Rosens – Chapter 79 – Heart Failure And Acute Decompensation

Front 1

Definition of high output failure and ddx

Back 1

hyperdynamic state with CO and ¯O2 extraction with pulmonary/peripheral edema because diastolic dysfunction and circulatory overload
§ hyperdynamic state results in myocardial damage over time

§ DDx:

1.anemia,

2.hyperthyroid,

3.AV fistula,

4.Paget’s disease,

5.thiamine deficiency,

6.sepsis

Front 2

Def low output

Back 2

o low output – most common; ¯CO (systolic dysfunction), filling pressures (diastolic dysfunction), systemic O2 extraction

Front 3

HF R sided vs L sided

Back 3

– useful in acute CHF as gives indication as to which chamber failing
o Rarely isolated
o Useful clinically for etiology and treatment

§ L - Anterior MI: hypotension, pulmonary edema, S3

§ R - Inferior MI: increased JVP, no pulmn edema, hypotension responsive to fluids

Front 4

HF · Systolic vs Diastolic – allows specific tx

Back 4

o Systolic
§ impairment of contractility (¯CO)
§ Seen well on echo – impaired stroke volume and EF
§ Often have a component of systolic dysfunction
§ usually caused by myocyte destruction: AMI,

o Diastolic (1/3)
§ Caused by impaired relaxation (low intracellular energy), increased wall thickness, increased myocardial interstitial collagen
§ more prominent at older ages
§ caused by ischemia, cardiomyopathies caused by chronic HTN, AS

Front 5

PATHOPHYSIOLOGY

Back 5

Primary insults in heart failure myocyte loss and volume overload which lead to pump dusfunction
· This results in a compensatory response to maintain CO:
o Activation of renin-angiotensin-aldosterone system which results in
§ Increased volume via aldosterone
· Initially natriuretic peptides released by the heart (including BNP) promote diuresis and act counter to the R-A-A hormone system
· Tx with diuretics

§ Increased vascular tone via angiotensin II resulting in increased afterload and preload (moves the myocytes along the Frank-Starling curve)
· Tx with ACEi and ARBs

o Activation of sympathetic nervous system which causes increased levels of catecholamines and results in increased afterload and preload
§ NO made by the vascular endothelium plays a role in counter-balancing this
§ Tx with b-blockers

· These compensatory mechanisms result in a number of physiological effects:
o Increased SVR/afterload
o Increased preload
o Increased HR

· This perpetuates a viscious cycle leading to further cardiac ischemia, myocyte loss, remodeling, and decreased LV function leading to further CO impairment thus starting to cycle over again.
· Eventually these “compensations” lead to decompensation

Front 6

renin angiotensin system

Back 6

Front 7

ETIOLOGY OF CHRONIC HEART FAILURE

Back 7

· Things that increase the workload of the heart:
o Hyperdynamic states
§ AV fistula
§ Hyperthyroid
§ Beri-Beri
§ Paget’s
§ Anemia
§ Sepsis

o Increase afterload (both pulmonary and systemic)
§ HTN
§ Valvular heart disease
§ Pulmonary HTN
§ COPD

· **Rememberpulmonary causes of heart failure is termed Cor Pulmonale**

· Things that decrease the muscle power of the heart
o Ischemia – CAD, AMI
o Cardiomyopathy
§ Infective – myocarditis, endocarditis, pericarditis
§ Inflammatory – amyloidosis
§ Toxicologic – EtOH
§ Drugs – adriamycin
§ Degenerative – idiopathic, HOCM
§ Post-partum
§ Anatomic – congenital heart disease
§ Tachyarrhythmia associated cardiomyopathy

Front 8

ETIOLOGY OF ACUTE DECOMPENSATED HEART FAILURE

Back 8

Dietary indiscretions
o Medication non-compliance
o Disease Progression
· Increased afterload
o HTN crisis
o Valvular dysfunction
o Physical, environmental, emotional stress (increase catecholamines)
o Acute PE
· Decreased output
o Ischemia
o Arrhythmia
o Acute myocarditis
o Disease progression
· Increased demand
o Thyrotoxicosis
o Pregnancy
o Anemia

Front 9

NYHA classification

Back 9

I- no limitations - asymptomatic during usual daily activities

II - slight limitation - mild symptoms with ordinary activities (dysp,fatigue,CP)

