Tips for Decision Making When Faced with Cardiac Diseaseksvm.agri.huji.ac.il/info-pages/cardio-lecture.pdf · 2003. 8. 9. · Tips for Decision Making When Faced with Cardiac Disease:

Tips for Decision Making When Faced with Cardiac

Disease:When Should Therapy

Start?

Dan Ohad, DVM, PhD, Diplomate ACVIM

(Cardiology)

האוניברסיטאי מיסודה של האוניברסיטה העבריתהוטרינריבית החולי ם . בית ד ג ן–הק ר יה החקלאית

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Mechanisms of SomeCardiac Drugs

ACE-I (↓Ald, ↓AT-II) ↓Preload, ↓Afterload

Diuretics (↓Na+, ↓Ald) ↓Preload

Digoxin A strong (-)chronotrope,

a weak (+)inotrope

Theo/Aminophylline ↑Φ ofBronchioli

“AAD”↑↓Anti/Pro-arrhythmic?

Heart Disease ≠ Heart Failure

• Myocardial Failure ≠ CongestiveHeart Failure

• Tx for either oneeither one (e.g. Myocardial Failure 20 to DCM, vs. fluid retention 20 to CHF): as soon as it as soon as it is diagnosedis diagnosed

• Treat non-congestive cardiac symptoms when identified (even when no CHF is present)

• The biggest dilemma: Should asymptomatic heart disease be treated?

In Moderate-to-Severe Chronic CHF, Definitely Treat

• Benazepril - ↓62% mortality over 56 days in dogs with CHF; Enalapril -↑survival by >100% (the “BENCH” Study: J Vet Cardiol, 1:7-18, 1999; the “LIVE”Study: JAVMA 213(11):1573-7, 1998 )

ACE-Iinhibitors indicated in systolic heart failure, when tolerated.

• Other cardiac agents indicated PRN

• Side effects (e.g. hypotension =>azotemia => GI signs): rare and result from combination-Tx (“polypharmacy”) responsive to ∆

±

ModerateCHF :

*ACE-I (BID)(± low dose ?Spironolactone)

*Fusid(moderatedose)

Digoxin

C.S. w/oCHF:

*ACE-I(SID)

*Fusid( lowdose)

±Digoxin

Severe CHF :

*ACE-I (BID)+Nitrate+Amlodipineor Hydralazine

*Fusid(highdose)+Thiazide

+PotassiumSparing Diuretic

Digoxin

?Vesnarinone?Pimobendan

RefractoryCHF :

Fusid IV, Oxygen, No Stress

Nitroprusside Dobutamine IV;±Dopamine IV, Amrinone or Milrinone IV

*Fusid (dogs, cats, horses) & Enalapril (dogs) are the only ones approved

or

ACE-I Are the First Line of Defense:

When Already in CHF:

Daily Resting Respiratory Rate

10

35

60

0 5 10 15 20 25 30

Day of Month

RR

(cyc

les/

min

)

Move between stages based on trends of ∆ in RR

Why is it Safe to Use Digitalis Glycosides?

Efficacy

Toxicity

Dose (mg/kg)

Is it Necessary to “Prophylactically” Treat Asymptomatic Patients?

• Chronic Valve Dz is a slowly progressing disease

• After developing murmurs, dogs may remain asymptomatic without any therapy for many years.

• “Prophylactic” therapy for asymptomatic dogs involves treatment over several years (↑$$ / ?↑S.E.)

Mechanisms of Some Cardiac Drugs

ACE-I ↓Preload, ↓Afterload

Diuretics (↓Na+, ↓Ald) ↓Preload

Digoxin A strong (-)chronotrope,

a weak (+)inotrope

Theo/Aminophylline ↑Φ ofBronchioli

“AAD”↑↓Anti/Pro-arrhythmic?

(↓Ald, ↓AT-II)

Should I Use ACE-I in Compensated Heart Dz, Prior

to the Onset of CHF?

• This “should” be beneficial if the disease has already ↑RAAS* (which is ↓by ACE-I).

