Cardiology CHF Weinberg 1027-9-10a

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October 26, 2010 CARDIOLOGY: CONGESTIVE HEART FAILURE

Dr. Weinberg 9a-10a

ASSESSING HF

Patient Hx, PE, Labs & Dx tests

DX EVAL OF NEW ONSET HF1. First you want to determine the type of cardiac dysfxn. So I showed you an echo there

w/ big bad heart function of about 40% thats SYSTOLIC HF.NORMAL Heart on ECHO

This is normal heart function on ECHO, but it can be a diastolic dysfxn heart if theyre inHF. This is a 39 y/o. This is a parasternal view and you can see how its contractingnormally. (Compares to HF ECHO he showed earlier) See how that squeezes much betterand its not nearly as big and contracting a whole lot better. This is nice normal EF ofabout 50% at rest and the ventricle squeezes very well. If you saw this person come in w/

HF then this would be diastolic dysfxntheyre failing even though they have normalheart function. Diastolic dysfxn is defined as what? An EF thats greater than 40% andpersons w/ SSx of HF. Why is diastolic dysfxn occur? B/c the diastolic phase of the heart

still requires energy and requires ATP to relaxit doesnt relax normally and pressures goup in diastole and they wind up in pulmonary edema. The same hemodynamicmechanisms, but its based upon diastolic rather than systolic dysfxn. Thats what thispatient is about.

Points out from top to bottomRV, LV, AV, MV, and the pulmonic valve from differentaspects on the Echocardiogram live action. Pulmonic insufficiency is that little orangeflame out there.

Of patients w/ HF, 1/3 is systolic, 1/3 is diastolic, and 1/3 is both systolic & diastoliccombined. How you define which one is which is based on Echo and other criteria, but its

a sticky situation.2. Determine Etiology

Is it ischemic HD, valvular HD, or is there a toxin around or a viral process? Youdetermine the etiological process.

3. Define a prognosis4. Define a guide to therapy

INITIAL WORKUP

EKGwhat can I see on an EKG and how valuable is an EKG? You get an idea, but youmay see a completely normal heart, but it can still be ischemic heart disease. I can get anidea if the person had a prior MI, LVH, arrhythmias, ST segment changes, QT intervals,

and all kinds of conduction problems. What makes the heart pump? Electricity, and it thatdoesnt work then the pump doesnt work well. If the electrical wires in the heart (His-PKJsystem) dont work then the heart wont squeeze as well.

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GENERAL MEASURESLifestyle Modifications

So lifestyle modifications, weight reductionwhy do I want to lose weight? Its not justwater weight, but if I have less tissue to preserve then youre better off. Theres a term

referred to as cardiac cachexiameans dramatic wasting of their muscles. They donthave any fat or muscle around so cardiac cachexia is when you dont have a lot of weightaround then the heart can continue to meet its demands. How does smoking come intoplay here? Increases vasoconstriction and the insult of myocardial plaques, so youretrying to reduce problems theyre going to have. Nicotine is a direct vasoconstrictor andobviously is a risk factor for further development of CAD. So if I have another myocardialinsult, my hearts only going to get worse.

Your heart is a pump to meet metabolic demands, so if I dont get enough oxygen therethe heart has to work harder. If I destroy my lung tissues/alveolar beds b/c Im smoking,

then Im only making my heart have to work even harder. So then youre fighting twodifferent causes nowpulmonary (diffusion of O2 and carbon monoxide/dioxide arentable to diffuse and the heart fails). So avoid Etoh and other cardiotoxic substances.

Exercisewhy? People who exercise do better than people who dont. Im not telling yousomeone who is a NYHA 3 or 4 patient thats going to go out to the gym and exercise, butthe more they do the better off they are. So if you have a sedentary patient, they dopoorly, but the people who get up and go out and do things and are part of thecommunity do better. The ones that dont want to go out and do anything justdeteriorate, so theres physiology, pathologic, and psychologic ways these peopledeteriorate and they wind up w/drawing from their family and things get worse.

