Loop diuretic blocks the Na/K+/CL transprt in the luminal membrane of the ascending ____ __ _____ resulting in increased luminal concentration of Na, K, Mg Ca and diuresis. This enhances venodilation and decreases cardiac preload.
loop of henle
Thiazide inhibit the Na/Cl pump in the early part of the ____ _______ ____ resulting in a negative sodium balance.
distal convoluted tubule
Aldosterone antagonists inhibit aldosterone receptors in the ____ ____ which blocks the action of the Na/K/H pump resulting in decreased reabsortion of Na and reduced excretion of K+
loop diuretics are efective in patients with.....
impaired renal function and CHF
Avoid in pregnancy
Potassium sparing diuretics are used in what situations?
Class III-IV CHF, post MI with LV dysfunciton
what is the side effect of potassium sparing diuretics like aldactone?
they have a weak androgen effect which can cause gynecomastia and ED!
avoid if creat clearnace <20 (related to potassium sparing may increase risk of hyperkalemia)
central acting A2 agonists are indicated mailnly for what situations?
resistat or malignant HTN or when multi drug therapy is needed.
(aldomet, catapres, wytensin, tenex)
what kind of agent is clonidine?
also known as catapress
it is a central acting agent---A2 agonist
what kind of anti-hypertensive is aldomet?
also known as a-methyldopa
it is a central acting agent----A2 agonist
How/where do the A2 agonists work?
exert effects on vasomotor center of brain limiting sympathetic outlow to the heart and blood vessels.
little direct cardiac or renal effects so no lipid or electrolyte influence but lots of SE!
So what are the SE associated with central acting A@ agonists? They reduce BP to normotensive in 30- 50% of persons when other meds don't; so why aren't they used more?
SE include sedation, postural hypotension, dry mouth, bradycardia, impotence, withdrawal syndromes, depression and dizzyness!
minimal potential for othostatic hypotensio but additive drug interactions especially with CNs depresants
remember clonidine should NEVER BE ABRUPTLY STOPPED!
Name the protype peripheral Alpha 1 antagonist.
Name the central Alpha 2 agonist?
how does Doxazosin, a peripheral A1 antagonist work?
blocks sympathetically mediated vasocintriction responses and thereby reduces vascular resitance.
when do you consider a drug like doxazosin?
consider a peripheral alpha 1 agonist as an "add on" treatment to other antihypertensives
SE include postural hypotension, syncope, tachy, dry mouth, fluid retenition, headache and dizzyness
what kind of atihypertensives are minoxidil and hydralazine?
direct acting vasoldilators
very potent can cause fluid retention and tachycardia
when are direct acting vasodilators like hydralazine used?
in patients with CRF or refractory HTN
hydralazine requires some special considerations, what are they?
address fluid and heart rate control
usually intiated by a subspecialist and
watch for a lupus like syndrome
what are the prefered HTN drug treatment combinations?
ACEI/ARB + diuretic
ACEI/ARB + CCB
CCB + diuretic or BB+ diuretic
CCB (dihydropyridien) + BB
DRI +diuretic or DRI +ARB
what are not likely to e effective combination therapies for HTN (what should not be ordered together)?
ACE+ARB can be used in selct CHF's with protienurea
RAAS+BB can be seen in CHF and CAD
BB+ Central A2 agents b/c both interfere with sympathetic nervous system an lead to brady and HB, rebound HTN if withdrawns abruptly.
HTN and minorities:Although treatment is similar for all demographic areas, socioeconomic factors and lifestyle barries can influence BP control. What else should you be aware of when choosing medications for HTN management in minorities?
prevelance in AA is increased
AA demonstrate reduced BP response to monotherapy with BB, ACEIs or ARBs compared to diuretics or CCBs.
what is LVH an independent risk factor for?
regression of LVH occurs with aggressive BP management including lifestyle changes and all classess of drugs except....
hydralazine, minixidil and probably clonidine and prazosin.
ARB, ACEI, CCB most effective
PAD is equivient in risk to ischemic heart disease. true or false?
Any class of drugs can be used in most PAD patients. true or false?
aging autonomic nervous system can lead to postural changes so monitor for side effects b/c this can increase comorbidity and mortality. true or false
in the elderly discuss issues with diuretics, ACE.ARB and CCB
Diuretics: plateau in higher doses with more SE. avoid with hx of incontinence
ACEI/ARB: well tolerated, monitor renal fx
CCB, longer acting preparatons prefered, fewer SE
oral contraeptives may increase BP but does HRT raise BP too?
no HRT does not!
what antihypertensives should be used for pregnant, or women who may become pregnant?
methyldopa, BB and vasodilators.
