Cardiovascular Flashcards
HTN potential complications
heart disease, kidney damage, stroke; causes end-organ damage
HTN 3 classifications
primary- unknown cause, secondary- caused by another factor and need to target underlying cause, malignant- HTN crisis
when classifying HTN
use the higher of either SBP or DBP out of range
prior to administering medications for HTN…
encourage lifestyle modifications for 1-3 months like reducing Na Sugar Alcohol fat, exercising, reduce stress
causes of primary HTN
aging, family hx, Af-Am, sedentary lifestyle, smoking, alcohol, HLD
causes of secondary HTN
resulting from other conditions; cardiovascular disorders, renal disease, endocrine diseases, pregnancy, meds, sleep apnea
assessing HTN
History: fam Hx, current meds, perception of disease; Signs/symptoms: dietary pattern, headache, visual changes, neuro assess, lab tests; Physical Exam: obtain 2 BP on both arms supine and standing, compare to prior, weight, JVD, increased HR, dysrhythmias, S3, CXR shows enlarged heart
lab tests for HTN
cardiac biomarkers, chem panel for electrolytes and liver, assess for end-organ damage, hypernatremia
common end–organ damage resulting from HTN
cerebrovascular damage, vasculopathy, heart disease, nephropathy
cerebrovascular damage resulting from HTN
acute HTN encephalopathy (confusion), stroke, vascular dementia, retinopathy (can cause retinal detachment
vasculopathy from HTN
atherosclerosis, aortic aneurysm
heart disease from HTN
left ventricular hypertrophy, CAD, MI, HF, atrial fibrillation
nephropathy from HTN
proteinuria, renal failure
non-pharmacological interventions for HTN
weight reduction, dietary sodium restriction (2g/day), reduce alcohol and caffeine, exercise, smoking cessation, stress reduction, monitor BP often
older adult considerations
isolated systolic HTN d/t age related loss of elasticity to carotid and aorta, difficult to treat d/t low DBP, medication issues because of failure to remember/polypharm/expensive/increased incidences of orthostatic hypotension
why does orthostatic hypotension occur
when standing up, all blood flows out of head due to gravity causing drop in BP
HTN urgency
BP >180/120, no evidence of end-organ damage, pharmacologic interventions are used to normalize BP within 24-48 hours
coronary atherosclerosis
fatty plaque accumulates on artery walls blocking off/narrowing vessels reducing blood flow to myocardium; plaques can rupture; symptoms arise d/t enough blockage to cause ischemia
when do symptoms of cardiac ischemia occur
left main artery reduced by 50%, any vessel reduced by 75%
coronary artery disease
narrowing/obstruction of 1 or more coronary arteries d/t atherosclerosis; causes inadequate perfusion and oxygenation of myocardial tissue
coronary artery disease can lead to
HTN, angina, dysrhythmias, MI, heart failure, death
collateral circulation
vascular system is generated around the obstruction/plaque to bypass; takes about 10 years to form
modifiable risk factors for CAD
BMI > 30, DM, HTN, alcohol use, high hDL and low LDL, tobacco use
non-modifiable risk factors for CAD
65+, Fam HX or genetic predisposition
LDL cholesterol
brings plaques into the arteries
HDL cholesterol
removes lipids from the arteries
CAD manifestations
early is asymptomatic, chest pain, dyspnea, syncope, cough/hemoptysis, palpitations, excessive fatigue
diagnosing CAD
EKG: ischemia = ST depression, infarction = ST elevation; Lipid: cholesterol is elevated (LDL vs. HDL), stress tests, Cardiac cath.