Other Medical Considerations

HTNtreat it, otherwise AL will be up and if thats up youll wind up failing.Hyperlipidemia and all these other things can cause further progression of disease.

Coronary revascularizationwhat does that do? It increases more blood flow to the heartvessels. Hibernating myocardium is tissue that is alive thats not functioning b/c its notgetting enough blood flow to it. You increase the blood flow to it and myocardial functionreturns. We can define that by using Rubidium and a PET scan to see what is hibernatingmyocardium and how to preserve it.

Anticoagulationis used w/ regard to people who have had AF, thrombus and accumulatein the heart.

Immunizationobviously b/c you dont want them getting sick again

Sodium restrictionhow much should these people get? Its tough, they should get 2grams a day and thats like eating cardboard, so these people dont pay attention to it.

Daily weights




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Close outpatient monitoringone of the biggest problems w/ these people is you wind up

sending them out on medicines (diuretics, ASA, BB, ACEi, statins, etca ton of medicine!)these people wind up taking their meds for about 6 months or they wind up only taking a

couple of them for multitudes of reasons (psychological, financial, etc.).

PHARMACOLOGIC MANAGEMENT

What medicines are out there?DIGOXIN

Digoxinis an old time medicine. How does it work? Na ATPase inhibitorSo now whatdoes it do? It increases the inotropy of the heart. Do people live longer w/ it? It reducesSx and hospitalizations, but the debate is on for whether it reduces M/M. We do know thatpeople do better symptom-wise w/ Digoxin. Its one of the meds we use at the end ratherthan the beginning. It reduces SNS & RAAS activation. It decreases risk of HF progressionand hospitalization, but you dont live any longer.

What is it like doing? Its like placing a carrot in front of the donkeymakes you go a littlefaster but you will NEVER get back to normal, but it will give you some relief.

DIURETICS

Used to relieve fluid retention & improve exercise toleranceless volume onboard=reducing preload brings you back on the F-S curve and reduces VEDV, thenreduces pressures on the heart and brings you back on the curve. You dont want to bringthem too far back on the curve, b/c then the patient gets hypotensive. It was shown onthat little curve there, that they hypo-perfuseso theyre on a really tight range of whatsthe best volume to give people. You treat them well, you send them home and they wind

up back in the hospital quickly, b/c people are hemodynamic and things are alwayschanging (volume they take in, catecholamines that come out, PNS, etc. you cantcontrol all of that), so you give them these static drugs (if they take them) and youexpect them to do well out of the hospital, but it doesnt always work so well. You needconstant monitoring/therapy at home for them, otherwise theyre back to the hospital soquickly.

Other drugs will work better, but you have to watch for electrolyte depletion. What do youhave to watch for w/ the most common electrolyte to deplete? Potassium, b/c when you

get hypokalemicyou get more arrhythmias. These people die from arrhythmias fromHF.

We know as they require more diuretics, the prognosis is worse.

ACEi I showed you the RAAS and where it happens, so where do the ACEi work? ACE comes outat the lungs, so ACEi blocks the conversion of AI to AII and prevents functional




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deterioration. You want these meds on board for the long-term, these are NOT acutemanagement of these people (acute management is getting rid of volume & increasingcatecholamines and getting them out of that acute hemodynamic phase). This phase is

the neurohormonal phase, so you want to prevent the interaction of the RAAS, b/c theydo poorly when its unmediated.

Relieves Sx, improves exercise tolerance, reduces M/M and its pretty good stuff andtheres a multitude of studies out there that show that these drugs really prevent peoplefrom dying that are in HF w/ poor heart function. Theres limited data on people w/diastolic dysfxn, but these people do better, die less, and theyre not back to normal byany means, but they do better by far w/ ACEi on board.

You want these people to be on an ACEi. Nobody has lived longer w/ diuretics or digoxinon board, but you definitely do better w/ an ACEi on board, b/c it blocks thatneurohormonal pathway (that if over time is left unattenuated will be deleterious on theheart).