ACEI and ARB are CONTRAINDICATED!
ACEI & ARBS work well to control BP and slow progression of renal failure. true or false/
is there a relationship between elevations in BP and renal failure?
which class is first line for DM with HTN?
ACEI or ARB
dyslipidema and hypertension require agressive management. where is the emphasis of treatment?
diet low sat fat, cholesterol, Na, ETOH
hyperlipidemic agents PRN
client with essential tremor and HTN, what med should you consider to impact both of these issues?
noncardioselecive b-blocker (inderal)
what about persons with hyperthyroidism, what antihypertensive agent should you order?
BB like propranolol
how about with migraine and HTN?
noncardioselective BB inderal
nondihydropyridine CCB like verapamil, diltiazem
with BPH and HTN what med can you consider?
a-blockers doxazosin (cardura) or Tamsulosin (Flomax)
what if someone has HTN and Raynaud's what med should you consider?
CCB nifidipine (dihydropyrdine)
what if they have OA and HTN? What medication can you consider to lower BP and affect OA?
someone with peri-operative HTN should recieve what medication for their BP?
those with dyslipidema and HTN, you should consider puttig them on what anti-hypertensive agent?
Emergency medicine prinicple; who gets admitted?
BP>180/120 with acute TOD or those without acute TOD?
TOD=target organ damage and inlcudes, eyes, brain, heart & kidney.
hsopitalize those with acute organ damage.
treat everyone with immediate combination of oral antihypersive and follow up for both. one in and one out within 7 days.
what is the BP that would delay surgery?
180/110 lower it then go to surgery.
lower it with BB
have them take BP medication right up until surgery and resume ASAP following surgery.
what is pseudo HTN?
oder patients typically can have this as a result of vascular stiffness.
if BP cuff is too small BP will be too high or too low?
cuff should be 80% of arm circumfrence.
what is better, increasing dose or multidrug therapy?
multidrug therapy. can consider combo pills to increase compliance but they may be more expensive.
describe how to do home BP monitoring for somone with white coat HTN making office BP unrealiable to base treatment or treatment respose.
five consecutive days.
each day take 3 measurements 5 min apart in the am and pm
toss the first 2 days of measurements
average the remaining
average the first measurement of each triplicate set.
define resistant HTN
BP that remains above goal despite the concurrent use of 3 anti-HTN agents of different classes.
one of these agents should be a diuretic
evaluations of pt's with resitant HTN referrred to specialty clinics have consitently found tx resistance was in part due to improper use of diuretics. what should you consider reltated to diurteics and resitant HTN?
increase HCTZ from 12.5 to 25mg
change HCTZ to chlorthalidone
change to a loop if CR>1.5 or GFR<30mL/min
increase low dose loop to BID
use a mineralocorticoid receptor antagonisit like aldactone or amiloride
what are common things that interfere with HTN medication efficacy?
ETOH use, NSAIDS
decongestants, diet pills, cocaine
secondary causes of HTN (4)
obstructive sleep apnea
renal parenchymal disease
renal artery stenosis
what's the issue with sleep apnea and HTN?
intermittent hypoxemia and or increased upper airwya resistance induces an increase in SNS.
what is the BP control for patients with renal disease/
<130/80 or lower
use ACEI/ARBs they work and slow progressionof RF
a rise in cr. as amuch as 30% above baseline with ACEI/ARB is acceptable and not a reason to withold tx unless hyperkalemia develops (>5.5)
Na resitriction will help and use diuretics
With an intra adrenal abnormality you will have an increase in aldosterone and electolye imbalance hypokalemia. Also you will see HTN and in younger persons. dx should be confirmed by CT if labs suggest primary hyperaldosteronism. what is the tx for bilateral adrenal hyperplasia?
if adenoma is found surgery will be requried.
paradoxical worsening of HTN with ACEI
recurrent pulmonary edema in moderate-severe HTN
presence of abdomial bruit
what should you consider?
reno artery stenosis!
dx with reanl duplex, spiral CT, MRI, renal angiogram
stop ACEI/ARB, PTCA stenting or surgery to improve renal perfusion and stop HTN!
General treatment guidelines for mild HTN stage I.