• ↓8%-28% mortality in mild / asymptomatic heart failure and early activation of the RAAS in humanNON-valvular Dz

• BUT: Tx in most of these cases: polypharmacy; some severe pts included (~↑estimated impact)

* [“RAAS” = “Renin-Angiotensin-Aldosterone System”]

ACE-I Prior to the Onset of CHF? (Cont’)

• ↑survival (601 vs. 314 days) in asymptomatic ("occult") male (>>female) Doberman DCM with ACE-I (O'Grady MR et al, Abst, J. Vet. Int. Med. 11:138, 1997)

• ↑RAAS in some mildly MR-affected CKCS dogs, but many fall within the normal range

• In these MR-dogs, ↓RAAS from 4.6 months prior to decompensation RAAS is not activated at the time of CHF onset

Traditional Recommendations for Tx of

Asymptomatic Mitral Regurgitation:

“Rely on radiographicprogression”

• Start conservative ACE-I when LAE

•↑Aggressiveness when LVE (± RVE)

• Add Digoxin & Furosemide when symptomatic CHF (if echo available, use also %SF).

1. LAE

2. LVE

3. LVE & RVE

4. PE (Interstitial)

5. PE (Alveolar)

Radiographic Progression of MR

CHF:

Reasons for TraditionallyRecommended Tx for Asymptomatic Mitral

Regurgitation

• This strategy might have stemmed out of some pressure from drug-representatives and from RDVMs interested in clear guidelines

• Due to small sample sizes in Vet. Med., it is based on theory / clinical impression / speculation & extrapolation from human pts, rather than on hard evidence.

Human Clinical Trials Consist of Thousands of Patients; Veterinary Studies

Look at < Tens - Hundreds:

• “IMPROVE” Study n = 58J Vet Intern Med. 9(4):234-42, 1995

• “LIVE” Study n = 110

JAVMA 213(11):1573-7, 1998

• “BENCH” Study n = 70J Vet Cardiol, 1:7-18, 1999

• “COVE” Study n = 211

J Vet Int Med 9(4):243-52, 1995

• “VETPROOF” Study n = 139

(Abst) J Vet Intern Med 13:246, 1999• “SVEP” Study

n = 229

(Survival when already in CHF)

(Prevention of CHF)

The Scandinavian Veterinary Enalapril Prevention study:

229 Cavalier King Charles Dogs

J Vet Intern Med 2002;16(1):80-8

The “SVEP” Study of Spontaneous MR in 229

CKCS Dogs (x 4.5 years)• Placebo: n

= 113• Onset of CHF:

1130 d• # of CHF cases: 50

• Enalapril 0.38 mg/kg: n = 116

• Onset of CHF: 1150 d

• # of CHF cases: 48

• ∆ (1.7%) was statisticallyinsignificant

(P=0.8 as per a Kaplan-Meyer analysis)

• “Survival plots” of the 2 groups tracked almost perfectly over time (see next slide)

• It would take ~1200 dogs to show a ∆ of ~40% in this setting: Clinical significanceis questionable at best

≠

Long term Enalapril in asymptomatic dogs did not delay the onset of CHF, regardless of cardiomegaly or dose

% of Dogs Remaining in Study (Until Reaching CHF)

P = non significant

Conclusions Re Onset of ACE-I Tx

• When data available, a drug should be used because it DOES work, NOTbecause it “SHOULD” work

• Okay to start ACE-I ± Dig in asymptomatic DCM

• Not yet justifiable to start Tx in asymptomatic MR

• ↑Aggressiveness (dose / frequency /# of drugs) along with ↑severity /progression of Dz (e.g. RR)

• Know when to refer a case to a specialist

The Ideal Referral Process

The need is recognized by RDVM & client

Reason for referral, clinical info, & expectationsare communicated to specialist

Specialist evaluates patient

Specialist communicatesfindings & recommendations to client & RDVM

Client, RDVM, and specialist decide about future care as a team

1

2

3

5

4

Problems can occur at each of these steps!

Specialists are an extension of your clinic!

They can:–Confirm your Dx –Narrow your DDx-list

–Determine the etiology for CHF

–Provide recommendations for Tx & follow-up visits

–Help with prognostication

Refer when Facing:

• A diagnostic challenge with a clinicallymeaningful dilemma (not any “teaching case”)

• A case refractory to Tx

• A case containing conflicting data.

