Test three Flashcards
hemodynamic hallmark of htn
persistently increased SVR
risks of htn
age
alc/tobacco
diet (sodium)
obesity
low socio-econ status
stress
men under 55; women over 64
black
sedentary
DM
high serum lipids
contraceptives
examples of 2ndary htn
coarctation of aorta
renal artery stenosis
Cushing
cirrhosis
neuro disorders, like brain injury
sleep apnea
pregnancy
clinical manifestation of htn
fatigue
activity intolerance
dizziness
palpitations
angina
dyspnea
complications of htn
target organ diseases affecting heart, brain, vasculature, kidney, and eyes
What does atherosclerosis in subclavian artery do?
causes false low read on side where narrowing occurs
Things to remember when taking BP
-feet on floor, sitting up
-take 2 readings on arm with highest BP, 1 min apart
-document if using forearm
-use proper cuff size
Nurse teaching ab htn care
Take BP at home! –> teach them how to and what is normal
-take it first thing in the morning and then at night b4 bed
Stress adherence to meds and decreasing risk factors
Beware of high-sodium antacids, appetite suppressants, and cold/sinus drugs
Avoid hot baths, lots of alc, and strenuous exercise w/in 3 hrs of taking vasodilation drugs
Drugs for htn
Adrenergic inhbiting agents - decrease SNS by working on peripherally and on vasomotor cento to inhibit NE release or block adrenergic receptors on blood vessels
ACE inhibitors - prevent AI to AII; reduce vasoconstriction and NA+/H2O retention
A-II receptor blockers- prevent A-II from binding to blood vessel walls
CCBs - increase Na excretion and cause vasodilation by stopping Ca+ from entering cells
Direct vasodilators- relax smooth muscle and reduce SVR
Diuretics - reduce plasma volume and reduce vascular response to catecholamines
htn drug side effects
-orthostatic htn
-dry mouth
-sex problems
-frequent voiding
*careful with NSAIDs
htn crisis manifestations
hypertensive encephalopathy
-headache, nausea/vomiting, seizures, confusion, coma, eyes
renal insufficiency
Cardiac decompensation
-MI, HF, pulmonary edema, chest pain, dyspnea
Aortic dissection
-chest and back pain, reduced/absent peripheral pulse
Road to CAD
endothelial injury + inflamation –> atherosclerosis –> CAD
Risks for CAD
age
men under 75; women over 75
whites
genes
lipids
Bp > 140/90
DM
tobacco
inactivity
waist over 40 or 35
BMI over 25
Possibly glucose, psych and hcy
CRP
protein made by the liver
nonspecific marker of inflammation
increased in ppl with CAD
a/w unstable plaqes and oxidation of LDL cholesterol
lipid measurements risks
cholesterol > 200
triglycerides > 150
LDL > 100
HDL < 60
Developmental stages of atherosclerosis
Endothelial injury
-htn, tobacco, hyperlipidemia, hcy, DM, infection, toxins
Fatty streak
-lipids infiltrate smooth muscle
Fibrous plaque
-collagen covers fatty streak
-lumen is narrowed
-blood flow is reduved
Complicated lesion
-plaque rupture
-thrombus formation (platelet adhesion)
-vessel occlusion
clinical manifestation of CAD
Angina - manifestation of reversible myocardial ischemia
dyspnea and orthopnea
edema
nocturea
cough
Drugs that restrict lipoprotein production
Statins - block synth of cholesterol and increase LDL receptors in liver (monitor liver enzymes and creatine kinase for toxisity and rhabdomyolysis)
Niacin - decreases synthesis of VLDL and LDL
(flushing (aspirin), pruritis, GI issues, orthohypo, hcy (folic acid))
Fibric acid derivatives - decrease hepatic synth of VLDL
(increases effects of warfin and antihyperglycemic drugs –> also statin myopathy)
Omega 3 fatty acids for super high triglycerides
Drugs that increase lipoprotein removal
Bile acid sequestrants - increases conversion of cholesterol to bile acids to reduce total cholesterol and LDL
(GI side effects; reduced absorption of other drugs)
injected PCSK9 inhibitors - lower LDL
(used with diet and max statin)
Drugs that decrease cholesterol absorption
Ezetimibe (Zetia)
decreases absorption of dietary and biliary cholseterol
-combine with statins
-don’t use if your livers fucked up
Antiplatelet therapy
low does aspirin or Clopidogrel
Prinzmetal’s angina
occurs at rest in response to coronary artery spasm
happens in ppl with migrains, Raynauds, smoking, or stress
a/w cold weather
Triggers for angina in those with chronic angina
physical exertion
temp extremes
stess
heavy meals
tobacco
stimulants (coke or amphetamines)
pathophysiology of chronic angina
