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nursing 141 > cardio (class 7) > Flashcards

cardio (class 7) Flashcards

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1
Q

hypertension

A

SBP > 140 DBP > 90.
prehypertension 120-139 & 80-89.

SBP-max pressure on walls of arteries while heart pumping.

DBP- min pressure between beats while heart filling

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2
Q

primary hypertension

A

without an identified cause; 90-95% all cases.

factors: age, alcohol, cigarette smoking, DM, elevated serum lipids, excess dietary Na, low K, Mg, Ca, gender, family hx, ethnicity, obesity, sedentary lifestyle, socioeconomic status, stress.

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3
Q

hypertesnions s/s

A

silent killer-asymptomatic. HA.
secondary symptoms fatigue, decrease activity tolerance, dizziness, palpitations, angina, SOB.
HTN crisis: nosebleeds, HA, dizziness, dyspnea, anxiety.

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4
Q

secondary hypertension

A

5-10% cases. elevated BP with specific identifiable cause. suddenly develop high BP can be severe.

causes: renal disease, cirrhosis, narrowing of aorta, endocrine disorders, meds, neurologic disorders, PIH, sleep apnea, medications.

clinical findings: unexplainged hypokalemia, abdominal bruit, variable BP with hx tachycardia, renal disease.

treatment: aimed at underlying cause

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5
Q

diagnostic tests HTN

A

urinalysis, CBC, BUN, creat clearance, glomerular filtration rate, electrolytes, glucose & Hgb A1C, lipid profile, ECG.

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6
Q

complications HTN

A

heart disease: coronary artery disease- artherosclerosis. left ventricular hypertrophy heart failure & dysrhythmia.

cerebrovascular disease: cerebral artherosclerosis & stroke, carotid atherosclerosis=TIA and stroke.

Peripheral vascular disease: speeds up peripheral atherosclerosis.

nephrosclerosis ischemic damage.

retinal damage.

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7
Q

antihypertensive meds

A

goal BP < 140/90 ideal 120/80.

diuretics; thiazide, loop diuretics, k+ sparring diueretics.

beta-andrenergic blockers.

centrally acting sympatholyics.

vasodilators

angiotensin-converting enzyme ACE inhibitors.

angiotensin II recetpros blockers ARBS.

calcium channel blockers.

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8
Q

CAD

A

disease is leading cause of death in US. can lead to MI & contribute to heart failure.

atherosclerosis

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9
Q

CAD major contributing factors

A

NONMODIFIABLE: age, gender, ethnicity, family hx, genetic inheritance.
MODIFIABLE: elevated serum lipids. elevated BP, tobacco use, obesity, DM, HTN, metabolic syndrome.

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10
Q

Angina

A

clinical manifestation of cardiac ischemia RT increase oxygen demand and/or decrease o2 supply.
C/O pain, pressure, heavy, squeezing, epigastric burning, can radiate.

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11
Q

chronic stable angina

A

intermittent predictable pain/pressure relived when precipitating factor removed, med controlled.

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12
Q

silent ischemia

A

more common in DM

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13
Q

prinzmetal’s angina

A

at rest, pain RT coronary artery spasm

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14
Q

unstable angina

A

emergency, new or worse pain, pain at rest, or with minimal exertion, can indicate impending MI.

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15
Q

diagnostic tests CAD & angina

A

labs: serum lipids, cardiac enzymes.
chest xray: cardiac contours, heart size, fluids around heart. electrocardiogram: 12 lead assess the hearts electrical function/conduction, thythm, tele.
stress test.
cardiac cath.

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16
Q

P wave

A

depolarization of the atria

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17
Q

QRS complex

A

depolarization of the ventricles

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18
Q

T wave

A

repolarization of the ventricles

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19
Q

Heart failure

A

chronic, progressive clinical syndrome resulting from any structural or functional disorder that impairs the ability of the heart to fill with or eject blood.