• An arrhythmia-case that is complicating case-Mngmnt

• A client who wants a second opinion.

Refer when You Need to:

• Confirm your Dx and / or Tx approach in a specific case

• Reduce interpretation error rates.

• Improve the image of your practice.

Whenever you feel you need to

“Know When to Refer”(Cont’)

• Refer BEFORE terminal Dz-stages, when something can still be done for the patient

• Avoid referring following numerous “shotgun”-Tx attempts, especially if the Dx is not final

• NOT every cardiac case should be referred

Know How to Refer:It’s All About

Communication & Expectation-

Management!

• What you consider as inconvenient or too expensive is not always so to your client

• Eventually many clients may expect a referral, being familiar with the concept from human medicine

• Mutual respect & effective communication between parties is key

Know How to Refer (Cont’):

Communicate the following:• Problem(s) / Client Complaint(s)• Relevant test results (not copy of

whole medical record)

• Current medications (dose & frequency)

• Response to these drugs• Previous drugs that are

discontinued and why• What client has been told

about this referral (not “this is a teaching case” at “no charge”)

• Your own expectations from specialist

נ/ ז _____:מ שקל___________:גזע____ :סוג ______ ר"י ד"הופנה ע_____ :גיל

וממ צאי בדי קה פי ז יקל י תהי סטוריה ר לוונטית ל מ ערכת ה לב וכל י הדם

:מבדל ת / אבחנה משוע רת / סיבת ההפניה

________________________________________________________________________

:תצפיות הב על י ם ע י יפות כללית יר ידה ב סבול ת מא מץ ) ופרודוקטי ב ילח/ י בש ( ש י עול

אנורקסיה חו סר מנו חה לילי אורטופנאה טכ יפנאהדיספנאה טכ יקרדיה

Pu / Pd מ שקל יתר קכקסיה ות / עוו ית אבוד הכרהפתע- קריסת ____ ___________________________________________: אחר הג דלת הבטן/התרחבות

:ממצאי בדיקה פיזיקלית (QAR*) ערנות שקטה)∗(BAR גבוהות : רמת הערנות ו הפעילות

דליריו ם ת ש י שות / רביצה / בינונ י / קל (משקל - תת ) ח מור/ ב ינוני / קל ( מ שקל יתר תקין :מצב גופני

לדקה_____ : במנוחהקצב נש י מות אסצי ט ס )ח מור י ב שות לחות:ריר יות

"מוזרקות "ח יו ורות כח ולות/ אפורות בצב ע תקין

בצב ע אדום עזצהובות מה יר מ יד י אי ט י מ ידי במה ירות תקינה:(CRT)מלו י ני מ י ח וזר

) וחזק מהצפוי( הולם חלש חזק ומלאbpm__:דופקנמוש -בלתי

“Pulsus Parvus & Tardus” Jugular Pulse “Pulsus Paradoxus” חוקיות ללאסדירות - אי "מרו חקי ם", חלש י ם חזקים ו ברור י ם :S1(S &2(קולות הלב

-פאן הולוס יס טול י ת___מתוך ___ דרגה :ות / אוושהס י ס טול ית

באמצ ע הס י ס טולה בתח ילת ה ס י ס טולה דיאס טול ית

הלב מ ש מאל - בב ס י ס מ ש מאלהלב- בח ודהלב מ י מ ין- בח וד

) בקו האמצע/ מ ש מאל / מ י מ ין (ס טרנאלית - פארא הצווארי/באזור עורק

Crescendo-Decrescendo (“Diamond-Shaped” = “Ejection Murmur”)Band-Shaped (“Plateau” = “Blowing”) Decrescendo

נעדר/ מזדמן / מת מ יד :(Gallop) ”מקצב דהירה"מפו צל 2S קול"קליק סי ס ט ולי ":קולות לב אחרי ם

ב כל האונות) וס יקולאריי ם-ברו נכו( תקינים :קולות ראה(Wheezes)"שריקות" / "צפצופים "

(Crackles / Rhonchi) קרפיטצ יה ש ל נאדיות :)אונות/ אונה ( מ יקום קולות שא ינם תקינ י ם -