occurs when myocardial cells become hypoxic w/in 10 s of coronary occlusion
lactic acid irritates myocardial nerve fibers and transmits pain messages
Characteristics of chronic angina pain
usually substernal, but can radiate
doesn’t change with position or breathing
lasts 5-15 mins
subsides when precipitating factor resolves
Diagnostic studies for chronic angina
12-lead ECG
Echo –> patient lies on left side
Exercise test (no caffeine 24 hrs b4; no smoking or exercise b4; stop if chest pain, wild VS change, or ECG change)
Nuclear cardiology - IV dipyridamole to mimic exercise, then inject isotope and do imaging –> observe for SOB, dizziness, nasea
Labs - troponin, CK-MB, lipids, CRP
Drug therapy for chronic angina
SA nitrates -dilate blood vessels (SL NGT can be used prophylactically)
Aspirin - inhibits cyclooxygenase to prevent clot formation
LA nitrates - reduces frequency of angina
ACE inhibitors - for those at high risk for cardiac event; can also reverse ventricular remodeling
BBs - for MI, LV dysfunction, or HTN –> decrease myocardial O2 demand
CCB - if can’t use BBs
Coronary catheter and angiography and PCI
-radiation and dye to view coronary arteries
-take baseline creatinine first to monitor renal func
-premedicate with corticosteroids if allergic to dye
-hydrate if CKD
-NPO 6-12 hrs
PCI
-balloon angioplasty
-don’t do if 3 vessel CAD and/or significant left main coronary artery disease
ACS parts
prolonged ischemia from decline of once stable atherosclerotic plaque
partial block = UA or NSTEMI
full block = STEMI
UA pain vs MI pain
UA
-new in onset
-occurs at rest
-worsens
MI
- Severe and persistent
- doesn’t get better with nitrate or rest
-heaviness, pressure, burning, crushing, tightness
-20+ mins
-might have epigastric pain that antacids won’t help
What to do with patient on the way to the hospital and once you get there?
-SL NTG and chewable aspirin
-morphine if they get to hospital w/o having these things
Start to consider coronary angiography and PCI
-ECG –> if STEMI, PCI w/in 90 mins
-thrombolytic if no cath lab (w/in 30 mins of arrival)
PCI
first, cardiac catheterization to locate blockages, see collateral circulation, and evaluate LV function
Put BMS or DES into blocked artery
If bad LV function, possibly IABP and/or inotrope
**very few need CABG
Thrombolytic Therapy
-for ppl with chest pain less than 12 or 24 hrs and STEMI
-GET BASELINE LABS and start 2-3 IV lines
-meds can be given in one IV bolus or over 30-90 mins
-serum cardiac biomarkers rapidly rise 3 hrs after
-start heparin bc risk of re-clotting
*Now you can move them to PCI facility
*complications = bleeding –> apply pressure or ice
absolute contraindications to thrombolytic therapy
-intracranial hemorrhage ever
-known structural/vascular abnormality
-intracranial neoplasm
-stroke in past 3 months
-recent head or facial trauma
-recent intracranial or intraspinal surgery
-severe uncontrolled htn
-active bleeding
-suspected aortic dissection
Surgery options for ACS
CABG
-requires sternotomy and CPB
-for left coronary artery, 3-vessel disease, DM, CKD, LV dysfunc
MIDCAB –> no sternotomy or CPB
-IMA is sutured to left anterior descending or right coronary artery
OFCAB
-sternotomy, but no CPB
-done on beating heart
-less blood loss, renal dysfunc, postop afib, and neuro issues
Transmyocardial laser revascularization
-for ppl with advanced CAD who aren’t candidates for traditional CABG
-laser makes channels in heart to let blood flow to ischemic areas
Drug therapy after an MI
IV nitroglycerin
aspirin
BBs
anticoagulants (LMWH or UH)
glycoprotein IIb/IIIa inhibitors if PCI anticipated
ACE-i sometimes; CCBs if issues w/ BBs
Nursing interventions for ACS
- Pain assessment using PQRST
- position patient upright and give O2 NO MATTER WHAT
- Establish IV line
- give NG, MORPHINE, and O2 for chest pein
- maintain ECG monitoring (PVC and Vfib after MI are common)
- assess vitals frequently along with I and O
**look for heart failure: dyspnea, tachycardia, pulmonary congestion, distended neck veins
Phases of ACS recovery
- hospitalization
-msy or may not be able to ambulate –> depends on severity
-start with sitting up, ROM, self care, then work on walking
-focus on pain, anxiety, dysrhythmias - Early recovery
-2-12 weeks in outpatient place
-increase activity
-teach ab risk factor reduction - Late recovery
- physical activity program
-therapeutic lifestyle changes
-some med supervision