cardiac catheterization
angiogram used to diagnose CAD; injection of dye into arteries to identify atherosclerotic plaques blocking off blood flow (plaques do not light up)
treatment of CAD
tobacco cessation, manage HTN, low cal sodium cholesterol fat and increased fiber diet, control DM, stress reduction, alcohol reduction, pharmacological management
angina pectoris
chest pain d/t ischemia from lack of oxygen; can be caused by obstruction or spasm
variant angina (prinzmetal)
caused by coronary vasospasm commonly caused by smoking or cocaine
symptoms of prinzmetal angina
occurs at rest without provocation, triggered by smoking, transient ST elevation during pain, associated with AV block or ventricular arrythmias, occurs with or without CAD
treatment of prinzmetal angina
smoking cessation, calcium channel blockers
stable angina
caused by myocardial atherosclerosis
stable angina symptoms
caused by exertion and usually last 5-10 minutes, aggravated by cold exposure or stress, stable onset duration severity and relieving factors, relieved by rest
stable angina treatment
nitrates, beta blockers, calcium channel blockers, aspirin
unstable angina (pre-infarction)
due to ruptures or thickened plaque with platelet and fibrin thrombus
unstable angina symptoms
angina of increasing intensity frequency or duration, occurs at rest or with minimal activity, lasts > 15 min, pain unresponsive to NTG
unstable angina treatment
oxygen, pain meds, nitrates, beta blocker, clopidogrel, aspirin (antiplatelet), statins, tPA (dissolves clot)
angina manifestations
pain, dyspnea, pallor, sweating, dizziness/syncope, palpitations/tachycardia, HTN, digestive disturbances
tests to diagnose angina
EKG (normal in stable angina), cardiac enzymes, stress test, cardiac catheterization
acute management of angina
pain assess and management, IV access, O2, continuous vitals, EKG q10min, NTG, rest semi-fowler, reduce anxiety
long term management of angina
lifestyle modifications similar to CAD, medication adherence, understanding the disease
medications for angina
nitrates, beta blockers, calcium channel blockers, antiplatelet therapy
older adult cardiac considerations
diminshed pain that may effect symptoms, recognize chest pain like symptoms such as weakness, indigestion, fatigue, pharmacologic testing for operation clearance, monitor med doses cautiously
Percutaneous coronary intervention (PCI)
balloon angioplasty- balloon expands inside artery to open up plaque; intracoronary stenting- can be done with or without balloon pre-dilation (mesh to hold artery open); atherectomy- removing plaque
coronary artery bypass graft (CABG)
taking artery from one spot of body and placing it in different area to bypass plaque or obstruction
cardiac procedures
cardiac catheterization, PCI, CABG
peripheral arterial disease
reduced blood flow to peripheral vessels leading to decreased oxygenation; results in oxygen demand exceeding the supply and can lead to ischemia then necrosis (then gangrene)
gangrene
wide spread tissue death
what causes decreased blood flow in PAD
atherosclerotic plaque leading to narrowing of vessels
symptoms of peripheral arterial disease (PAD)
ischemic ulcers, diminished/absent pulses, sharp stabbing pain, cramping (claudication), loss of hair, dry scaly skin, cold gray/blue skin, dependent rubor (reddish-gray) skin
venous insufficiency due to
prolonged venous HTN that stretched and damaged valves decreasing blood flow back toward heart
symptoms of venous insufficiency
venous congestion/stasis, edema, brown discoloration along ankles up to calf, stasis ulcers, cellulitis, pulses present
if pulses are diminished in venous insufficiency, then due to…
edema
ankle brachia index
test used to determine if individual has peripheral arterial disease; if brachial pressure > ankle pressure = PAD; value should be about 1
ankle-brachial index formula
ankle pressure/brachial prsssure = 1; if lower than 1 = PAD
nursing interventions of PAD
refrain from elevating above heart, walk until claudication (cramp) then rest then repeat, avoid crossing legs, avoid caffeine and tobaccos,
PAD treatment medications
antiplatelet therapy: ASA, clopidogrel; phosphdiesterase III inhibitor: cilstazol; HMG CoA reductase inhibitors: high dose statins
PAD treatment endovascular
angioplasty with/without stent; balloon; atherectomy
PAD surgical management
bypass grafts
venous insufficiency nursing interventions
compression stockings, avoiding prolonged standing, avoid constructive clothing, elevate legs above heart (10-20 minutes every few hours); sequential compression device; if user present the compression stocking over dressing
arterial ulcer
punched out, deep, round shape, thin shiny skin, dry; d/t inadequate oxygen supply
venous ulcer
leg swelling, dark red purple brown hardened skin, torn skin near ankle, scaling and redness around wound, usually wet; d/t pooling of deoxygenated blood
treatment of ulcers
pharmacological: anti-septic, antibiotic; compression; cleansing and debriding, topical therapy: petroleum jelly to surround tissue; wound dressing (semi/occlusive to avoid fluid loss); skin graft; hyperbaric chamber; negative pressure (wound vac.)
