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NUR 323-Exam 2 > Chap. 28, 29, 31: HTN, BP, Heart failure, Heart Disease > Flashcards

Chap. 28, 29, 31: HTN, BP, Heart failure, Heart Disease Flashcards

1
Q

What is normal, prehypertension, Stage I hypertension and Stage 2 hypertension

A

Normal: <120/80
Prehypertension: 120-139/80-89
Stage 1: 140-159/90-99
Stage 2: 160/100 or greater

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2
Q

What is mean pressure and how is it calculated

A

Mean pressure is the average amount of pressure exerted during the cardiac cycle.
Calculation: diastolic X 2 + systolic/3

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3
Q

What is pulse pressure:

A

Difference between systolic and diastolic pressure

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4
Q

What are methods for prevention of HTN

A

Diet, exercise, stress reduction, adequate sleep, low alcohol intake, avoid smoking, low salt/cholesterol in diet

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5
Q

goal bp for adults over 60? Goal bp for pts with CKD or DM

A

> 60: 150/90

CKD or DM: BELOW 140/90

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6
Q

What are the treatment strategies for HTN in patients who do not have compelling conditions?

A

Stage 1: Thiazides for most; may consider ACE-I,ARB,BB, CCB or combination

Stage 2: 2 drug combo for most: thiazides and ACE-I, OR ARB, Or BB, OR CCB.

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7
Q

What are compelling conditions, in order of most significance to least?

A

Heart failure, post MI, High CV risk, DM, CKD, and recurrent Stroke prevention

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8
Q

What are initial therapy options for patients who have heart failure?

A

Thiazides, BB, ACE-I, ARBs, Aldost. Antagonists

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9
Q

What are initial therapy options for patients who are post MI

A

BB, ACE-I, Aldosterone Antagonists

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10
Q

What are the initial therapy options for patients who have high CV risk

A

Thiazides, bb, ace-i, ccb

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11
Q

What are the initial therapy options for patients with diabetes

A

thiazides, BB, ACE-I, ARBs, CCBs

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12
Q

What are the initial therapy options for patients with CKD?

A

ACE-I, ARBs

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13
Q

what are the initial therapy options for patients with recurrent stroke prevention?

A

Thiazides, ACE-I

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14
Q

What drugs affect preload, afterload, and contractility

A

Preload: amount of pressure exerted during passive ventricular filling (end of diastole): Diuretics

Afterload: Resistance that the left ventricle needs to overcome to circulate blood. ACE-I, ARBs, and CCBs

Contractility: ability of the heart to contract effectively: BBs and Digoxin

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15
Q

What is a risk of using Beta Blockers

A

they suppress the SNS so the body does not respond to a “flight or fright” response. They also can cause bronchospasm and glucose intolerance.

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16
Q

What are the risks of both CCBs, ACE-Is,

A

CCBs: heart block, CHF, constipation

ACE-Is: cough, hypotension, cost

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17
Q

what are long term risks of HTN

A

CV: SHF, IHD,
Brain: CVA, encephalopathy
Kidney: small vessel necrosis, renal artery disease

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18
Q

factors that affect Pulse rate

A

Age, gender, stress, exercise, fever, medications, hypoglycemia, hypovolemia, pain, position changes, disease processes.

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19
Q

what is the difference between hypertensive urgency and hypertensive emergency? What are the treatment goals of each?

A

Hypertensive Urgency: Elevated hypertension without any evidence of impending or progressive target organ damage. (nosebleeds, severe h/a, anxiety). Rx: oral antihypertensives with a goal of normalizing BP within 24-48hrs.

Hypertensive Emergency: Severe hypertension that must be lowered immediately with evidence of progressive or impending target organ damage. (hypertension of pregnancy, acute MI, dissecting Aortic aneurysm and intracranial hemorrhage) all conditions assoc. w/hypertensive emergency. Rx: IV therapy, with 20%-25% reduction of BP within 1st hour of treatment, a further goal to 160/100 over 6hrs and then continued reduction of BP over several days.

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20
Q

which portion of the BP tells you about the CO, stroke volume, and peripheral vascular resistance, which best identifies risk for decreased tissue perfusion or end organ damage?

A

Systolic: tells about CO and stroke volume
Diastolic: tells about peripheral vascular resistance
Mean: identifies risk for decreased tissue perfusion or end organ damage.

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21
Q

What are the common medications used in heart failure and when are they indicated?

A

Common medications: Diuretics: decrease preload, Dilators: decrease afterload: ACE-I, ARBs, CCBs
Digoxin: Improve contractility: BBs, Digoxin

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22
Q

when and where does mitral regurgitation occur

A

between S1 and S2.

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23
Q

S1 represents what

A

the pulse beat. it is also when the AV valves close

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24
Q

S2 represents what

A

closure of Semilunar valves

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25
Q

where would you hear the sounds of mitral stenosis

A

After s2. (mid diastole when valves s/b open)

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26
Q

what S/S would you see in ACUTE heart failure:

A

Increased BNP, resp. alkalosis, cool, clammy skin, pale extremities, (decreased tissue perfusion), Increased HR, s/s of hypoxia. May have murmors in systole.