/ אמצע י ת / קדמית ) / (י מנ ית/ ש מאלית () ב טנית/ גב ית ) / (אחור ית

ס וף ה נש יפה/ שא יפה : ע יתו י הופעת ם ב מ חזור הנשי מה-

∗ BAR = Bright, alert & responsive QAR = Quiet, alert & responsive

The Specialist Will:

• Spend more time “milking” relevant Hx from owner

• Examine & perform additional tests as needed

• Explain Dz, Monitoring processes, Tx (including expected response & S.E.),Prognosis, and Follow-up recommendations to owner, orally & in writing

• Often will recommend more frequent monitoring & follow-up visits at RDVM’s

• Communicate the above to RDVM• No major procedures should be

performed prior to discussion with RDVM

The Specialist Should Not:

• “Bad-mouth” the RDVM (or let other personnel in his facility do that)

• Agree to become the primary-care provider of the patient

• Practice a discipline outside his/her area of expertise

• Accept a case w/o a referral,unless has already seen this patient before will also contact RDVM as if a referral

Anti-Arrhythmic Therapy:

VPCs / VT

Types & Frequency of Arrhythmia and Conduction Disturbances in 95 Dogs Screened From 3000

Consecutive Cases

• VPCs43

• APCs14

• Atrial Fib.13

• 10 AVB12

• 20 AVB12

• VT 8

• PAT3

• Atrial Flutter2

• 30 AVB2

• R-BBB2

• L-BBB2

Total: 113

Which of These 2 VPC Cases Needs Tx More?

(http://www.isrvma.org/article/cardiac2.htm)

The QRSComplex

• It's duration is measured from the onset to the offset of the QRS-complex• Represents ventricular depolarization; ( => Has to be followed by a T-wave)

• Can be prolonged (widened) with:

1. ? Myocardial hypertrophy2. ? Hyperkalemia

3. Ventricular Premature Complexes / VT

4. Ventricular Escape Complexes / Rhythms

5. Bundle Branch Block (R-BBB or L-BBB)

The one thing in common to # 3-5, is slowtrans-myocardial conduction, on a cell-to-cell basis (≠ via the fast conducting His-Purkinje system).

T

Ventricular PrematureComplex (VPC): [The most common arrhythmia]

QRS

T

TTp

QRS

T

TTp

Ventricular PrematureComplex (VPC): [The most common arrhythmia]

QRS

T

TTp

Ventricular Tachycardia (VT) (≈a series of VPCs)

["SMVT" vs. "NSMVT" vs. "SPMVT" vs. "NSPMVT"]

Ventricular Escape Complex / Rhythm

(note the long pauses and the dissociation from P-waves)

Bundle Branch Block (note the constant association with P waves)

Ventricular Escape Complex / Rhythm (note the long pauses and the dissociation

from P-waves)

Bundle Branch Block (note the constant association with P waves)

Bundle Branch Block

(≠)

VPCs (the most commonarrhythmia)

(≠)

"Fusion" between Sinus & Ventricular-Escape Mo

TT

P T

When Treating: Do Not Confuse VPCs with Ventricular Escape Complexes

(http://www.isrvma.org/cardiac.htm)

Hemodynamic Effect of APCs ("Pulse Deficits")

Hemodynamic Effects of AF & One VPC ("Pulse D

To Treat, Or Not To Treat?• Depending on rate & duration, rhythm disorders

may have a fundamental effect on the efficiency of the heart as a pump (especially when efficiency is already hampered).

• Many arrhythmias are transient or too sporadic to even compromise hemodynamics, let alone threaten life.

• Cardiac rhythm is easily monitorable arrhythmias are only seldom overlooked, and often distract us from "real" issues.

• Mere recognition does not automatically justify intervention.

• First, use the Hx & PE to determine whether BP & perfusion are compromised. Treat the Dz before you treat the rhythm, unless this is a true emergency .

When You Decide AAD-Tx is Warranted:

If this is not an emergency, Do not use it before:

• Tx of CHF, if present. (when chronicAAD-Tx is considered)

• D/C, followed by ↓ of concurrent, offending drugs (e.g. Digoxin).