DIURETICS, ACEiReduces the number of sacks on the wagon so the donkey can pull it better

BETA BLOCKERS

Why do you think BBs work? They decrease myocardial O2 demand (MO2D), and itsbeneficial in patients w/ CAD. Functionally, though, what does it do? DecreasesHR=negative inotropic (seems counterintuitive, but studies show giving people BB helpsthem live longer too).

BB have cardioprotective effects due to blockade of excessive stimulation of the SNS.

Thats really what this is all aboutit blocks that excess catecholamine (B1, B2, all that

stimulation thats happening) so that deleterious long-term effect (5 years, not a bignumber but people do better). If you dont give it to them, 50% are dead w/in 5 years. Ifyou do give it to them, people do much better and live longer.

Short term effects: BB decrease myocardial contractility (thats a bad thing b/c you canpotentiate HF and make them worse), so you may have to back off then rechallenge themand give them more over time. See it says here increase in EF after 1-3 months of useso the heart function may get better, b/c it prevents remodeling of the ventricle (if theheart is going to recover). There is some selection here for people that arent going to dowell in the first month or twothese people will die, but others will do better b/c they canaccommodate on their own.

Long-term placebo-controlled trials have show Sx improvement in patients treated w/

certain BBs, but not all of them.Combined w/ conventional therapy, BBs reduce combined risk of M/M or diseaseprogression and do better.




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So now Ive given you two drugs that you look at your patient and tell them take thisdrug and you will live longer. They have to be able to tolerate it, but most of them willand theyll live longer.

Youre giving this to LV systolic dysfxn patients, who have poor LV function. This is notgoing to be your diastolic dysfxn patient.

BBs limit the donkeys speed, thus saving energy is the overall concept for this so theyare able to keep going.

ALDOSTERONE ANTAGONISTS

There are two out there that are shown to be beneficial, now these are another type ofdiuretic, but they are K+ sparing. It makes your K+ go higher, so you get morearrhythmias too.

These are used in people that are in NYHA Class 3 & 4 HF (high frequency patients thatwind up getting into trouble and die from HF just as much as they die from arrhythmias.

You give these patients Aldactone or Eplerenone and those people do better over time,but they also have a loop diuretic on board (lasix) and now they have a K+ sparingdiuretic (aldosterone antagonist).

ARBs

These work the same mechanism as the RAAS and are generally given to people whoCANNOT tolerate ACEi. It should not be considered equal or superior to an ACEi.

Some of the reasons people cant tolerate ACEi, are some develop renal failure,hyperkalemia, intractable cough they cant tolerate, and those patients dont do as wellso you give them an ARB. Those people have shown in several studies that they do betterthan if they werent on a RAAS blocker, but clearly not as well as patients on an ACEi.

These are drugs you need to have people on board for.

Angiotensin ReceptorsAII receptors wind up causing vasoconstriction, growth promotion, anti-apoptotic (celldeath), pro-fibrotic, pro-thrombotic, and pro-oxidant (oxidation of LDL & ROS

generatedfurther deterioration of heart muscle). If you stimulate these prognosticAngiotensin receptors, you generally do poorly.

PART IV: ASSESSMENT AND TREATMENT OF HF PATIENTS




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Treatment Approach for the PatientTreatment Approach for the Patient

with Heart Failurewith Heart FailureStage AStage A

At high risk, noAt high risk, no

structural diseasestructural disease

Stage BStage B

Structural heartStructural heart

disease,disease,

asymptomaticasymptomatic

Stage DStage D

Refractory HFRefractory HF

requiringrequiring

specializedspecialized

interventionsinterventions

TherapyTherapy

Treat HypertensionTreat Hypertension

Treat lipidTreat lipid

disordersdisorders

Encourage regularEncourage regular

exerciseexercise

Discourage alcoholDiscourage alcohol

intakeintake

ACE inhibitionACE inhibition

TherapyTherapy

All measuresAll measures

under stage Aunder stage A

ACE inhibitors inACE inhibitors inappropriateappropriate

patientspatients

Beta-blockers inBeta-blockers in

appropriateappropriate

patientspatients

TherapyTherapy


under stage Aunder stage A

Drugs:Drugs:

