Murray_The Role of Primary Care in CHF

The Role of Primary Care
in CHF and Acute MI Care
By: Andrew Murray DO PGY4
Heart failure
 Classification
 Stage A description and therapy
 Stage B description and therapy
 Stage C description and therapy
 Stage C alternative therapeutic options
 Stage D description and therapy
How we classify heart failure now
Heart failure risk factors for AHA Stage A
 HTN
 CAD
 DM
 Obesity
 Valve Disease
*However at this stage there are no heart failure signs or symptoms, nor are there any abnormalities of cardiac
structure or function. *
Stage A is essentially primary prevention
 UKPDS addressed tight glucose control (7.0% H1AC) vs control (7.9%
H1AC) and while the results suggested a decrease in microvascular
complications and MI it was not statistically significant. Therefore
keeping DM close to goal (less than 8.0% H1AC) is an appropriate
target.
 JNC 8 BP guidelines
What about lipids?
Lipid therapy choices:
 Statins
 Niacin
 Bile acid sequestrants
 Ezetimibe
 PCSK9 Inhibitors
 Probucol
 Fibrates
 Combination therapy?
Finally…
 Diet: Mediterranean is a great
option, minimize sodium intake,
eliminate fast food, smoking,
minimal alcohol if any
 Exercise: At least 30 minutes of high
intensity 3-5 times a week. For a
goal reach 70% of age predicted
maximal heart rate. (220-age*0.7)
 Obesity goals: England study has
suggested the benefit of bariatric
surgery. Regardless weight loss is
challenging at best, must
remember 3500 calories is one
pound.
 Valve disease and CAD watch with
echo, stress test. Adapting and
controlling other aspects of heart
disease risk factors will help as well.
Stage B Secondary Prevention
 Most heart failure patients are in this stage
 Mortality is <5%
 EF is now reduced, continue Stage A measures.
 BB must be started as well. While in the short term they decrease heart rate
and contractility in the long term they improve contractility (3-6 months).
Correlated with better results based on dose and absence of scar tissue.
Cannot be stopped as abrupt cessation may cause significant worsening of
cardiac function.
 Watch out for high grade AV block, significant hypotension, and effects on
asthmatics.
 ACEIs are important to start to reduce afterload, preload and wall stress.
They augment renal blood flow, reduce aldosterone, and antidiuretic
hormone as well as preventing ventricular remodeling.
 However: cough or allergy switch to ARB. Watch out for significant renal failure,
angioedema dysgeusia (metallic taste), hyperkalemia, and hypotension.
How do these drugs work?
What about renal function?
Stage C, symptoms start
Tertiary Prevention
 Hospitalizations begin occurring, mortality increases to 10-30%
 Important to engage the patient with a Heart failure clinic if not already
enrolled (as Jen McCambridge PA talked about earlier, other medical
therapy Entresto/sacubitril and valsartan, Corlanor/Ivabradine, etc..)
 Salt restriction becomes very important to help prevent fluid overload. Talk to
your patient in depth about avoiding high salt foods such as: chips, crackers,
canned food, preserved meat, fast food. The simplest way is to tell them to
eat fresh food, if it doesn’t go bad in 7 days don’t buy it.
Stage C medications and
interventions:
 Diuretic therapy:
 RALES trial: Spironolactone decreases
mortality and heart failure hospitalization.
Improves symptoms as well. Watch for
hyperkalemia.
 SHEP trial: Diuretic therapy for HTN reduces
new onset heart failure. Minimum dose
should be used to avoid overdiuresis which
activates RAAS and causes hypotension,
prerenal azotemia, hyponatremia
,hypokalemia, and hypomagnesemia.
Start with furosemide and progress to BID
and/or torsemide or bumetanide. Consider
thiazide diuretics if doses of 120mg BID or
more is needed.