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20
Q

causes of HF

A

primary: CAD, MI, HTN, rheumatic heart disease, congenital defects, pulmonary hypertension, cardiomyopathy, hyperthyroidism, valve disorders, myocarditis.
precipitating: anemia, infection, hypothyroid, dysrhythmias, bacterial endocarditis, pulmonary disease, nutritional deficiencies, hypervolemia

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21
Q

acute HF

A

pulmonary edema, interstitial edema.
s/s tachypnea > 30 RR, anxious, pale, clammy, & cold skin, dyspnea, respiratory distress, frothy, blood-tinged sputum, rales/rhonchi/wheeze, often fluid overload.

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22
Q

chronic HF

A

s/s depend on pt age & extent of underlying CV disease.

FACES
f-fatigue
a-activity limitation
c-cough/chest congestion
e-edema
s-SOB
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23
Q

systolic failure

A

decreased pumping function.

caused by: damage to cardiac muscle, increased afterload, abnormalites(valve dysfunction)

24
Q

diastolic failure

A

inability of ventricles to relax & fill.

caused by: stiff ventrivles
s/s rt congestion behind ventricle & high pressure.
dx- pulmonary congestion, pulmonary HTN, ventricular hypertrophy with a normal EF.
often mixed systolic & diastolic

25
Q

Left HF

A

causes CAD & HTN.

s/s pulmonary congestions SOB, cough, orthopnea, crackles, murmur. decreased output fatigue, dizziness, syncope.

26
Q

RIGHT HF

A

causes: pulmonary disease, LHF.

s/s RT venous pressure in systemic circulation=edema, ascites, JVD.

27
Q

s/s HF

A

fatigue, dyspnea, orthopnea, tachycardia, edema, nocturia, skin changes, behavioral changes, chest pain, weight changes.

28
Q

diagnostics HF

A

ABGs, B-type natriuretic peptide, liver function tests, chest xray, 12 lead EKG, nuclear imaging studies: thallium scan, echocardiography, exercise stress test, cardiac catheterization.

29
Q

BNP: B-type natriuretic peptide:

A

protective mechanism, released by the myocytes of the ventricles in response to excess stretch created by volume overload.

BNP levels correlated with the degree of left ventricular dysfunction

30
Q

medications for heart failure

A

diueretics- for volume excess.

RAAS inhibitors- decrease workload. ACE/ARB, aldosterone antagonists, direct renin inhbitors.

vasodilators

beta adrenergic blockers.

neprilysin inhibitors-entresto

positive inotropes- digoxin

antidysrhythmics

anticoagulants if afib.

31
Q

anemia

A

results in reduced oxygen carrying capacity of blood.

32
Q

anemia s/s

A

depend on degree & if onset is gradual or acute and are RT tissue hypoxia.
increase HR, increase R, angina, fatigue, SOB, pallor, HA, dizziness

33
Q

anemia causes

A

decreased RBC production or imaired HgB synthesis.
Altered HgB synthesis: iron dificiency, chronic inflammation. Altered DNA synthesis: B12 or folic acid deficiency. bone marrow failure.

increased RBC loss/destruction acute or chronic blood loss, increased hemolysis.

34
Q

nutritional anemias

A

iron deficiency: most common, Fe supply inadequate. low RBCs, microcytic, hypochromic, malformed RBS.

s/s spoon shaped nails, cheilosis, smooth, sore tongue, pica.

35
Q

vitamin B12 deficiency:

A

B12 animal sources. unable to absord due to lack of intinsic factor secreted by gastric mucosa. other absorption problems (gastic bypass, ETOH, chronic gastritis) dietary defiecincy in vegans.

s/s pallor, slight jaundice, weakness, diarrhea, sore beefy red tongue, also neuro symptoms with deficiency.

36
Q

Folic acid deficiency

A

green, leafy vegs, fruits, cereals, and meats, intestinal absorption.
RBCS megaloblastic cells. inadequate intake in chronically undernourished elderly.
impaired metabolism: ETOH suppresses folate metabolism, some meds.
impaired absorption: celiac, med-related
increased needs: pregnancy, dialysis, hemolytic anemais.

S/S gradual onset of pallor, weakness, glossitis

37
Q

megaloblastic anemia

A

clincal s/s: beefy red tongue, sore, anorexia, nausea, vomiting, abd pain, weakness, tachycardia, B12 only: neuro: parasthesias; gait ataxia; impaired thought.

labs: cobalamin, folate leves, HgB/Hct, MCV, test for IF antibodies.