nursing intervention for ulcer
restore skin, improve mobility, promote adequate nutrition (high protein, VitC, VitA, iron, zinc)
lymphangitis
acute inflammation of lymphatic channels; red streak up arm
lymphadenitis
lymph node infected; large red and tender; can become necrotic; present in groin, axilla, cervical (neck)
lymphedema
can be primary (no known cause) or secondary (d/t increased lymph); increase in lymph d/t obstruction of vessel
treatment of lymph edema
ambulatory-compression stockings, manual drainiage, physiotherapy, skin care
types of heart failure
left ventricular failure (most common), right ventricular failure (often result of left vent. failure), systolic failure (HFrEF), diastolic failure (HFpEF)
systolic heart failure (HFrEF) vs. diastolic failure (HFpEF)
systolic failure is heart failure with reduced ejection fraction meaning problem with contraction and ejection; diastolic failure is heart failure with preserved ejection fraction meaning problem with relaxing and filling
systolic HF
decreased ventricular output d/t decreased contraction; low output causes baroreceptors to stim. SNS to vasoconstrict and increase contraction (increase HR and contractility); heart tries to compensate with natriuretic peptides (diurese and vasodilate)
end result of sytolic HF
workload of heart increases, contractility decreases, increased end diastolic blood volume, then ventricular dilation
diastolic HF
cardiac cells die during systolic HF and muscle becomes fibrotic which can lead to diastolic HF (decreases stretch and filling); stiff ventricles resist filling causing less blood in ventricles and decreases CO; low CO causes increased workload for heart causing HF to become worse
in simple terms, systolic or HFrEF…
impairs contractility leading to low ejection fraction from weak and thin heart muscle
in simple terms diastolic or HFpEF…
impairs filling and relaxation of heart due to stiff and thick heart muscle; diastolic has normal EF
diagnosing HF
history and physical, echocardiogram to show EF and ventricle size, chest Xray to show cardiomegaly, EKG, labs- cardiac enzymes/BNP, stress test, catheterization
congestive heart failure
pulmonary congestion due to diastolic heart failure; increase pressure of pulmonary venous blood volume forcing fluid into pulmonary tissue and impairing gas exchange
manifestations of congestive HF
dyspnea, crackles, low O2 sat, S3 heart sound (ventricular gallop = extra sound)
managing HF
avoid caffeine, low soidum/low fat/low cholesterol diet, flluid restriction, potassium rock foods if taking K wasting diuretic, balance activity and rest, monitor weight gain and signs of fluid retention, lifestyle change, medis (ACEI, diuretics, digoxin, BB)
right sided HF manifestations
peripheral venous congestion: JVD, hepatomegaly, cardiac cirrhosis, renal failure, peripheral edema, ascites; commonly caused by cor pulmonale or Left sided heart failure
left sided HF manifestations
increased venous pulmonary pressure: pulmonary edema (dyspnea, orthopnea, paroxysmal nocturnal dyspnea), hypoxic ischemia, encephalopathy
EF range (normal)
echocardiogram shows around 55-70%
signs/symptoms of low cardiac output
decreased activity tolerance, muscle wasting/weight loss, weakness, anorexia/nausea, lightheadedness, AMS/confusion, tachycardia at rest, oliguria, pallor/cyanosis,
gerontologic cardiac considerstions
may have atypical signs such as fatigue, weakness, somnolence; have decreased renal function
risk factors for developing HF
old age, cigarette smoking, obesity, poorly managed diabetes, metabolic syndromes, CKD, HTN, CAD
