CONGESTIVE HEART

FAILURE
A MATTER OF LIFE OR BREATH
Capt. Mike Timmons EMT-P
David Miramontes MD FACEP NREMT
OBJECTIVES
Congestive Heart Failure Explained
Cardio-Endocrine-Renal-Pulmonary System
dysfunction as new paradigm
Pathophysiology of Congestive Heart Failure
Signs & Symptoms
Right-sided vs Left-sided Congestive Heart Failure
Treatment Modalities Medications and CPAP
DCFEMS Acute Pulmonary Edema Protocol
Putting it all Together
CHF-New paradigm
Congestive Heart Failure should be
named.
Cardio-Endocrine-Renal-Pulmonary
System dysfunction
CHF is a multisystem disease that is not
simply caused by physical Heart disease.
Studies at to Cause
National Health and Nutrition
Examination Survey (NHANES I)
Ischaemic heart disease 62%
Cigarette smoking 16%
Hypertension 10%
Obesity 8%
Diabetes 3%
Valvular heart disease 2%
(much higher in older populations)
Epidemiology of
Heart Failure
Heart failure is caused by any condition which reduces the
efficiency of the myocardium or heart muscle through
damage or overloading.
Myocardial Infarction
(Muscle death and scarring)
Heart Valve Disease
Hypertension causes Hypertrophy
(thick stiff Ventricle that fills poorly)
Cardiomyopathy
Heart Muscle disease causes Ventricle Dilation, scarring
Toxic Myopathy (Stimulants, Cocaine, HIV)
Pathophysiology of Congestive
Heart Failure
In a healthy heart increased filling of the
ventricle results in increased force of
contraction
(by the FrankStarling law of the heart) and thus a
rise in cardiac output.
In heart failure. this mechanism fails. As the
ventricle is overloaded with blood beyond the
point where heart muscle contraction is most
efficient, ejection fraction decreases resulting
in partial fluid overload in a euvolemic state.
Pump versus Pressure
PUMP Issues
Hypertrophy an increase
in physical size of the
myocardium, Which is
caused by the terminally
differentiated heart
muscle fibers increasing
in size in an attempt to
improve contractility.
This may contribute to
the increased stiffness
and decreased ability to
relax during diastole.
Afterload=Back pressure
High Blood pressure at the
Aortic Valve decreases the
ejection of blood from the
Ventricle as cardiac work is
used to generate pressure to
overcome this back pressure
instead of physical
contraction that ejects blood
from the left Ventricle
Exercise Intolerance
As the heart works harder to meet normal
metabolic demands, the amount cardiac output
reserve that is needed in times of increased
oxygen demand (e.g. exercise) is reduced.
This contributes to the exercise intolerance
commonly seen in heart failure. Since the heart
has to work harder to meet the normal
metabolic demands, it is incapable of meeting
the metabolic demands of the body during
exercise or increased activitywalking
High Blood Pressure
The increased peripheral resistance and
greater blood volume place further
strain on the heart and accelerates the
process of damage to the myocardium.
Causative Factors:
Vasoconstriction (Renin-Angiotensin )
Salt Retention (Aldosterone)
Water Retention (Naturetic Peptide)
Renin Angiotensin
RENIN
Renin is released when
Blood Flow to Kidneys is
decreased
Sympathetic Stimulation
to Kidney also triggers
renin release
Angiotensin I
Peptide pro-Hormone
released from the Liver
Activated by Renin
Converted to
Angiotensin II by
Angiotensin Converting
Enzyme
Becomes potent
Vasoconstrictor
Stimulates release of
Aldosterone
Aldosterone
Steroid Hormone from adrenal gland
Works at Kidney to retain sodium
resulting in water retention in
vasculature
Increases blood volume=Fluid Retention
Medication-Spiranolactone blocks this
action.
Exact opposite of Naturetic Peptide
Right-sided failure
Backward failure of the right ventricle
leads to congestion of systemic
capillaries.
This generates excess fluid accumulation
in the body.
1. Edema
2. Ascites
3. Scrotal Edema
Right Heart Failure
Can result from multiple vascular and
organ issues.
Examples
Pulmonary hypertension
Cor Pulmonale
Left Heart Failure
Right failure
As the right heart ejected blood volume
decreases relative to preload, the
pressures increase in the venous
system. This results in venous overload
and increases in interstitial fluid volume.
Most often seen as gravity dependent
pitting edema of the ankles.