RASS Review
Stage C medications and interventions continued:
 RADIANCE and Digoxin study suggest a benefit to patients in sinus rhythm with
heart failure by reducing the risk of hospitalization, improving clinical stability,
however mortality is not improved
 V-HeFT I and II trials suggest hydralazine and isosorbide dinitrate reduce
mortality and improve symptoms in heart failure, however not as much as ACEI
or BB
 PRAISE, PRAISE II, V-HeFT III prove that CCBs should be avoided and due to
negative inotropic properties can worsen heart failure
 OAC -warfarin for HF in NSR only with a history of systemic emboli, PE, or visible
thrombosis on echocardiography
 ICD if EF is 35% or less
 Cardiac resynchronization therapy -after maximal medical therapy with NYHA
class 3 symptoms, sinus rhythm, EF 35% or less, QRS>120 msec. Atrial fib patients
may also benefit
Acute exacerbation admissions
 Tests: Physical exam, history, chest x-ray, ECG, BNP, oxygen saturation
 Most important is perfusion/congestion status to predict outcome and
guide therapy:
Acute CHF: Basics
●Airway assessment and continuous pulse ox
●Supplemental oxygen and Bipap
●Vital signs assessment, Position of Comfort
●IV access and Continuous cardiac monitoring(arrhythmias are a serious concern from electrolytes or
failure)
●Diuretic therapy(loop diuretics ie furosemide turosemide bumetanide; high doses may be necessary,
onset of action is about 30 minutes after dose)
●Early vasodilator therapy (Nitro gtt, remember sublingual nitro = 80mcg/min of nitro gtt and has
about the same onset)
●Fluid status monitoring (foley, strict Is and Os, daily weights, especially important for discharge
weight, as well as 2 gram Na restriction)
Acute exacerbation: Advanced
 Reduced systemic perfusion and decreased
urine output suggest shock requiring urgent fluid
resuscitation
 If fluids don’t help IV inotropic support is
important(i.e. dobutamine and/or milrinone,
maybe dopamine) but do not give with
dynamic left ventricular outflow tract
obstruction and BP/Rhythm monitoring must be
continued.
 Pulmonary edema and hypoxia require IV loop
diuretic therapy (Bolus or Infusion), IV morphine.
Elevations in creatinine may improve as the
edema resolves and renal perfusion improves.
 If loop diuretics don’t cut it don’t forget about
hydrochlorothiazide or metolazone (perhaps
better in renal failure, inconclusive evidence)
 Mineralcorticoid can be used but a higher dose
will be necessary
 UNLOAD and CARRESS-HF trials suggest
ultrafiltration has no benefit over diuresis for
acute exacerbations and in fact was inferior at
96 hours in regards to renal function and
adverse events
Post-Acute Exacerbation
 After the patient stabilizes home heart failure
medications and volume status should be
optimized
 Cardiac rehab
 Heart failure clinic
 Patient education
 Early outpatient follow-up with home health as
needed to help with long term management
 Average stay in skilled nursing is 13-15 days
 Bundled payments, important to prevent
readmission to complete all of the above
Future directions of acute HF therapy
 Relaxin/serelaxin-recombinant human relaxin-2 a naturally
occurring human peptide vasodilator. RELAX-AHF trial
demonstrated improvement in dypsnea and lower CV death.
 Hypertonic saline and furosemide-by increasing the osmotic
effect it helps increase the intravascular volume and improve
renal perfusion
 Continuous aortic flow augmentation/CAFA- extracorporeal
pump pulls arterial blood from a peripheral artery and
recirculates it through the aorta by a second arterial access
site augmenting pulsatile cardiac output reducing peripheral
vasodilation and cardiac load. MOMENTUM trial had
promising results in improving cardiac performance but a
significantly higher rate of major bleeds (16.5% compared to
5.1%)
Stage D (End Stage HF)
 Continue therapy from Stage A to C
 Mortality increases to 30-80% due to sudden cardiac death, CHF
exacerbation, or other cause
 Considerations:
 LVAD
 Cardiac transplant
 Chronic IV inotropic support: not proven to benefit. Some palliative use but
safety and efficacy has not been proven. Carries the risk of arrhythmia, central
line infections and complications.
 May also be time to consider palliative care, hospice
Acute MI
One of the leading causes of death in the Western World
 How do we diagnose it?