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27
Q

what are some CAUSES of ACUTE heart failure

A

new onset dysrhthmia, myocardial ischemia, infection, valvular collapse

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28
Q

What are the S/S of Chronic Heart Failure

A

S/S: Increased JVD, periph. edema, Na retention, HTN, renal insufficiency: PND, S3, Rales in Bases, dysrhythmias, cardiomyopathy, increased Na, Cl, Increased BNP and enlarged cardiac shadow

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29
Q

What is Cor Pulmonale and what are the S/S

A

Cor Pulmonale: a type of right sided HF as a result of high pulmonary pressure (low O2 and high CO2)
S/S: elevated hr, rr, low bp, low O2 sat, low UO, edema, LOC alteration dusky membranes, delayed cap refill, distant in bases, upper lobe rhonchi.

30
Q

what are S/S of CHF and treatments

A

S/S: increased RR and HR, low O2 sats, S3, bilateral pitting edema, rales

Rx: Oxygen, sit up, loop diuretics

31
Q

what is included in a perfusion assessment

A

LOC (1st thing), UO, VS

32
Q

what is the difference between primary and secondary hypertension

A

Primary (essential) unknown etiology

Secondary due to a known cause

33
Q

the pulse corresponds to the closing of which valves

A

Atrial valves

34
Q

S2-S1 is what

A

diastolic filling

35
Q

S1-S2 is what

A

systolic ejection

36
Q

aortic or pulmonary regurgitation will be heard

A

in diastole. Normally semilunar valves are closed in diastole

37
Q

when will mitral and tricuspid stenosis be heard

A

in diastole (normally av are open soundlessly in diastole).

38
Q

Mitral or triscuspid regurgitation is heard

A

in systole between s1-s2

39
Q

how is diastolic or systolic heart failure diagnosed

A

Echocardiogram. Both are a type of LEFT Sided HF.
Systolic: ejection fraction <45%
Diastolic: ejection fraction >45%.

40
Q

what are the causes of systolic HF, what is the pathophysiology of this condition

A

Causes: early HTN, Aortic stenosis, CAD, Arhythmias, myopathy. Path: enlarged ventricles fill with blood as there is a problem with ejection and contraction

41
Q

What are the causes of diastolic HF, what is the pathophysiology of this condition

A

HTN, Aortic stenosis late

Problem with ventricles becoming stiff and fill less than normal.

42
Q

how is systolic and diastolic heart failure treated

A

Systolic: Diuretics, ACE-I, BB limit fluids, mon. F&E, fibrotic disease
Diastolic: Diuretics, ACE-I, BB, CCB: need adequate fluids and vasodilators, hypertrophy

43
Q

what are s/s of pulmonary HTN

A

Low O2, high CO2

44
Q

How is pulmonary HTN treated, diagnosed

A

Dx: BNP, ABGs, PE, ECGs
Rx: O2, diuretics, bronchodilators, vasodilators

45
Q

what are nursing interventions for pulm. HTN

A

HOB raised, frequent position changes, treat hypoxia and hypercapnia.

46
Q

what are the differences between right and left sided heart failure

A

RSHF: heart cannot pump blood effectively and cant accommodate blood from venous return
s/s: edema of lower extremities, ascites, enlarged liver, anorexia, nausea, abd. pain, gen. weakness, increased capill. hydrostatic pressure, JVD, impaired circulation, weight gain

LSHF: LV cannot effectively pump blood into aorta and systemic circulation
S/S: dyspnea, cough, pulm. crackles, low O2, nocturia, SOB at rest, tachypnea, orthopnea, S3, decreased cardiac output, decreased stroke volume, crackles at bases, weight gain, Cap. refill > 3sec.

47
Q

What is Dilated Cardiomyopathy (DCM)

A

Most common form, significant dilation of ventricles without simultaneous hypertrophy. Ventricles have increased Systolic and Diastolic volumes, decreased Ejection Fraction

48
Q

What are the S/S of DCM

A

increased volume, decreased ejection, wt. gain, edema, SOB,

49
Q

how is DCM diagnosed and treated? What are some nursing pearls

A

Dx: hx, exam, ecg, cardiac cath. myocardial biopsy, diastolic murmur.
Rx: Diet (decrease Na, beta blockers, pacemaker, ACE-Is, ARBs, diuretics
Pearls: CHF, Ventricular/atrial dysrrhythmias, emboli. MOST COMMON

50
Q

What is Restrictive Cardiomyopathy (RCM)

A

the most rare type of cardiomyopathy that is caused by amyloids/infiltrative disease. This is a DIASTOLIC dysfunction.

51
Q

What are the S/S of RCM

A

dyspnea, non.prod. cough, chest pain,

52
Q

how is DCM diagnosed and treated? What are some nursing pearls?