• Correction of Acid/Base Imbalance

• Correction of Electrolyte Imbalance (when either acute or chronic AAD-Tx

is considered)

• Correction of Hypoxia

Use Reason, Not Dogma, For Tx of Ventricular

Arrhythmia• VPCs often raise non-proportional concerns

and trigger AAD-Tx based on both unrealistic assessment of risk, and unrealistic expectation for benefit.

• This bias is reinforced by the ease of VPC recognition, by many textbooks, & by extrapolation from human CAD.

• Although SVTs tend to be viewed more tolerantly, in veterinary pts they usually attest to a more severely compromised cardiac function than ventricular arrhythmias do.

Chronic AAD-Tx

• SCD may occur in some DCM or SAS or "Boxer dog Cardiomyopathy" cases that also manifest frequent VPCs, and may warrant AAD-Tx. Tx of the underlying Dz in these high-risk pts should still precede chronic AAD-Tx.

• The merit of chronic AAD-Tx should be periodically challenged by empirical discontinuation.

• ↓ in the # of VPCs can only attest to a pharmacological effect, not to a clinically relevant benefit.

• AAD-Tx should be continued only if some ↓of C.S. is seen.

Chronic AAD-Tx for SCD-Prevention is Ineffective!

• An arrhythmia such as VF can be the manifestation of death, rather than the reason for it. AAD may not necessarily prevent this from happening.

• Although cardiac patients at the greatest risk of dying due to arrhythmia are identifiable, AAD-Tx can often not prevent "arrhythmogenic death". It may actually (sometimes) cause it.

Do not be tempted to use AAD to prevent"sudden, arrhythmogenic death".

• Use AAD to control hypotension / fainting / episodic weakness / intractable or acutely exacerbated heart failure, if these are clearly arrhythmia-related (e.g. based on sustained, severe ↑ or ↓ of HR).

Acute AAD-Tx of "Traumatic Myocarditis"

• Often diagnosed with HBC / GDV / Extra-cardiac Dz.

• Traumatic "Myocarditis" is a speculation & a misconception. There is no ventricular trauma with GDV or splenic neoplasia, & no evidence for myocardial Dz even when trauma *is* present.

• The typical "Accelerated Idioventricular Rhythm" is only ≤ 170/min and does not compromise LV-filling or SV or CO, unless VPCs are both very premature & frequent, and/or independent organic heart Dz is present.

• It is usually self-limiting, and is reversible despite of, not thanks to AAD-Tx. AAD-Tx does not improve survival of GDV cases.

Idioventricular Rhythm

• Typically seen with extra-cardiac Dz (e.g. "Traumatic Myocarditis"...)

• Usually faster than a ventricular escape rhythm, but not much faster than the background NSR 2 foci "compete" over setting the pace

• RSA-driven transition often shows fusion morphology

• Typically hemodynamically stable & self-limiting

Lack of Hemodynamic Effects of an Accelerated(Idio)ventricular Rhythm-

NO NEED FOR TREATMENT!!!

HR~120/min

(HR=260/minVentricularTachycardia:

Be Methodological

• Determine the real (cardiac or extra-cardiac) underlying problem, and establish a cause & effect relationship between ventricular arrhythmia & C.S.

• Use other Tx (e.g. O2-Tx / volume expansion / volume reduction / blood transfusion / anti-CHF-Tx) as needed, prior to acute AAD-Tx, unless arrhythmia directly impairs ventricular function. Otherwise AAD-Tx will fail.

• Once you decide to use AAD-Tx, be fully committed to it: empiricism with drug choice & methodical dose-titration are often inevitable. Don't give up before your options are exhausted.

Again, When AAD-Tx *IS*Warranted :

If possible, Do not use it before:

• Tx of CHF, if present.

• D/C, followed by ↓ of concurrent, offending drugs (e.g. Digoxin).

• Correction of Acid/Base Imbalance

• Correction of Electrolyte Imbalance (e.g. correct ↓K+ or ↓Mg++)

• Correction of Hypoxia

!תוד ה

האוניברסיטאי מיסודה של האוניברסיטה העבריתהוטרינריבית החולי ם . בית ד ג ן–הק ר יה החקלאית

03-9688533) שעות24( חי רום 03-9688525 – פקס 03-9688588 -טלפון לקביעת תורי ם