cardio (class 7) Flashcards
hypertension
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
primary hypertension
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.
hypertesnions s/s
silent killer-asymptomatic. HA.
secondary symptoms fatigue, decrease activity tolerance, dizziness, palpitations, angina, SOB.
HTN crisis: nosebleeds, HA, dizziness, dyspnea, anxiety.
secondary hypertension
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
diagnostic tests HTN
urinalysis, CBC, BUN, creat clearance, glomerular filtration rate, electrolytes, glucose & Hgb A1C, lipid profile, ECG.
complications HTN
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.
antihypertensive meds
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.
CAD
disease is leading cause of death in US. can lead to MI & contribute to heart failure.
atherosclerosis
CAD major contributing factors
NONMODIFIABLE: age, gender, ethnicity, family hx, genetic inheritance.
MODIFIABLE: elevated serum lipids. elevated BP, tobacco use, obesity, DM, HTN, metabolic syndrome.
Angina
clinical manifestation of cardiac ischemia RT increase oxygen demand and/or decrease o2 supply.
C/O pain, pressure, heavy, squeezing, epigastric burning, can radiate.
chronic stable angina
intermittent predictable pain/pressure relived when precipitating factor removed, med controlled.
silent ischemia
more common in DM
prinzmetal’s angina
at rest, pain RT coronary artery spasm
unstable angina
emergency, new or worse pain, pain at rest, or with minimal exertion, can indicate impending MI.
diagnostic tests CAD & angina
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.
P wave
depolarization of the atria
QRS complex
depolarization of the ventricles
T wave
repolarization of the ventricles
Heart failure
chronic, progressive clinical syndrome resulting from any structural or functional disorder that impairs the ability of the heart to fill with or eject blood.
causes of HF
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
acute HF
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.
chronic HF
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
systolic failure
decreased pumping function.
caused by: damage to cardiac muscle, increased afterload, abnormalites(valve dysfunction)
diastolic failure
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
Left HF
causes CAD & HTN.
s/s pulmonary congestions SOB, cough, orthopnea, crackles, murmur. decreased output fatigue, dizziness, syncope.
RIGHT HF
causes: pulmonary disease, LHF.
s/s RT venous pressure in systemic circulation=edema, ascites, JVD.
s/s HF
fatigue, dyspnea, orthopnea, tachycardia, edema, nocturia, skin changes, behavioral changes, chest pain, weight changes.
diagnostics HF
ABGs, B-type natriuretic peptide, liver function tests, chest xray, 12 lead EKG, nuclear imaging studies: thallium scan, echocardiography, exercise stress test, cardiac catheterization.
BNP: B-type natriuretic peptide:
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
medications for heart failure
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.
anemia
results in reduced oxygen carrying capacity of blood.
anemia s/s
depend on degree & if onset is gradual or acute and are RT tissue hypoxia.
increase HR, increase R, angina, fatigue, SOB, pallor, HA, dizziness
anemia causes
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.
nutritional anemias
iron deficiency: most common, Fe supply inadequate. low RBCs, microcytic, hypochromic, malformed RBS.
s/s spoon shaped nails, cheilosis, smooth, sore tongue, pica.
vitamin B12 deficiency:
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.
Folic acid deficiency
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
megaloblastic anemia
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
polycythemia
increased production RBCs. Impaired circulation due to increased blood viscosity.
polycythemia vera
chronic chromosomal mutation with increase RBCs, WBCs and platelets. uncommon (HCT > 55%)
secondary polycythemia
hypoxia driven increase oxygen demand (high altitudes, smoking, COPD)= increase EPO most common.
hypoxia independent-malignant or benign tumors.
teach primary polycythemia
not preventable. perform phlebotomy. monitor I&O hydration. prevent stasis & DVT exercise ASA. meds (leukemia risk)
secondary polycythemia
controlling chronic pulmonary disease. smoking cessation. avoid high altitudes. monitor I&O hydration. prevent stasis & DVT.
peripheral arter disease pathophysiology
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
PAD risk factors
4 most significant:
cigarette smoking, hyperlipidemia, hypertension, diabetes.
other: obesity, hypertriglyceridemia, family hx, sedentary lifestyle, stress.
intermittent claudication
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.
PAD diagnositc testing
doppler utrasound. angiography to detect the location and extent of the disease process. MRA is alternative to angiography
PAD treatment
smoking cessation.
medications: antiplatelet agents: aspirin, plavix, ticlid,. ace inhibitors. trental, pletal.
risk factor modification: control DM, HTN, wt, exercise therapy, surgical therapy.
Buerger’s disease
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.
Raynaud’s
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.
Raynaud’s assessment:
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.
raynauds diagnosis
persistent symptoms, HX.
raynauds treatment
prevention: keep warm, wear gloves, avoid injury, increase perfusion, smoking cessation, stress management.
medication: calcium channel blockers, vasodilators, alpha blockers.
chronic venous insufficiency s/s
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
care of venous vascular disease
compression, moist environment wound dressings, nutritional evaluation & education, activity: avoid prolonged standing/sitting or crossing legs. comparison of arterial and venous ulcers.
arterial disease
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
venous disease
pulses +, cap refill < 3 sec, ulcers, pain dull ache heaviness, skin brown discoloration, thick, hardened, indurated, warm, itchy