140-159/90-100 with no additonal risk factors, DM or TOD
lifestyle diet ,
monthly BP re-eval in 6 months
consider 1st line Rx
General treatment guidelines for mild HTN stage I
140-159/90-100 with risk factors, or disease?
DASH, monthly BP's re-eval in 3 months or less
start 1st line Rx
General Treatment Guidelines for moderate HTN Stage II
if risk factors TOD or DM start 1st line or combo after confirmation and diagnostic evaluation
General Tx Guidelines for Severe HTN Stage II
start full dose of 1st line agent and a 2nd agent (diuretic)
re-eval in 1 week
if improved but elevated change to another 1st line agent at full dose.
reassess in 2-4 days if still elevated consider further titration or addtion of another agent
reasses weekly until DBP<100
How often should newly dx HTN patient visit?
monthly until goal reached
then q 3-6 months
how often to check potassium and creatine in HTN patients?
1-2 times yearly
can you consider reducing doses and number of agents afer 1 year below goal?
when to refer to a specialist?
when a secondary cause of HN is suspected
if BP remains elevated after 6 mo of tx
outcomes do imrove when referred to a HTN specialist.
CV disease lead to progressive LV disease which lead to ..
NYHA Class is based on the patients current symptoms and describes the patient's functional limitations. As a dynamic scale the patients class may go up or down depnding on the improvement or worsening of his HF condition.
TRUE OR FALSE?
The ACC/AHA heart failure stage A-D classifies and describes HF evolution progressively through the stages. not a dynamic scale it only goes one way (donwhill). Is the NYHA Class sytem incorporated into the A-D staging?
why yes it is!
If HF is not a disease state how is it described/
A clinical syndrome that is dynamic with signs and sx that wax and wane over time with tx.
the average life expectancy for a person with 1 hospitalization for HF is 5 years!
what is this the definition of :
structual or functional impairment of either venticle to fill or to eject blood--unable to meet metabolic needs of the body.
CHF referst o LV systolic dysfunction: specifically an enlarge, blood congested LV
these are the cardinal signs of something, what?
dyspnea, fatigue, fluid retenion (pumonary &/or periphral)
heart failure or CHF
High out put HF--normal heart challenged with excessive metabolic demand and the heart fails to meet the need. what situations might you conside this situation?
Low output HF cause about 90% of all HF cases. It occurs when diminished volume from a weakened heart muscle fails to meet normal metabolic needs. It may be left, right or biventrilcular.
sytolic dysfuntion is seen with?
diastolic dysfunction is seen with?
LV dysfunction is most common usually after myocardial injury, infection, or valvular disorders. RV dysfunction may accompany LV with infaract or progression of left to right failure.
HF is a clinical syndrome that represents the end point of many diseases name 5
DM (endocrine disturbance)
how does HF begin?
the process begins with an intial injury that leads to adaptation. Over time, what begins as normal adaptive proces results in LV remodeling, culminating in LV dysfunction and the development of HF
what is this?
abnormal dilation of the ventircles and resultant thinning of the myocardial wall with dereased stretch and contractile strength.
what is this?
left and or right ventricular hypertrophy often asymmetrical, which usually involves the interventricular septem, impairing outflow through the aortic valve
HOCM: hypertrophic obstructive cardiomopathy
high risk for SCD d/t arrythmia
what is this?
Disease of myocardium that causes stiffening of the myocardium causing pressure within the ventricles to rise with small increases in volume. Thus, accentuated filling ocurs in early diastole. Reduced LV filling volume leads to reduced SV & low CO (fatigue, lethargy) whearas increased filling pressures cause pulmonary and systemic congestion.
RCM restrictive cardiomyopathy
S&Sx of left and right HF.
what is arrhythmogenic RV cardiomyopathy?
progressive fibrofatty replacement of the RV and to some degree LV myocardium which creates a proclivity for lethal arrhythmias, especially with exertion.
what is octopus pot cardiomyopathy?
Takatsubo, similar to restrictive :bulging ventricle with limited outflow.
also know as stress cardiomyopathy.
most commo in midle-aged women
which cardiomopathy is most common?
what kind of murmur will you find with hypertrophic cardiomyopathy?
aortic stenosis murmur-sytolic murmur-turbulance.
diminishes with maneuvers to increase venous return like squating and increases with valsalva or position changes which decrease preload.
what is systolic heart failure?
develops form a weakened heart muslce and pump failures
what causes diastolic heart failure
results from end-organ damage as a result of long-standing HTN
what is diastolic heart failure
the venticle can't relax and accept an adequate volume of blood during diastole, EF will be normal or increase >55%
describe restrictive heart failure.
rigid ventricles due to fibrosis (radiation therapy, sarring) or infiltration (amyloid, sarcoid) or scleroderma or tumor.
treatment options are very limited.