III-moderate limitation - symptoms noted with minimal activity

IV- severe limitation - symptoms at rest

Front 10

HF CXR

Back 10

· Order of appearance of X-ray findings
1. Increased heart size, cardiothoracic ratio >50%
· usually noted first b/c usually Hx of prior CHF or may have DCM, etc
2. Large hila with indistinct margins
3. Prominence of superior pulmonary veins; CEPHALIZATION OF FLOW
4. Fluid in the interlobar fissure
5. Pleural effusion
6. Kerley B lines (base on the pleural surface of the lung and extending horizontally a variable, but usually short, distance toward the center of the chest).
7. Alveolar edema

Front 11

Signs and symptoms HF

Back 11

Front 12

NIPPV

what does it do and whats the evidence

Back 12

o Increases FRC
o Increased oxygenation
o Decreased sympathetic tone
o Decreased LV preload b/c of intrathoracic pressure
o Decreased work of breathing (decreased metabolic demands of respiratory muscles)
o Relative afterload reduction

o Vital FMR, et al. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database of Systematic Reviews 2013, Issue 3.

reduced mortality significantly(NNT 13)
§ reduced intubation significantly(NNT 8)

Gray A, Goodacre S, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J Med 2008;359:142-151

§ Severe APE excluded
§ Findings: no difference in mortality or intubation rates
§ There was greater mean improvements at 1 hour in terms of patient-reported dyspnea, heart rate, acidosis, and hypercapnia.

Li H et al. A comparison of bilevel and continuous posi- tive airway pressure noninvasive ventilation in acute cardiogenic pulmonary edema. Am J Emerg Med. 2013 Sep;31(9):1322-7. PMID: 23928327. \

no diff cpap/bipap

Front 13

Morphine

Back 13

No evidence that it venodilates centrally, there are Swan studies to suggest that it increases CVP
o Sympatholytic: decreased HR, BP, contractility, MVO2
o ADHERE registry (Emerg Med J 2008;25:205-209) shows morphine is an independent predictor of mortality, and is associated with increased ICU admission, days on a vent, and hospital length of stay.

o Amal Mattu suggests that the only reason to use it is for anxiolysis but benzos do that better anyway.
o If you are going to use it: 2 - 5 mg iv prn to effect

Front 14

Nitrates

Back 14

o Mainstay of treatment
o Increases nitric oxide which increased cGMP :. vasodilation
o Low dose is primary venous VD, decrease preload
o High dose is arterial VD, decreased BP, afterload (esp in HTN patients)
o Potential for coronary artery VD and reduction of ischemia
o Watch for hypotension: usually responds to fluid challenge

Front 15

What level of hypotension should NTG be stopped?

How much to give?

Back 15

o Depends on patient; SBP 75 and talking is OK, SBP 90 and decreased LOC not OK

o Sublingual tab/spray: rapid onset, big doses, duration 30 min
§ 400mcg/spray, consider giving sprays while starting IV NTG
o Patch has poor absorption with diaphoresis!
o IV: start 10 ug/min and increase by 10 ug/min q5min to effect (may need up to 300 ug/min; can be more aggressive with starting dose and titration is adequate BP

Front 16

Nitroprusside

Back 16

o Potent vasodilator: venous decreases preload, arterial decreases afterload
o More arterial dilation than nitroglycerin
o Drug of choice with hypertensive crisis and APE
o Continuous infusion, BP monitoring mandatory
o Coronary steal phenomenon = nitroglycerin better with MI b/c of possible coronary steal where less diseased vessels dilate and steal blood flow and increased risk of hypotension
o Thiocyanate toxicity possible: increased agitation, lactic acidosis (especially with renal failure); can also cause methemoglobinemia
o Convert to po therapy ASAP: ACE, NTG, hydralazine

Front 17

Lasix

1. how does it work?

2. dose and how to give?