Graded on a scale from +1 to +4
Right-sided failure
As the body becomes overloaded with fluid
from congestive heart failure, swelling
(edema) of the ankles and legs or abdomen
may be noticed. This can be referred to as
"right sided heart failure. As the right
heart chambers fail to pump venous blood
to the lungs to acquire oxygen fluid builds
up in gravity-dependent areas such as in the
legs
Peripheral Edema
Vasoconstriction, Salt and fluid retention produce
an increased hydrostatic pressure in the capillaries.
This increased pressure forces additional fluid out
of the blood vessels into the tissue.
This results in edema (fluid build-up) in the tissues
Left-sided failure
Backward failure of the left ventricle
causes congestion of the pulmonary
vasculature, and so the symptoms are
predominantly respiratory in nature.
Backward failure can be subdivided into
failure of the left atrium, the left
ventricle or both within the left circuit
CHF Signs and Symptoms
Cardio
Fatigue
Exercise Intolerance
Edema
Chest pain
Paroxysmal Nocturnal
Dyspnea (PND)
Pulmonary
Dyspnea
Cough
Poor Resp. reserve
Hypoxia
Not Hypercarbia
Decreased lung
Compliance
Decreased Oxygen
Diffusion
Anti-hypertensives
Relaxation of smooth
muscle
Widens blood vessels
Lowers systolic blood
pressure
Vasodilator
Widens the blood
vessels, decreasing
vascular pressure.
Results in appropriate
redistribution of fluids
Therefore allowing
more blood flow
Anti-hypertensives
Clonidine
Centrally Acting in the
Brain

2
receptors in the
brainstem
Decreases sympathetic
tone
Decreases peripheral
Vascular Resistance
Lowers Blood Pressure
Also used for ADHD
Tics
Withdrawal Symptoms
If stopped suddenly
Rebound hypertension
Very Dangerous rise in BP
occurs
Lasix
Hydrochlorothiazide(HCTZ)
Bumex
These inhibit reabsorption of Na+ into
the kidneys and sodium and water are
excreted.
Metoprolol
Atenolol
Propanolol
Amiodarone
(Has Beta, Potassium
Channel blocker
effects)
Useful by blocking
the beta-adrengergic
receptors of the
sympathetic nervous
system
the heart rate slows
Allows for longer
filling time
Promotes ventricular
relaxation
Nifedipine
Diltiazem
Verapamil
Amlodipine
Felodipine
Used to dilate blood
vessels
Lowers Afterload and
Blood pressure
Used mostly with
CHF in the presence
of ischemia/spasm
ACE Inhibitors
Blocks Angiotensin
1
to
Angiotensive
2
Ace Receptor blockers
Blocks the
ANGIOTENSIN
2
RECPTOR
Anti-hypertensive
Decreases Afterload
Increases Renal blood flow
Sodium Excretion
Protects from Diabetic Nephropathy
Spiranolactone
Blocks Endocrine
hormone
Aldosterone
Pushes out Sodium
and Water into urine
Resorbs Potassium
DCFEMS DEPT. PROTOCOLS
1. Initiate General Assessment and Universal Patient Care.
2. Support airway and provide supplemental Oxygen per Airway
Maintenance
and Supplemental Oxygen protocol.
3. If the patient is conscious and in moderate to severe
respiratory distress with
adequate respiratory effort, apply Continuous Positive Airway
Pressure
Device (CPAP) and titrate to a pressure of:
4. PLACE THE PATIENT IN A POSITION OF COMFORT.
EMTS WHO HAVE COMPLETED THE IV TRAINING
MODULE AND ADVANCED EMTS MAY INITIATE IV
ACCESS.
5. ESTABLISH AN IV OF NORMAL SALINE KVO OR SALINE
LOCK.
DCFEMS Dept. Protocols
1. ADMINISTER NITROGLYCERIN. ALS PROVIDERS MAY
ADMINISTER 1ST DOSE EVEN BEFORE IV ACCESS IS
ESTABLISHED.
CAUTION - WITHHOLD NITROGLYCERIN OR CONSULT
MEDICAL CONTROL IF:
- THE PATIENT HAS A SYSTOLIC BLOOD PRESSURE
110 MM/HG.
- THE PATIENT HAS TAKEN ERECTILE DYSFUNCTION
MEDICATIONS WITHIN THE PAST 24 HOURS (I.E.
VIAGRA, CIALIS, OR LEVITRA).
