptly or rebound hypertension may occur
Present measures to manage hypertension as health practices beneficial to everyone (not a long list of “don’ts)
Sexual dysfunction is common side effect
Encourage patients to talk to doctor about this
