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99 Cards in this Set
- Front
- Back
what is normal blood pressure
1 |
systolic less than 120
diastolic less than 80 |
|
what is pre-hypertension
1 |
systolic 120-139
diastolic 80-89 treatment: lifestyle changes |
|
what is stage one hypertension
1 |
systolic 140-159
diastolic 90-99 treatment: medications |
|
what is stage two hypertension
1 |
systolic greater than 160
diastolic greater than 100 treatment: medications |
|
why is diabetes a risk factor for
hypertension 1 |
diabetes do not process fats
correctly this leads to atherosclerosis |
|
why is alcohol a risk for hypertension
1 |
alcohol causes constriction of blood
vessels |
|
how is stress a risk factor for
hypertension 1 |
releases catecholamines
epinephrine and norepinephrine makes heart beat faster blood vessels constrict and raise blood pressure |
|
what is the diagnosis of
hypertension based on 1 |
elevated reading of 3 times or more
over a period of a week or longer |
|
what is the presentation of hypertension
1 |
asymptomatic
may complain of HA or dizziness or blurry vision presents as effects on target organs |
|
what is the target organs presentation in hypertension
1 |
CAD
CVA-HTN is the number one risk factor for CVA PVD CRF blindness-eyes only place can visual damage to blood vessels damage is irreversible |
|
what should be the foundation
of treatment for hypertension 1 |
lifestyle modifications
|
|
what are the classifications of drugs used for hypertension
1 |
beta blocker-lol
ace inhibitor-pril angiotensin receptor antagonist arbs-sartan calcium channel blockers direct vasodilators diuretics |
|
what is the diuretic drug of choice
for hypertension 1 |
hydrochlorothiazide-HCT
|
|
what is the mechanism of
action of diuretics in hypertension 1 |
inhibits kidneys uptake of water lowering
blood volume decreases blood return to heart leads to decreased cardiac output |
|
what are the three groups of diuretics
1 |
thiazide diuretics hydrochlorothiazide
loop diuretics furosemide potassium-sparing amiloride |
|
what are some complications of diuretics
1 |
diuretics can raise plasma triglyceride
and low-density lipoprotein cholesterol levels monitor your patient’s lipid levels thiazide diuretics can also increase blood glucose levels used cautiously in patients with diabetes |
|
what is the mechanism of action
of adrenergic inhibitors beta blockers 1 |
blocks beta stimulation
decreases the workload of heart by dilating blood vessels decrease O2 demand lowers heart rate |
|
what are some complications of beta blockers
1 |
nonselective beta-blockers depress the tachycardia
associated with hypoglycemia use a cardioselective betablocker in patients with diabetes can increase serum triglyceride levels and decrease high density lipoprotein (HDL) cholesterol levels. worsen depression and cause sexual dysfunction |
|
what is the mechanism of action
of direct vasodilators 1 |
relaxes vascular smooth muscle and dilates vessels
decreases peripheral resistance lowers blood pressure |
|
what is an example of a direct vasodilators
1 |
Hydralazine (Apresoline)
|
|
what is the mechanism of action
of ace inhibitors 1 |
blocks conversion angiotension I
to angiotension II a potent vasoconstrictor leads to dilation of blood vessels |
|
what is a major side effect that
would cause a pt to be taken off an ace inhibitor 1 |
constant cough
|
|
what is another function of ace inhibitors
1 |
they preserve renal function
first-line treatment for patients with hypertension diabetes heart failure impaired renal function |
|
what drugs should diabetics take for their
renal protective qualities 1 |
ACE inhibitors
|
|
what is the mechanism of action
for calcuim channel blockers 1 |
blocks calcium going into cell
to decrease excitement of cell to make heart beat slower all CCB lowers blood pressure they take the workload off the heart by relaxing muscle and taking away O2 demand |
|