DiureticsDiuretics

ACE inhibitorsACE inhibitors

Beta-blockersBeta-blockers

DigitalisDigitalis

Dietary saltDietary salt

restrictionrestriction

TherapyTherapy


under stages A,B,under stages A,B,

and Cand C

Mechanical assistMechanical assist

devicesdevices

HeartHeart

transplantationtransplantation

Continuous (notContinuous (not

intermittent) IVintermittent) IV

inotropicinotropic infusionsinfusions

for palliationfor palliation

Hospice careHospice care

Stage CStage C

Structural heartStructural heart

disease withdisease with

prior/currentprior/current

symptoms of HFsymptoms of HF

Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management ofHunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of

Chronic Heart Failure in the Adult, 2001Chronic Heart Failure in the Adult, 2001

Referred to as Stages A-D or its also known as NYHA Classes 1-4

How do you want to treat these people?

STAGE Ahigh risk patients, but no structural diseaseTreat the HTN (preventprolongation and reducing AL on the heart), b/c HTN causes HF, MI, CVA, renal failure and

these are the things you are treating. DMsame kind of things and you want to treathyperlipidemiabring down the lipids, get rid of the Etoh. Depending what your patientsare already on, you use the ACEi to start with for first line treatment depending on what

other processes they have going on (ex. if they have proteinuria, DM w/ HTNuse anACEi to start with).

STAGE B

have structural HD & ASx

just b/c they have accommodated (b/c ASx) theycan do just as badly as people who have Sx. So Stage B patients, who are ASx w/

structural HD, and the EF is 30% they have accommodated but those people still do




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just as badly w/ sudden death as patients w/ Sx. Treat them w/ ACEi, BB, and some dontusually need diuretics b/c the EDVs are ok and theyre ASx.

STAGE Cstructural HD w/ Sxobviously if they have Sx, you have to treat them and

you do so w/ diuretics first, then use other meds combod w/ salt reduction, etc.STAGE Dpatients are just sitting there at rest and cant do anything. Those are thekinds of patients that have mechanical assist devices, ventricular remodelization,resynchronization therapy, and they do Latissimus dorsi flap muscles, and all sorts ofthings out there that theyre trying. But when all of those things arent working, then youwant to use cardiac Hospice care, b/c these people are going to die (9 months is usuallythe limit for them).

CARDIAC RESYNCHRONIZATION THERAPY

Increase the donkeys (heart) efficiencyHow does that work? We talked about the heart squeezing and it usually contractssynchronously (Left wall & septum are going at the same time). If you have a BBB,

particularly a LBBBthe left side doesnt contract as well as the right side of the LV. Wedo resynchronization therapy and put a pace maker into the RV apex and another wireinto the coronary sinus into the lateral wall to try to stimulate two areas of the heart tocontract synchronously. This is only two areas, so how well does it really work? Peoplegenerally do better and you may get an EF thats 20% moved up to 30% w/resynchronization therapy. Ideally, it would be nice to put a whole electrical systemoutside of the heart to make it contract synchronously, but short of that now we are stillable to make it contract a little more synchronously.

SUMMARYOverall, HF is a chronic process & progressive disease process. Its not curable but it istreatable.

Most guidelines promote lifestyle modifications, management w/ medications (ACEi, BB,Dig, diuretics, etc.).

About 15% of all HF patients may need resynchronization therapy. You have to do closefollow-up and make adjustments as needed.

This last part was just some things to go overthe first part is REALLY KEY info onneurohormonal, SNS stimulation, CO, SV, HR, dealing w/ what HF is all about, systolic &

diastolic HFbasic idea of HF/concepts.



Cardiology CHF Weinberg 1027-9-10a

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