Back 17

MOA: inhibits 2Na/Cl co-transporter in thick ascending loop of Henle :. increases Na and water excretion and decreases preload; also diuretic induced neurohormaonal changes of PGE2, ANP
o Effect is seen quicker than renal effects thus likely a pulmonary vasodilator (this has been shown in swan ganz studies)
o Watch for hypokalemia/magnesemia

o Dose 1mg/kg iv but may require much more with renal failure
o Can give massive doses with renal failure (max is 1000 mg); risk hearing loss
o Doses < 100mg can be pushed, > 100mg should be infused

Front 18

· ACE-I in acute CHF

Back 18

ACE-I good in acute setting for afterload reduction
o Captopril 6.25 mg – 25mg po
o Give dose if already on ACE-I, be very careful if not already on
o Do NOT give if critical Aortic Stenosis (afterload redution, increased gradient, reduced coronary perfusion)

Front 19

Niseritide

Back 19

o Recombinant BNP

o VMAC trial (Industry sponsored trial), JAMA 2002; 287:1531-40.
§ DBRCT, n=500
§ Primary E.P. = PCWP
§ Secondary E.P. = Sx at 3H
§ Results
§ ↓ PCWP (and improved other cardiac indices)
§ No improved Sx relief at 24hrs
§ No difference in mortality at 18/12 (25% for nesiritde, 21% Nitro, p=0.32)
§ Equivalent to Nitro (at best)
§ Significant hypotension, bradycardia, renal dysfx
§ Trend to higher MR
o JAMA, 2005. Pooled analysis of 860 patients
§ MR was 7.2% v 4.0% , p=0.059(niseritide –v- std Tx)

Front 20

Treatment of APE in Hypotensive Patients

Back 20

1.Fluids

2. Dopamine

3. Dobutamine

4. norepi

5.milrinone

Front 21

Fluids fluids for APE?

Back 21

o Clinically, small fluid challenge and monitor response of BP and possible worsening of oxygenation
o Small boluses 250 ml NS over 10 min
o Repeat prn if respiratory status not deteriorating
o Should increase BP if hypotension due to hypovolemia
§ REMEMBER that these patients are often hypovolemic overall they just have a redistribution of fluids to their lungs

Front 22

Dopamine - for APE?

Back 22

o Low doses: 2-5 ug/kg/min: dopaminergic; renal/splanhnic vasodilation
o Moderate: 5-15 ug/kg/min: beta adrenergic; increased contractility, HR
o High doses: > 15 ug/kg/min: alpha adrenergic; vasoconstrict all vessels, increases BP, HR, contractility (may ppt ishcemia, may worsen pulmn edema - venodilator can reduces worsening of Ped)
o Venoconstriction at low doses may increase wedge pressure and increase edema
o Indication = hypotension SBP 70 - 100 with s/s of hypoperfusion failing fluid challenge:10-20 ug/kg/min

Front 23

Dobutatmine for APE?

Back 23

Mainly B1 agonist, some B2 and some alpha
o B1 is +ve ionotrope and B2 is a venodilator
o May lead to hypotension by vasodilation if CO doesn’t increase much
o Excellent for normotensive, caution with borderline hypotension, don’t use alone in hypotensive (May norepi for vasoconstriction)
o Excellent choice for AMI: increases cardiac function without worsening ischemia by increasing heart rate
o Dose is 5 - 25 ug/kg/min: start 2 and increase to 20 ug/kg/min
o Indication = hypotension SBP 70 - 100 with NO s/s of hypoperfusion after fluid challenge

Front 24

· Norepinephrine

Back 24

o Mostly alpha agonsist (some beta)
o Drug of choice for volume repleated profound hypotensive (SBP < 70)
o Goal: temporary management until IABP, PTCA, surgery
o Start at 0.1 ug/kg/min and titrate up to 2-3 ug/kg/min
o Indication = hypotension SBP < 70 failing fluid challenge

Front 25

MI and cardiogenic shock with acute pulmonary edema

Back 25

· Needs cath lab or PTCA ASAP
· Shock trial showed no benefit of thrombolysis
· Elevate BP with dopamine then lysis is next best option if cath lab not available
· Avoid negative inotropes: no BetaBlockers!
· R/o mechanical complications of MI
o ?RV infarct
o Valve rupture (?murmur)
o Free wall rupture (?PCE w/US)
o VSD (?murmur)
o Consider AoD

Front 26

ACEi systolic dysf in HF

Back 26

Decrease mortality and hospitalization rates
· Every patient should be on an ACEi
· If cough, switch to ARB
· Target is ramipril 10mg/d, captopril 150mg/d

Front 27

Angiotensin Receptor Blockers (ARBs) systolic dysf in HF

Back 27

Used for contraindication or intolerance of ACE-I
· Increasing evidence of benefit in addition to ACE-I thus may be added for persisting CHF symptoms once other meds are maxed
· Losartan (cozaar), Valasartan (Diovan)

Front 28

BetaBlockers in HF?