The dilated cardiomyopathies tend to lead to what kind of dysfunction
initially loss of LV contratile strength leads to pulmonary congestion
diastolic failure takes place in the presnce of normal LV systolic function. True or False?
you hear an S3 with increased end diatolic volume and client has EF <40% what type of dysfunction and where is it?
sytolic dysfunciton d/t dilated LV
client has normal herat size and contractility. normal or increased EF >45-75%. what type of pathology and dysfunction, why is the EF so high?
this is a diastolic dysfunction seen with normal LV systolic function.
the small LV chamer is able to eject a high fraction of the low volume it holds, that is why EF is high. it's all relative!
Diastolic heart failure what sound will you hear? why?
S4, increased filling (diastolic) pressure.
what are the signs of diastolic heart failure?
S4, JVD, liver enforgement/tenderness, LE edema, pulmonary congestion.
what are the main components of diastolic HF? preload or after load?
preload, even small amount of fluid creates high LVEDP.
what are the main compnents of systolis heart failure?
decreased contractility and afterload needs to be reduced.
recommended for all patients with current or prior sx of HF and reduced LVEF
indicated in all patient with a recent or remote history of MI regardless of LVEF or presnce of HF
anyone with reduced LVEF with/without HF or MI
What 3 BB are proven to reduce mortality in HF treatment?
metoprolol succinate ER
what are the recommendations for BB in HF?
recommended for allstable patients with current or prior sx of HF and reduced LVEF.
use bisprolol, carvedilol or Lopressor ER
ayone with a recent or remote hx of MI regarless of LVEF or HF
anyonw w/o hx of MI wh have a redued LVEF w/o HF sx.
Aldosterone antagonists, like Inspra and spironolactone (aldactone), are a class IIb recommendations in HF. when and why should they be considered?
b/c aldosterone production in the adrenal cortex is stimulated by renin release in the kidneys from under perfusion. Aldosterone increases Na+ and water retention.
Inspra and spironoloactone block aldosterone recetors and promote Na+ and water excretion thereby reducing preload.
what's the deal with ARB's and HF?
use whenever ACEI would be used but can't be used d/t intolerance
the recommendations for a hydralizine-nitrate addition to HF treatment is a class IIb "reasonable to consider". what do you need to know to consider this therapy? like when would you choose it?
reasonable in persons with rediced LVEF whae are already on ACEI/BBB for sx HF and still have sx
reasonalbe for AA who are NYHA III or IV and alredy on everything else.
might be ok in stage C HF with reduced LVEF who can't take ACEI/ARB b/c intolerance, hypotension or renal insufficiency.
what about digoxin and HF?
can be beneficial stage C with reduced LVEF.
it is a sx improvement not a mortality benefit
does prevent hospitalizations but has a narrow theraputic window and requires really good management esp with renal issues to prevent toxicity.
what is the salt restriction in HF?
what is the diuretic recommendation for HF?
for those who are stage C: diuretics and salt restriction are indicate in patients with current or prior sx of HF and reduced LVEF who have evidene of fluid retention
ACC/AHA/NASPE recommend what in past-Mi patients with EF <30%?
what are the current ICD indications based on NYHA functional class?
NYHA Class I: EF ,30%w/prior MI
NYHA Class II-III: EF <35%
NYHA class IV: if meet criteria for BV pacing
LBBB is more prevalent with impaired LV systolic funtion, so what?
leads to widened QRS and potentiates dyssynchrony and delayed ventriclar activation which means decreased jpumping efficiency in the already weak muscle.
What will you find with syssynchrony as it relates to cardiac function and symtoms?
reduced diatolic filling time
post systolic regional contraction (contraction after aortic valve closes)
bottom line: decrease in SV!
what besides ACEI can prevent or reverse LV remodeling in HF patients?
Which HF patients needs CRT therapy?
cardiac resynchronization therapy
have QRS duration >120 (cardiac dyssnynchrony)
are sx despite OPT
in primary care if you suspect HF what is the clinical obligations?
to determine the cause of the exacerbation and treat or admit.
patient presents with
new DOE, PND ororthopnea,
liver congestion expressed as an elevated INR, abdominal tenerness or ascites-
what should you be considereing for dx?