 Signs & Symptoms
 EKG changes
 Biomarkers
 Treatment?
 Acute
 At discharge
 After the MI
 Secondary prevention
 Tertiary prevention
 Evaluate primary prevention?
Symptoms:
Diagnosis
o Severe sudden prolonged chest
pain radiating to the left arm,
shoulder, neck jaw.*
Signs:
o
Levine’s sign
o
S3 or S4 gallop
o
Hypotension
o
Tachycardia
o
o Palpitations
Low grade fever,
Tachypnea
o
Restless, agitated
o Syncope
o
JVD
o
Crackles
o
Left ventricular heave
o Nausea & vomiting
o Weakness
o Dizziness
o Second wind phenomena(repeat
the same activity without
symptoms)
o Walk through angina(keep going
and the pain resolves)
Levine’s Sign
*Older patients, diabetics, and women may present without chest pain*
AMI EKG Findings
 MUST obtain and review within 10 minutes of arrival
 ST elevation must be present in two contiguous leads
 How to remember contiguous leads:
LIILI
SSAALL
How do 2 contiguous leads localize the infarct?
What about LBBB?
 Modified Sgarbossa Criteria for ventricular paced or LBBB
 1) > or = 1 lead with > or = 1mm of concordant ST elevation
 2) > or = 1 lead of V1-V3 with > or = 1mm of concordant ST depression
 3) > or = 1 lead anywhere with 1mm STE and proportionally excessive discordant
STE, as defined by > or = 25% of the depth of the S wave
Biomarkers
 Troponin or cTn come from the myocardial contractile
apparatus making it highly specific for myocardial
damage
 3 isoforms: cTnC binds calcium, cTnI inhibits actin-myosin
interaction, cTnT binds tropomycin
 cTnI elevates in 3-12 hours, 24 hours peak, returns to normal
in 5-10 days assuming no other events or interventions
 cTnT elevates in 3-12 hours, 12 to 48 hours peaks, returns to
normal in 5-14 days assuming no other events or
interventions
 Due to improvement in cTn assays CK-MB, CK, myoglobin
are no longer recommended or needed for detection.
False negatives occur in up to a 1/3 of patient’s CK-MB
levels even during an MI.
When is an elevated
troponin not a heart
attack?
Differential Causes of Elevated Troponin
 Cardiac trauma: Surgery, Biopsy, Penetrating, Blunt trauma
 Toxins: Sepsis, Chemotherapeutic agents (anthracyclines, alkylating agents,
anti-metabolites, anti-microtubules), snake venom, vasoactive substances
(methamphetamine, cocaine)
 Myocardial Inflammation: Infiltrative cardiomyopathy (amyloid) as well as
infectious neoplastic or inflammatory
 Demand ischemia due to PE, LVH, RVH, CHF
Crotalus horridus
Timber Rattlesnake
What’s the difference between a type 1 or 2 MI?
So how do we diagnosis AMI?
 ACC criteria
 Elevated troponin plus at least one of the following:
 1) Symptoms of Ischemia
 2) ECG changes consistent with ischemia (ST elevation, ST depression
greater than or equal to 1mm, or new LBBB)
 3) New pathologic Q waves (greater than or equal to 0.04 mm wide
and/or 1/3 the QRS height)
 4) Imaging evidence of a new wall motion abnormality or new loss of
viability in an area of myocardium
Medications:
 1) DAPT with Asa (324mg) and Ticagrelor (180mg)-Brilinta is now preferred over
Clopidogrel (Superior to Clopidogrel )and Effient (Less bleeding risk then Effient)
 2) Beta blocker therapy, usually the equivalent of 75mg of Metoprolol PO, 5mg IV
*3 doses as tolerated (IV is 1:5 the PO dose, hold for high grade AV block,
HR<55bpm, hypotension, acute pulmonary edema may need to hold with
asthma)
 3) Sublingual nitro at 0.4mg q5 min or Nitro gtt started at 5mcg/min and titrated
to effect (avoid in hypotension)
 *no nitro with inferior wall infarcts or with phosphodiesterase inhibitors*
 4) Start heparin IV 70units/kg with 4000units bolus then a gtt at 12units/kg/hr
titrated to protocol (likely factor Xa soon)
 *alternatives or additions include low molecular weight heparin, bivalirudin or
fondaparinux*
 *can consider the GP 2B/3A inhibitors Abciximab, Eptifibatide, Tirofiban*
 5) Therapy based on distance to PCI, either Cath lab or Fibrinolysis
Iowa mission lifeline is deploying a statewide protocol that has all the steps
written out along with appropriate facilities and steps along the way
https://www.heart.org/idc/groups/heart-public/@wcm/@mwa/documents/downloadable/ucm_463466.pdf
Secondary Prevention
Reducing the impact of the MI
 Stent has been placed now what?
