congestive heart failure

CONGESTIVE HEART FAILURE

“A MATTER OF LIFE OR BREATH”

Capt. Mike Timmons EMT-PDavid 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-PulmonarySystem 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 Frank–Starling 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 activity…walking

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. Edema2. Ascites3. 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• α2 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 hypertensionVery 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-adrengergicreceptors 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 Angiotensin1 to

Angiotensive2

Ace Receptor blockers• Blocks the

ANGIOTENSIN2RECPTOR

• 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 Maintenanceand Supplemental Oxygen protocol.3. If the patient is conscious and in moderate to severe respiratory distress withadequate respiratory effort, apply Continuous Positive Airway PressureDevice (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 IVACCESS.

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).


2. PROVIDE CONTINUOUS EKG AND QUANTITATIVE WAVEFORM CAPNOGRAPHY MONITORING (ETCO2) VIA NASAL CANNULA DEVICE.

3. APPLY NITROGLYCERIN PASTE:

4. ADMINISTER ENALAPRILAT IV IF SBP≥110 MMHG AND NO KNOWN SENSITIVITY TO ACE INHIBITORS (I.E. LISINOPRIL, CAPTOPRIL, AND MONOPRIL).


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).


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.


CPAP Benefits

1. Improves Pulmonary Mechanics2. Decreases Work of Breathing3. Increases Driving pressure of Oxygen

through the interstitial membrane.4. Decreases Pre-Load5. Improves Ejection Fraction 8-10%6. Decreases HR as there is a decrease in

cardiac workload.

02 ResQ Disposable CPAP• Set it and forget it !!!

– 5 cm H2O for COPD– 10.0 cm H2O. For CHF

• Uses 50psi DSS port not the flow meter

• Adjustable mask and Velcro straps

• Put nasal Capnographyunderneath for added FIO2

Amal Mattu, MD, FAAEM, FACEPAssociate Professor and Program Director

Emergency Medicine ResidencyUniversity of Maryland School of Medicine

Baltimore, Maryland

Emergency Cardiology Update:

The Articles You’ve Got to Know!!

Fluid-Pump -Pressure

preload

afterload

LV function

lungs

Pump Failure

DecreasedLV function

Pulmonary edema!!

lungs

Pump Cant keep up with Volume…..Less output through the Supply lineWater backs up in Drafting Tank

preload

Too Much Fluid

preload

afterload

LV functionPulmonary edema!!

lungs

Reduce After Load

Reduced 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

IncreasedAfterload=Back Pressure

Pulmonary edema!!

lungs

Poor LV functionIncreased Work

One inch booster line • High pressure & Poor Flow• Huge demands on the Pump

Fluid-Pump-Pressure

3. increasedAfterload= Back Pressure

2. decreasedLV function

Pulmonary edema!!

lungs

1. increasedpreload

Goals of Treatment

2. decreaseafterloadlungs

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. improveLV function

lungs

• Decrease Venous return=Preload• Lower back pressure=Better Flow• Slow Heart Rate-Decrease Adrenalin• Maximize Oxygenation (CPAP)

Goals of Treatment

1. decreasepreload

lungs

Decrease Fluid Volume !!!Nitro Cuts Venous returnDiuresis will naturally Occur

Goals of Treatment

1. decreasepreload

2. decreaseafterload

3. improveLV 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


Acute Heart Failure (Cotter, et al. Am Heart J 2008)

• What’s the problem with aggressive early use of diuretics?– Doesn’t 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


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


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


Question…• What about prehospital use of furosemide?


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)


15. Evaluation of Prehospital Use of Furosemide in Patients With Respiratory Distress(Jaronik J, Prehosp Emerg Care 2006)

• Reviewed 144 presumed prehospital dCHF pts.• Reviewed hospital records and BNP tests (level

> 400) to determine final diagnosis• Results…


15. Evaluation of Prehospital Furosemide(Jaronik J, Prehosp Emerg Care 2006)

• Non-CHF diagnosis in 42% – Furosemide considered “inappropriate”



• 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”



• 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


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


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%)



• Review article — Ben Lawner, DOPrehospital Management of CHFHeart Failure Clinics, Jan 2009

See attached PDF Article

Questions?

[email protected]

congestive heart failure

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