what two calcium channel
blockers also lower heart rate in addition to lowering blood pressure 1 |
Cardizem
Verapamil |
|
what is precaution for calcuim channel blocker
1 |
used cautiously in a patient with heart failure
myocardial contractility is already compromised |
|
what is mechanism of action for angiotensin receptor antagonist-arbs
1 |
blocks receptor sites for angiotension II,
so can’t vasoconstrict used more often because has less side effects |
|
what are lifestyle changes for HTN
1 |
reduce salt intake
exercise regularly limit alcohol intake adopt the DASH diet to decrease cholesterol intake diet is rich in fruits, vegetables, and low-fat dairy products (reduced saturated and total fat content) stop smoking |
|
how will a patient with chronic kidney disease
will benefit from an ACE or ARB 1 |
these drugs have been
shown to slow the progression of renal disease |
|
how do you evaluate the classifications of drugs
1 |
did the drugs get the outcome they were given for
ie. HCT-lower blood pressure beta blocker-prevent chest pain/angina |
|
how do you decrease blood pressure in
a hypertensive crisis 1 |
reduce BP by 25% in first hour
next 2-6 hours target BP 160/100: stage two HTN next 24-28 hrs gradual reduction |
|
what can too rapid decrease of blood pressure in hypertensive
crisis lead to 1 |
decreased cerebral coronary
decreased renal perfusion ie stroke MI renal failure |
|
what are some IV vasodilators
1 |
Nitroprusside (Nipride) 2 cc/hr
IV NTG (Tridil) IV Hydralazine (Apresoline)-push slowly |
|
what are some IV Beta Blockers
|
labetalol (Normodyne)
esmolol (Brevibloc) |
|
what are some IV Ace Inhibitors
1 |
enalapril (Vasotec)-push
|
|
how do you help pt to manage side effects of
antihypertensive drugs 1 |
gum and hard candy for dry mouth to prevent
increase drinking slow position changes for orthostatic hypotension discuss sexual function problems erectile dysfunction ie blame drug for problem |
|
what teaching is given to pt to prevent
nocturia with diuretics 1 |
take diuretics in morning
|
|
when is the best time to take vasodilators and
adrenergic inhibitors 1 |
early in the day
|
|
what is the one side effect
common to all hypertensive drugs 1 |
orthostatic hypotension
baroreptors in carotid artery sense position change and vasocontrict carotid arteries so blood won’t go to head barorecptors slow to sense changes with antihypertension drugs |
|
how often should pts exercise
1 |
5x per week for 30 min=non-sedentary
|
|
what is drug of choice to quit smoking
1 |
wellbutrin
|
|
what should you monitor your pt for while they are taking hypertensive
drugs 1 |
CHF
because can cause blood to back up into heart S/S of CHF JVD(seen at 45 degrees angle) edema (swollen feet) wt gain dyspnea |
|
what are the three coronary arteries we will study
1 |
RCA
LAD Circumflex artery as long is blood is pumping thru aorta, blood will get to coronary arteries Left Main bifurcates into LAD and Circumflex artery aka Widow maker if you knock out coronary arteries that supply left ventricle, it cannot push out 70% of heart's CO |
|
what does the RCA supply
1 |
rt atrium
rt ventricle SA node AV node posterior portion of left ventricle |
|
what does the LAD supply
1 |
intraventricular septum
anterior left ventricle lateral left ventricle |
|
what does the Circumflex Artery supply
1 |
left atrium
posterior left ventricle |
|
what are the causes of plaque formation
1 |
HTN
High Blood Cholesterol Heredity Carbon Monoxide-smoking toxic substances in blood |
|
where does cholesterol come from
1 |
1-liver (statins inhibit production
of cholesterol and increase HDL) happy cholesterol-HDL lousy cholesterol-LDL 2-diet |
|
how is diabetes a modifiable risk factor in CAD
1 |
if managed and kept under 100 will decrease risk associated
with getting CAD manage using Lantus-24hr coverage or insulin pump for tighter control |
|
what is angina pectoris
1 |
pain in chest