 Nitrates are stopped after the first day of hospitalization unless used
for angina/heart failure though can be discharged on PRN
 Opiates should be stopped fairly quickly
 Continue the Beta blockers
 Equivalent to 50-100mg of metoprolol BID
 DAPT for at least a year: Ticagrelor 90mg BID along with 81mg of
Asa daily
 There are some people who do not respond, can test P2Y12 or the Plavix
function tests
 Ensure medical compliance, in-stent thrombosis is frequently fatal
Prior to discharge:
 Statin therapy should be started 24-96 hours from admission with
high dose high potency statins
 Goal LDL<70 and CRP <2 add other agents as needed if goals not met
 ACEI and ARB has been found to be beneficial after AMI
 However watch out for hypotension, more than an a 0.3 increase in
creatinine, hyperkalemia, or side effects
 What is the EF after the procedure?
 The current rule is an EF of 35% or less 6 weeks after an MI qualifies for an ICD
 Aldosterone blockade
 only for those without significant renal dysfunction (creatinine less than 2.5 in
men 2.0 in women) or hyperkalemia with an EF less than 40% on a
therapeutic ACEI and have HF or DM
Tertiary Prevention
Soften the AMI effect
 Average STEMI stay is 4-5 days in hospital
 Average STEMI 12-15 days in skilled nursing
 Must quit smoking
 Weight loss should be addressed, can be candidates for bariatric surgery at a
minimum of 6 months post event
 Cardiac rehab along with an exercise plan and counseling is extremely effective
 Phases 1-4
 Improve symptoms, exercise tolerance, while reducing stress, lipids, weight,
smoking, and most importantly mortality
 New trials are unclear about alcohol, reduction to one drink a day at most is
advisable
 Improving glucose control in diabetics, keeping their H1AC as close to goal as
possible
 Repeat 3 month lipid checks with goal directed therapy
 Lifestyle Modification
Primary Prevention
Is there a role to prevent heart disease?
 Early lipid panel checks and goal directed therapy
 Education about weight loss and exercise
 Smoking cessation
 Dangers of alcohol and drug use
 Family history
 Risk stratification including early testing
 Asa daily after the age of 50
 Excellent BP and DM control
Questions?
References/ Sources
Colucci, Wilson S., MD, Stephen S. Gottlieb, MD, James Hoekstra, MD, and Susan B.
Yeon, MD. "Treatment of Acute Decompensated Heart Failure: Components of
Therapy." UpToDate. Wolters Kluwer, 23 Oct. 2015. Web. 4 Apr. 2016.
Korff, Susanne, Hugo A Katus, and Evangelos Giannitsis. “Differential Diagnosis of
Elevated Troponins.” Heart 92.7 (2006): 987–993. PMC. Web. 17 Apr. 2016.
Redfield, Margaret M. "Heart Failure: Diagnosis and Evaluation." Mayo Clinic Cardiology
Concise Textbook. By Richard J. Rodeheffer. 4th ed. Oxford: Oxford UP, 2013. 858-63.
Print.
Redfield, Margaret M., MD. "Pharmocologic Therapy of Systolic Ventricular Dysfunction
and Heart Failure." Mayo Clinic Cardiology Concise Textbook. By Richard J. Rodeheffer.
4th ed. Oxford: Oxford UP, 2013. 869-73. Print.