congestive heart failure
DESCRIPTION
EMS managementTRANSCRIPT
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).
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 SBP≥110 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 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
Cardiogenic Pulmonary Edema
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
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(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…
Cardiogenic Pulmonary Edema
15. Evaluation of Prehospital Furosemide(Jaronik J, Prehosp Emerg Care 2006)
• Non-CHF diagnosis in 42% – Furosemide considered “inappropriate”
Cardiogenic Pulmonary Edema
15. Evaluation of Prehospital Furosemide(Jaronik 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(Jaronik 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, DOPrehospital Management of CHFHeart Failure Clinics, Jan 2009
See attached PDF Article
Questions?