Back 28

Cardioselective: metoprolol, carvidolol
· Good post MI to reduce mortality by reduction of neurohormnal remodelling
· Not started in acute CHF phase
· Start slow: metoprolol 12.5mg bid

Front 29

Spirnolactone (Aldactone) - sys HF

Back 29

· Aldosterone antagonist thus decreases Na+ resorption and increases K+ retention
· Decreases mortality in class III/IV CHF
· NEJM 1999 RALES study: EF < 35% on ACE-I; trial stopped early b/c one year death rate was 35% vs 46% (ARR 11%, NNT about 10); also showed improved symptoms with spirnolactone therapy
· Potassium sparing diuretic thus watch K+ (esp with ACE-I + spirnolactone)
· Dose: 25 - 50 mg po od
· Triamterene (Triazide), eplerenone is a similar agent
· Who should be on spirnolactone?
o NYHA class III or IV (symptomatic on less than ordinary activity or symptomatic at rest)
o EF < 35%
o Already on ACE-I

Front 30

Lasix

Back 30

· Symptomatic control, no reduction in mortality
· Side effects: hypokalemia, hypomagnesemia, hypotension, gout
· Metolazone (Zaroxlyn) used for synergy if resistant to lasix: ideally given 2 hrs before lasix dose

Front 31

Nitroglycerin

Back 31

· Symptomatic control, no reduction in mortality
· Patch or oral pills
· Tachyphylaxis a problem thus patch only worn for 12hrs/day

Front 32

Digoxin

Back 32

·
· Symptomatic improvement but no effect on mortality
· Has been shown to decrease hospital admission rates
· Should NOT replace ACE-I, BB, spirnolactone which do decrease mortality
· Best indication: CHF + Afib + diastolic dysfunction
· Load iv: 0.5 mg then 0.25 mg until effect or 1.5 mg total
· Maintenance: 0.25 mg per day

Front 33

CCB + what other interventions?

Back 33

· CCB have no role in CHF managment
· Influenza and pneumoccocus vacination
· Fluid and salt restriction counselling

Front 34

ICDs

Back 34

· Increasing role of ICDs in CHF and CAD patients
· MADIT II showed a decreased mortality with ICD use compared to medical therapy in patients with LV EF < 30% post MI

· SCD-HeFT: sudden Cardiac Death in Heart Failure Trial
o ICD vs amiodarone
o N=2521
o NYHA class 2-3 and LVEF < 35%
ICD Amiodarone
o 3 yr mortality 17% 22%
o 5 yr mortality 29% 36%

Front 35

Chronic Resynchronisation Therapy (CRT) rationale?

Back 35

· Rationale: prolongation of QRS in patients with CHF has been shown to be an independant predictor of adverse outcomes
o QRS delay occurs in up to 30% of moderate to severe CHF patients
o QRS delay, especially LBBB, causes electrical and mechanical dyssynchrony in patients with depressed LV function which lead to decrease in stroke volume, EF
· CRT = pacing of RV and LV to cause simultaneous contraction and synchrony that has been shown to improve LV function

Front 36

CRT trials?

Back 36

CRT trials have looked at CHF patients with EF < 35%, QRS > 120 msec and LBBB and/or evidence of dyssynchrony on echo, normal sinus node function (NOT afib), appropriate chf therapy (ace-i, bb, etc)
· Pacer leads placed in the RV and the Coronary Sinus branch vein to achieve LV stimulation (a cardiac vein!)
· Studies: MIRACLE, InSync ICD, CONTACK CD
o All 3 studies showed symptom improvement

· COMPANION trial
o NEJM 2004
o Medical therapy vs CRT vs CRT + ICD
o Combined outcome of death or hospitalization
o CRT+ICD > CRT alone > medical therapy

Front 37

Diastolic Dysfunction

Back 37

· BetaBlockers: rate control for better filling
· ACE-I: benefit not well defined but should be used as most have some systolic component
· Treat underlying cause: HTN, valve dz, etc
· Can’t decrease preload too much b/c they are preload dependant: careful with diuretics and nitroglycerin