transient caused by myocardial ischemia(muscle hurts) lack of O2 in coronary arteries have ischemia when demand for O2 exceeds supply |
|
who is more susceptible to CAD
1 |
white males
African Americans more at risk for CRF |
|
what is stable angina
1 |
intermittent over long period of time
can be relieved by sitting down, taking deep breathes occurs with activity, tachycardia and emotional upset |
|
what will an ECG reveal about stable
angina 1 |
ST depression
ischemia |
|
what is the first thing that is
done for pt with chest pain 1 |
12 lead ECG to diagnose what is going on with heart
ST depression-ischemia ST elevation-injury |
|
what is the goal of drug therapy with stable angina
1 |
decrease O2 use or/and increase O2 supply
1-give nitrates to vasodilate coronary arteries 2-giveO2 3-beta blockers decrease O2 demands and workload off heart by lowering heart rate and dilating blood vessels 4-CCB if beta blocker don’t work 5-ACE to vasodilate coronary arteries better blood flow to coronary arteries |
|
what is a short acting nitrate
1 |
sublingual
|
|
why are pts placed on long acting nitrate
1 |
long standing stable angina and just live with it
can’t tolerate procedure to fix problem |
|
what are some other forms of nitroglycerin
1 |
nitroglycerin ointment-long acting, not exact
transdermal patch controlled release nitro-long acting Indur-long acting controlled release all day long |
|
what is Prinzmental’s angina
1 |
spasm, not CAD
give calcuim channel blockers on EKG: ST elevation-injury |
|
what is unstable, crescendo angina
1 |
progressive and unpredictable in once stable lesion
ischemia at rest or sleep |
|
what is the cause of USA
1 |
plaque instability-rupture constriction in artery or
thrombosis, occlusion, MI 20 mins to get clot busted or muscle die aspirin chewed to assimilate faster |
|
how does nitroglycerin work on USA
1 |
NTG does not take pain away even though it
dilates blood vessel area distal to clot not is being perfused with O2=ischemia =pain |
|
what can happen if lose left
ventricle with clot from USA 1 |
if lose pumping ability of left ventricle can go
into cardiogenic shock and die |
|
how does pt present with USA
1 |
chest pain-ischemia
dysrhythmia-cells irritable, not getting blood flow and fire irritably dyspnea diaphoresis N and V anxiety fatigue/weakness-decreased CO |
|
why use beta blocker for both
USA and stable angina 1 |
goal: decrease angina by taking workload off heart
reduce HR reduce contractility reduce blood pressure |
|
what are SE of beta blocker
1 |
tired
sexual dysfunction worsen depression bradycardia-slows HR and decreases CO keep HR above 60 bpm, if not hold meds (tachycardia also decreases CO) old hearts hold for meds for HR 55 hypotension |
|
what is education for beta blocker
1 |
don’t stop abruptly can increase angina attacks
monitor BP and pulse orthostatic intolerance-change position slowly |
|
what are contraindications for beta blocker
1 |
avoid non selective in pt with CHF
or COPD or asthma ie Lopressor beta stimulation opens bronchioles open up so pt can breath beta blocker can cause bronchioles to constrict |
|
what is the problem with grapefruit juice
with cardiac meds 1 |
teach pts to avoid grapefruits
while on cardiac meds can lead to increased blood levels of drugs leading to toxicity |
|
what is the action of beta blocker in CAD
1 |
lowers heart rate
reduces contractility |
|
what is the action of NTG in CAD
1 |
dilates coronary arteries-the drug of choice for anyone
having chest pain dilates veins-reduces preload-good drug for CHF lets extra fluid stay out in peripheral circulation not po, use SL, buccal and IV spray |
|
what is important teaching for NTG
1 |
if no relief after 3 doses 5 minutes apart call 911
if take too quick can get hypotensive from opening arteries too fast replace 6 months keep with you, away from body |
|
how can a pt develop reflex tachycardia
1 |
take NTG too quick