Treatment: supplements

38
Q

polycythemia

A

increased production RBCs. Impaired circulation due to increased blood viscosity.

39
Q

polycythemia vera

A

chronic chromosomal mutation with increase RBCs, WBCs and platelets. uncommon (HCT > 55%)

40
Q

secondary polycythemia

A

hypoxia driven increase oxygen demand (high altitudes, smoking, COPD)= increase EPO most common.

hypoxia independent-malignant or benign tumors.

41
Q

teach primary polycythemia

A

not preventable. perform phlebotomy. monitor I&O hydration. prevent stasis & DVT exercise ASA. meds (leukemia risk)

42
Q

secondary polycythemia

A

controlling chronic pulmonary disease. smoking cessation. avoid high altitudes. monitor I&O hydration. prevent stasis & DVT.

43
Q

peripheral arter disease pathophysiology

A

progressive thickening of walls, narrowing lumen, and decrease elasticity of arteries of the neck, abdomen, and extremities.

atherosclerosis is major cause.

4-5 times the risk of dying from MI/stroke.
strongly RT other CVD

44
Q

PAD risk factors

A

4 most significant:
cigarette smoking, hyperlipidemia, hypertension, diabetes.

other: obesity, hypertriglyceridemia, family hx, sedentary lifestyle, stress.

45
Q

intermittent claudication

A

ischemic muscle ache or pain precipiated by exercises which resolves in 10 mins or less with rest & reproducible. progress slowly atrophy of skin. delay healing of wounds lower extremities. amputation of extremity w gangrene.

46
Q

PAD diagnositc testing

A

doppler utrasound. angiography to detect the location and extent of the disease process. MRA is alternative to angiography

47
Q

PAD treatment

A

smoking cessation.
medications: antiplatelet agents: aspirin, plavix, ticlid,. ace inhibitors. trental, pletal.

risk factor modification: control DM, HTN, wt, exercise therapy, surgical therapy.

48
Q

Buerger’s disease

A

thrombosis & fibrosis occur inside the vessel. segmental: isolated UE, LE, single leg, foot, or hand. inflammatory cells invade artery wall, thrombus formation & vasospasm. progressive disease leads to scarring & collateral involvement.

s/s: pain, skin changes overtime, decrease distal pulses, ulcers.

incidence: smokers, men < 40.
tx: smoking cessation, foot care, prevent vasoconstriction, exercise, meds for symptomatic relief, surgery.

49
Q

Raynaud’s

A

episodic vasospastic disorder of small cutaneous arteries of fingers and toes.
disease: no identifiable cause.
phenomenon: secondary to disease or exposure.
common in young women 15-45.

50
Q

Raynaud’s assessment:

A

fingers, toes, ears, and nose change colors. patient describes coldness, numbness, followed by throbbing, aching, tingling, and swelling.

episodes lasts minutes to hours

precipitated by cold, emotional upsets, caffeine, tobacco use.

51
Q

raynauds diagnosis

A

persistent symptoms, HX.

52
Q

raynauds treatment

A

prevention: keep warm, wear gloves, avoid injury, increase perfusion, smoking cessation, stress management.
medication: calcium channel blockers, vasodilators, alpha blockers.

53
Q

chronic venous insufficiency s/s

A

brawny, brownish, leathery fragile skin, cyanosis if dependent, persistent edema in LEs, statis dematitis-itching with standing, ulcers above medial malleolus, pain increase if dependent, recurrent ulcerations & cellulitis

54
Q

care of venous vascular disease

A

compression, moist environment wound dressings, nutritional evaluation & education, activity: avoid prolonged standing/sitting or crossing legs. comparison of arterial and venous ulcers.

55
Q

arterial disease

A

pulses: dim or absent. cap refill > 3 secs, ulcers, pain: intermittent claudication, skin: rubor, pale elevated thin, shiny, taunt, hairless, cooler gradient down leg, thick toenails

56
Q

venous disease

A

pulses +, cap refill < 3 sec, ulcers, pain dull ache heaviness, skin brown discoloration, thick, hardened, indurated, warm, itchy

nursing 141 (18 decks)

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