HF=acute HF syndrome=exacerbation of HF
if just volume it may not be cardiac, consider renal function as cause of fluid
acute heart failure is caused by 3 overbearing cardiac conditions, what are they?
structural+valvular heart disease
Electircal+ atrial arrhythmias/bradycardia
name risk factors for the development of HF?
Obesity:dietary indiscretion (sodium)
ETOH men>2drinks daily women>1 drink/day
what are some differentials to consider with sx of HF:
pulmonary disease (asthma, COPD, pul HTN, PE)
anxiety and hyperventiation syndromes
what is the main reason for admission with HF?
cardiopulmonary congestion with high LV filling pressures
this leads to neurohormal activation-causing nor-epi release which causes vasoconstriction-which causes ishcemia- which worsens myocardial function. then LV dilation causes altered geometry of heart which causes valve distortion which leads to TV/MV regurge AKA valvular insufficiency which causes R sided failure
acute HF syndrome-who should be hospitalized?
hemodynamically significant arrhythmia (A-Fib)
ACS: EKG changes or isoenzymes suggestive of MI
Dyspnea at rest: associated with resting tach not so much changes in pulse ox.
nitro SL & or gtt (vasodilitation to decrease preload/afterload
waht symtoms do you evaluate when considering Acute HF syndrome (AHFS)?
S3 gallop/murmurs suggesting vlavular dysfunction
laterally displace or prominent PMI
what is the recommendation for follow-up after dc from hospital for AHFS?
phone call within 3 days of dc
7-10 days appointment
what are the goals of therapy with diastolic HF wth preserved systolic function?
slow HR relax myocardium and enhance ventricur diastolic filling time so use BB.
achieve adequate BP control to prevent TOD (ACEI/CCB)
adequate diuresis to maintain euvolemia
myocardial ischemia is related to what?
O2 supply and demand
which angina is this?
predictable c/p with exertion
when angina has accelrating symptoms what type of angina is it?
what is vasopastic angina?
this occurs with emotion and little or no activity
there is a postprandial and a microvascular angina what are these?
postparndial occurs after eating
microvascular occurs with increases in myocardial well stress and strain like with HTN or aortic stenosis
what are the unusual or minimal presentations of chest pain complaints in women compaired to men?
women fatugue SOB malaise "flu-like"
men chest squeezing, radiation to neck, jaw, arm
What do you know about angina pain that would help you determine it c/p complaint is likely to be angina?
almost never is sharp or stabbing
does not change with postion or respiration
lasts minutes (dull ache lasting hours is not angina)
usually substernal can radiate but pain above the nadible, below epigastrium or localized ot a small area over the left alteral chest wall is rarely angina
precipated by eating, exertion or stress and relieved by rest (and nitro SL)
patient complains of pain that increases with a deep breath what are you thinking?
what sympathetic nervous sytem repsonses are found during periors of true heart pain?
emotional repsonse to neurohumoral influences (anxiety, doom)
Although a normal EKG does not exlude severe CAD it dose it imply what about cardiac function?
normal LV with favorable prognosis
most patients with chest pain/suspected angina do NOT neeed an ech. True or False?
client with angina that occurs only with prolonged exertional activety and not at all with walking is what class of angian based on CCS classisfication scale?
client with angian pain walking >2blocks or more than 1 flight of stairs wi is what angina class (based on CCS system)
client with anginal pain walking <2 blocks or <1 flight of stairs has what class on angina?
describe the client with class IV angina
chest pain at rest
A client with known stable angina complains of any of the following symptoms to you, the PCP, what are your concerns?
new or worsening MR
hypotension or tachycardia
dynamic T-wave changes
new dysrhythmia or EKG changes
high risk for MI
complaints of the above sx suggest unstable angina which is a medical emergency
TIMI risk score has seven componants name them
>3 CAD risk factors
Prior coronary stenosis>50%
>2 anginal events in <24 hours
ASA in last 7 days
elevated cardiac markers
when the pretest probability of severe CAD is high what test should you assign?
coronary angiography-cathy lab
what are the ACC/AHA Class I recommendations for initial management and anti-ischemic therapy of patients with unstable angina and NSTEMI?
best rest, telemetry, O2, IV nitro, morphine (pain)
ACEI for persistent HTN in patients with LV systolic dysfunction or CHF