A

Dx: echo
Rx: Beta blockers, diuretics, anticoagulants, transplantation
Nursing Pearls: avoid nifidipine, increased sens. to digoxin

53
Q

what two neurotransmitters affect contractility of the heart

A

Acetylcholine: released by PNS: decreases heart rate
Norepinephrine: released by SNS: “beta adrenergic” fibers that increases heart rate.

54
Q

what is the formula for calculating cholesterol?

A

HDL + LDL+ triglycerides/5= Total Cholesterol

55
Q

what is endocarditis? What the two types

A

microbial infection of the endocardium. 2types: rheumatic and infective endocarditis

56
Q

what are the S/S of endocarditis?

A

fever, heart murmur, petechiae, small painful nodules (Osler nodes) on the pads of fingers and toes, Hemorrhages with pale spots: Roth Spots, splinter hemorrhages: red-brown lines and streaks.

57
Q

who is at high risk for developing endocarditis?

A

prosthetic heart valves, tattoos, piercings, history of endocarditis, IV drug use, defective heart valves, congenital heart defects.

58
Q

who should receive prophylactic antibiotics, which procedures

A

patients with artificial heart valves or previous known endocarditis.
Procedures: dental work, tonsillectomy, adenoidectomy, respiratory procedures (bronch), and surgery involving skin or muscle tissue.

59
Q

what is mitral regurgitation? what does it sound like and where do you hear?

A

mitral regurgitation is a condition in which blood flows back from the left ventricle into the left atrium during SYSTOLE. the leaflets do not close due to becoming thickened and fibrosed.

High pitched blowing sound at apex of the heart

60
Q

What are the S/S of mitral regurgitation?

A

severe CHF, dyspnea, fatigue, weakness, palpitations, SOB with exertion, cough

61
Q

what are some causes of mitral regurgitation

A

SLE, infective endocarditis, cardiomyopathy, ischemic heart disease,

62
Q

How does mitral regurgitation lead to heart failure

A

blood regurgitates into atrium during systole,
backward flow from ventricle leads to decreased blood flow from lungs into atrium.
Lungs become congested, which adds strain to left ventricle. Increased blood volume from atrium fills ventricle, causing vent. hypertrophy, ventricle dilatation, and SHF developes

63
Q

what is mitral stenosis, what are the causes

A

a condition in which there is an obstruction of blood flow from the left atrium into the left ventricle

Causes: rheumatic endocarditis thickens mitral valve leaflets and chordae tendineae leaflets fuse together and obstruct blood flow into the ventricle

64
Q

how does mitral stenosis lead to heart failure

A

right ventricle hypertrophies, which leads to dilation and increased heart rate and shortened diastole. The time for forward flow is reduced, the blood backs into pulm. veins.

increased heart rate leads to decreased cardiac output, which leads to increase in pulm. pressure.

65
Q

what are the s/s of mitral stenosis

A

Mitral stenosis: DOE, prog. fatigue, decreased exercise tolerance, decreased cardiac output, dry cough, wheeze, hemoptysis, palpitations, orthopnea, PND, repeated resp. infections

66
Q

What is aortic regurgitation and its causes

A

aortic regurgitation is a condition in which blood flows back into the left ventricle from the aorta during DIASTOLE

Causes: infective or rheumatic endocarditis, congenital syphillis, dissected aneurysm, blunt chest trauma, surgical replacement of aortic valve.

67
Q

what are the S/S of aortic regurgitation and where is this heard?

A

forceful heart beat, (head and neck) marked arterial pulsations, visible palpations at carotid or temporal art. exertional dyspnea, fatigue, orthopnea, PND, widened pulse pressure, water-hammer pulse

heard: high pitched blowing noise, 3-4intercostal space at left sternal border DIASTOLIC murmur

68
Q

how does aortic regurgitation lead to HF

A

blood from aorta returns to left ventricle during diastole, in addition to blood normally delivered by left atrium. The left ventricle dilates and hypertrophies leading to increased SBP. Arteries compensate for increased pressure by REFLEX VASODILATION in which peripheral arterioles relax, peripheral resistance is decreased and decreased DBP.

69
Q

what is aortic stenosis and its causes

A

Aortic stenosis is the narrowing of the orifice between the left ventricle and aorta
Cause: often degenerative calcifications, atherosclerotic arterial disease, DM, hypercholesteremia, HTN, and low HDL, rheumatic endocarditis

70
Q

what are the S/S of aortic stenosis and where is this heard

A

Exertional dyspnea, increased pulm. ven. pressure, orthopnea, PND, pulm. edema, dizziness, syncope, angina pectoris, pulse pressure may be low
Heard: lough systolic murmur over aortic area and apex of the left ventricle. Low pitched crescendo-deccrescendo, rough, rasping, and vibration.

71
Q

how does aortic stenosis lead to heart failure

A

left ventricle overcomes obstruction to emptying by contracting more slowly and with increased power, which leads to increased pressure on the left ventricle, as a result the ventricular wall thickens.

NUR 323-Exam 2 (7 decks)

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