not wait 5 minutes blood pressure goes down heart compensates by beating faster tachycardia can lead to more chest pain, ischemia |
|
what is procedure prep for cath
1 |
ask pt if have allergies or ever have procedure with dye
permit-signed NPO-in case needs surgery and had to be intubated IV fluids-to move dye out baseline BMP-assess creatinine(indicates kidney function) more significant than BUN which is effected by variations in dietary protein explain post procedure care |
|
why is a left sided cath done
1 |
to visual coronary arteries
extent of lesions perform intervention |
|
why is right sided cath done
1 |
so the pulmonary artery
catheter can measures pressures in the rt atrium rt ventricle PAPs O2 sats |
|
what complications looking for post cath
1 |
bleeding
kidney failure infarction from plaque MI |
|
what is transmural MI
1 |
full thickness
Q wave MI |
|
what is subendocardial MI
1 |
partial thickness
non Q wave MI |
|
why is it important to have 12 lead EKG done when
pt presents with CP 1 |
MI and USA present with the same symptoms
don’t know which one until a 12 lead EKG is done ST elevation=injury=MI ST depression=ischemia=USA presence of Q waves=all layers injured |
|
why are serial cardiac markers done
1 |
confirmatory of injury to heart
have time constraints that might not be helpful for a second event |
|
what are the cardiac markers used to confirm MI
1 |
CKMB-specific to cardiac muscle
Myoglobin-nonspecific to cardiac muscle Troponin I-cardiac specific sensitive test |
|
what is the supportive dx for MI
1 |
C-reactive protein-inflammation
serum electrolytes-Mg or K CBC-anemia could be source of MI get transfusion to correct CXR-congestion in lungs enlarged heart=heart failure BNP-enzyme made in HF |
|
what are two major complications of MI
1 |
1-dysrhythmia-#1 complication in 80% patients
can lead to fatal V-Fib or V-tachy leads to cardiac arrest 2-cardiogenic shock-15% infarcts on left anterior descending artery=left ventricle |
|
what is treatment for acute coronary syndrome/MI
1 |
MONA
Morphine Oxygen Nitrates Aspirin-main stay for cardiac care SA, USA, MI daily antiplatelet aggregator-no clots chew to liquid to absorb faster |
|
what is the standard treatment for USA and MI
1 |
90 minutes from door to cath lab to break clot
if no cath lab use thrombolytics |
|
what is drug of choice to break clot
1 |
thrombolytics
|
|
what are complications of thrombolytics
1 |
bleeding
|
|
what is rule for giving thrombolytics
1 |
if chest pain less than 6 hours in duration
complete invasive procedures prior to giving monitor neuro status, neuro status change could mean bleeding into head check to guiac or hemostat to assess for GI bleeding |
|
how do you evaluate the
effectiveness of thrombolytics 1 |
O2 restored to area where clot was at
ST elevation returns to normal chest pain resolves |
|
what is reperfusion dysrhythmias
1 |
complication of thrombolytic tx
now previous ischemic area is irritable and gets PVCs or dyrhythmias tx with antidysrhytmias-amiodarone drug of choice instead of lidocaine |
|
why is heparin given after thrombolytic tx
1 |
to keep area that had clot open
|
|
what is the standard concentration for heparin
1 |
25,000 units in 250 cc D5W
100 units in every 1cc D5W |
|
how is the therapeutic effect for heparin monitored
1 |
PTT 60-70 sec
2 1/2 time normal |
|
does heparin lyse a clot
1 |
no
prevents thrombus formation or extension of existing clot that has been lysed |
|
what is the complications of
heparin and what system need to be monitored for complications 1 |
bleeding
monitor neuro |
|
what do nitrates do in MI
1 |
vasodilates coronary arteries
decrease preload-hold fluid in arms and legs so not coming back to rt side heart decrease afterload dilates all vessels and aorta so heart does not have to pump harder stops workload of heart |
|
how are nitrates administered
1 |
topical-paste
only used prophylacticly sublingual 1 tab q 5 min up to 3 NTG IV 50 or 100 mg/250 cc D5W only in glass bottle not plastic |