DCFEMS Dept. Protocols
2. PROVIDE CONTINUOUS EKG AND QUANTITATIVE
WAVEFORM CAPNOGRAPHY MONITORING (ETCO2) VIA
NASAL CANNULA DEVICE.
3. APPLY NITROGLYCERIN PASTE:
4. ADMINISTER ENALAPRILAT IV IF SBP110 MMHG AND
NO KNOWN SENSITIVITY TO ACE INHIBITORS (I.E.
LISINOPRIL, CAPTOPRIL, AND MONOPRIL).
DCFEMS Dept. Protocols
5. IN INSTANCES WHERE BRONCHOSPASM IS PRESENT
WITH WHEEZING, ALBUTEROL 2.5 MG VIA NEBULIZER IN
LINE CIRCUIT WITH CPAP.
6. OBTAIN A 12 LEAD EKG IF TIME AND PATIENT
CONDITION PERMITS. IF MYOCARDIAL INJURY IS
SUSPECTED BECAUSE OF ST ELEVATION WHICH IS
EVIDENT IN TWO OR MORE CONTIGUOUS LEADS OR
CHEST PAIN IS PRESENT, ADMINISTER ASPIRIN 325 MG
PO AND TRANSPORT TO THE NEAREST CARDIAC
INTERVENTIONAL FACILITY (STEMI FACILITY).
DCFEMS Dept. Protocols
1. CONSIDER LASIX 20-40 MG IV. PEDIATRIC
PATIENTS: 0.5 MG/KG IV.
2. CONSIDER MIDAZOLAM 1-2 MG IV UP TO 5
MG OR IN PEDIATRIC PATIENTS: 0.1 MG/KG
IV UP TO 5 MG AS NEEDED FOR SEVERE
ANXIETY TITRATED TO ANXIETY REDUCTION
WITH A NOTED DECREASE IN ANXIETY
RELATED TACHYCARDIA.
DCFEMS Dept. Protocols
CPAP Benefits
1. Improves Pulmonary Mechanics
2. Decreases Work of Breathing
3. Increases Driving pressure of Oxygen
through the interstitial membrane.
4. Decreases Pre-Load
5. Improves Ejection Fraction 8-10%
6. Decreases HR as there is a decrease in
cardiac workload.
0
2
ResQ Disposable CPAP
Set it and forget it !!!
5 cm H
2
O for COPD
10.0 cm H
2
O. For CHF
Uses 50psi DSS port
not the flow meter
Adjustable mask and
Velcro straps
Put nasal Capnography
underneath for added
FIO
2
Amal Mattu, MD, FAAEM, FACEP
Associate Professor and Program Director
Emergency Medicine Residency
University of Maryland School of Medicine
Baltimore, Maryland
Emergency
Cardiology Update:
The Articles Youve
Got to Know!!
Fluid-Pump -Pressure
preload
afterload
LV function
lungs
Pump Failure
Decreased
LV function
Pulmonary edema!!
lungs
Pump Cant keep up with Volume..
Less output through the Supply line
Water backs up in Drafting Tank
preload
Too Much Fluid
preload
afterload
LV function
Pulmonary edema!!
lungs
Reduce After Load
Reduce
d
afterload
lungs
Use Five inch Supply hose from a Hydrant
Lower back pressure=Better Flow
Less Work on the Pump
LV function
High Afterload=CHF
Increased
Afterload
=Back Pressure
Pulmonary edema!!
lungs
Poor LV function
Increased Work
One inch booster line
High pressure & Poor Flow
Huge demands on the Pump
Fluid-Pump-Pressure
3. increased
Afterload=
Back Pressure
2. decreased
LV function
Pulmonary edema!!
lungs
1. increased
preload
Goals of Treatment
2. decrease
afterload
lungs
Bigger Hose=Less Resistance=Better Flow
Use Five inch Supply hose from a Hydrant
Lower back pressure=Better Flow
Less Work on the Pump
Goals of Treatment
3. improve
LV function
lungs
Decrease Venous return=Preload
Lower back pressure=Better Flow
Slow Heart Rate-Decrease Adrenalin
Maximize Oxygenation (CPAP)
Goals of Treatment
1. decrease
preload
lungs
Decrease Fluid Volume !!!
Nitro Cuts Venous return
Diuresis will naturally Occur
Goals of Treatment
1. decrease
preload
2. decrease
afterload
3. improve
LV function
lungs
Goals of Treatment
lungs
body
Pulmonary edema
Total body hypovolemia or euvolemia
Goals of Treatment
lungs
body
Cardiogenic Pulmonary
Edema
Note: more than 50% of patients with
cardiogenic pulmonary edema are
euvolemic!!
Treatment should be based not
necessarily on fluid removal, but on
fluid redistribution.
body
Goals of Treatment
Pulmonary edema
lungs
body
Goals of Treatment
Pulmonary edema
lungs
body
Goals of Treatment
lungs
body
Cardiogenic Pulmonary
Edema
Acute Heart Failure (Cotter, et al. Am
Heart J 2008)
Whats the problem with aggressive early use
of diuretics?
Doesnt work quickly in patients with Pulm. Edema
Literature: no immediate central preload benefit
Early rise in SVR, decrease in CO
MAKES CHF WORSE !!!!!!!!
Complications 24 hrs later if patient was euvolemic
Increase renal dysfunction worse prognosis
Cardiogenic Pulmonary
Edema
14. Acute Heart Failure
(Cotter, et al. Am Heart J 2008)
Focus of early therapy should be fluid
redistribution, not fluid removal
Preload and afterload reduction
Cardiogenic Pulmonary
Edema
Beyond Pulmonary Edema: Diagnostic, Risk
Stratification, and Treatment Challenges
of Acute Heart Failure Management in the
Emergency Department
(Collins, et al. Ann Emerg Med 2008)
Fluid overload vs. fluid maldistribution
Pts with maldistribution focus on vasodilation
rather than diuresis
Cardiogenic Pulmonary
Edema
Question
What about prehospital use of furosemide?
Cardiogenic Pulmonary
Edema
Prior literature has raised concerns
No immediate benefit
(Hoffman, Chest 1988)
Misdiagnosis rate 20-35%
If these patients are treated with furosemide,
potential complications, worse outcome
(Hoffman, Chest 1988)
(Wuerz, Ann Emerg Med 1992)
Cardiogenic Pulmonary
Edema
15. Evaluation of Prehospital Use of
Furosemide in Patients With Respiratory
Distress
(J aronik J , Prehosp Emerg Care 2006)
Reviewed 144 presumed prehospital dCHF pts.
Reviewed hospital records and BNP tests (level
> 400) to determine final diagnosis
Results
Cardiogenic Pulmonary
Edema
15. Evaluation of Prehospital Furosemide
(J aronik J , Prehosp Emerg Care 2006)
Non-CHF diagnosis in 42%
Furosemide considered inappropriate
Cardiogenic Pulmonary
Edema
15. Evaluation of Prehospital Furosemide
(J aronik J , Prehosp Emerg Care 2006)
Non-CHF diagnosis in 42%
Furosemide considered inappropriate
Sepsis, dehydration, pneumonia in 17%
Furosemide considered potentially harmful
Nine patients died
Seven had received furosemide inappropriately
Cardiogenic Pulmonary
Edema
15. Evaluation of Prehospital Furosemide
(J aronik J , Prehosp Emerg Care 2006)
Authors conclusion
Prehospital personnel now required to get online
medical control approval for furosemide
EMS systems should reconsider the
appropriateness of prehospital diuretic use
No evidence that early use of furosemide helps
anyway, even if it is dCHF
16. Morphine and Outcomes in Acute
Decompensated Heart Failure
(Peacock, et al. Emerg Med J 2008)
Background: MS is routinely used in dCHF
despite
Lack of good evidence proving benefit
Multiple studies demonstrating subjective and
objective deterioration
Harmful if prehospital dx incorrect
Cardiogenic Pulmonary
Edema
16. Morphine and Acute dCHF
(Peacock, et al. Emerg Med J 2008)
Reviewed data from ADHERE registry
20,782 patients (14% of total) received MS
No difference between MS group vs. non-MS group
in terms of age, VS, comorbidities
Cardiogenic Pulmonary
Edema
16. Morphine and Acute dCHF
(Peacock, et al. Emerg Med J 2008)
Results: MS was independent predictor of
Mechanical ventilation (15% vs. 3%)
Increased hospital stay (5.6 vs. 4.2 days)
Increased ICU admission (38.7% vs. 14.4%)
Mortality (13% vs. 2.4%)
Cardiogenic Pulmonary
Edema
Cardiogenic Pulmonary
Edema
Review article Ben Lawner, DO
Prehospital Management of CHF
Heart Failure Clinics, J an 2009
See attached PDF Article
Questions?
David.Miramontes@dc.gov
202-715-2856