Heart Failure : Heart Failure Information per the National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey as well as the 2009 Focus Update to the 2005 American College of Cardiology/AHA guidelines.
Published by the American Heart Assoc.
Prevalence : Prevalence 658,000 Annual ED encounters.
Nearly 80 % admitted.
Partially because there is little to guide disposition decisions.
As high as 50% of patients will return to the ED in the same year.
Why the high return rate?
What is Heart Failure ? : What is Heart Failure ? AHA says a “complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood”.
What are some structural causes?
Functional causes?
Structural and Functional : Structural and Functional What would a cardiac rhythm disturbance be classified as, structural or functional?
CHF? : CHF? Now referred to as “Heart Failure Syndrome”.
Acute is defined as 24 to 48 hours.
Subacute defined as greater than 48.
“Acute Heart Failure Syndrome”
Why is Congestive Heart Failure not always an accurate description?
Basic review : Basic review I find it easy to think of patients as having two hearts, right and left.
What does the right heart do?
Left heart?
Pulmonary edema, which heart is failing?
When might RHF be encountered?
Ventricular Remodeling : Ventricular Remodeling Any guesses on what this term means?
LV remodeling : LV remodeling Pts with HF have elevated levels of norepi, angiotensin II, aldosterone, endothelin, vasopressin and cytokines.
These neurohormonal factors increase the hemodynamic stresses on the ventricle causing sodium retention and peripheral vasoconstriction also causing myocardial fibrosis.
This causes hypertrophy and or dialation of the ventricle thus a“remodel”.
Simply put : Simply put If uncontrolled, increased heart rate, increased vessel pressures, increased volume and increased oxygen demand on the heart.
Coronary artery disease is “believed” to be the underlying cause of 2/3rds of pts with HF and low EF.
Roughly how much blood is ejected from the left ventricle with each beat. CO= SVxHR
Other causes? : Other causes? What are some other causes of HF?
Risk factors?
What medications are HF pt likely to be taking?
Rx Meds : Rx Meds Aldosterone antagonists
Inhibits sodium reabsorbtion in the collecting duct of the nephron in the kidney.
Increased diuresis and increased potassium.
These meds end with ONE. Spirorolactone, Canrenone, Pronnenone etc.
Rx Meds : Rx Meds Angiotensin converting ezyme inhibitors ACE-I.
Renin released from kidney forming angiotensin I, this acts on the adrenal gland to produce aldosterone. Also released, is the angiotensin covenerting enzyme (ACE) converting angiotensin I to angiotensin II.
ACE inhibitors block this conversion.
ACEI : ACEI Angiotensin II causes vasoconstriction, contributes to remodeling, stimulate the adrenal cortex to release aldosterone increasing volume and also releasing anti-diuretic hormone called....
So, ACE inhibitors are useful for a variety of reasons.
End in RIL. Enalapril, Ramipril, Lisinopril, Benzapril etc.
Endotheline Antagonists : Endotheline Antagonists Proteins that constrict blood vessels increasing blood pressure. Produced in the endothelium.
These end in TAN. Ambrisentan, Sitaxentan, Bosentan, Tezosentan.
Beta Blockers : Beta Blockers B-1 blockers lower heart rate and O2 demand of the heart while also increasing CO and potentially lowering blood pressure. These also decrease renin secretion.
These are only to be used in combination with ACE-I and diuretics.
End in LOL. Metoprolol, Carvedilol, Bisolprolol.
This is why your pt might not be tachycardic but still will likely be hypertensive in extremes.
Symptoms : Symptoms The majority of HF pts have symptoms due to LV function. Knowing this how might a pt present? Where does the fluid end up?
What is the most common complaint?
What might be a few other complaints?
Hint- remember all of the physiologic changes listed previously.
Subjective : Subjective Complaint of SOB.
Fatigue, exercise intolerance.
Weight gain
Swelling
Orthopnea
PND
Increased urine with decreased appetite
Objective : Objective Tachypnea with dyspnea. What is the difference?
Edema. Peripheral edema caused by which side of heart? May or may not be present.
Which heart typically fails first R or L?
JVD? May or may not be present.
Objective Cont.. : Objective Cont.. Almost ALL pts have elevated blood pressure when symptomatic. What is elevated?
Breath sounds. Rales or diminished bases.
Low sao2 when in extremis
Capnogram?
Other sx?
Treatment of LVHF : Treatment of LVHF Remember we are treating the S/S.
Oxygen! These pts are SOB.
No exertion.
Nitrates- Decrease preload and afterload, as well as dilation of the coronary arteries.
CPAP this not only “pushes the fluid out” but also DECREASES preload.
NEBS? : NEBS? Everyone has a different take on this one.
Mine.. If you think that there is a broncospasm component or hx of COPD or suspected pneumonia then yes.
If you are not sure and they are wheezing then yes. Risk to benefit?
Can somewhat be used diagnostically.
No continuous nebs and I stay away from Duonebs (Atropine).
RVHF? : RVHF? Remember, you are dealing with LVHF if pulmonary edema is suspected/present.
RVHF causes HYPOTENSION and peripheral edema.
Cardiogenic shock is rare and represented only 5% of HF cases. In this case you would be treating with pressure support. Simple.
Helpful rule outs : Helpful rule outs Check a temp. Maybe pneumonia with infiltrate. Remember edema is edema but pneumonia presents typically unilateral with fever, productive cough etc., and rarely in combination with marked hypertension and orthopnea.
But, they can have both!! Hf and pneumonia.
COPD. What are some rule outs?
PE Rule outs? VS?
Lasix? : Lasix? I just say no to Lasix. Why?
Lasix has not shown to be of benefit prehospitally and recent studies actually relate it to increased mortality and hospitalization with its use.
This is largely to do with poorly trained paramedics giving to pts with pneumonia.
Concentrate on getting a handle of the acute issues and allow the ED to confirm and continue with diuresis.
Diuretics : Diuretics Even in the Ed Diuretics have been shown to be “potentially harmful” and were widely adopted “without clinical trials” with no evaluation of “long term safety and efficacy”. Pts with “dyspnea and elevated BP appear to be the biggest risk”. According to AHA.
While at ED : While at ED HPI, PE, Chest x-ray, 12ld ECG, Trop, electrolytes, cell count.
X-Ray found to lack findings in 15% of cases.
Echo also useful.
These evaluations combined with BNP diagnose with 90% accuracy.
BNP? : BNP? “b” type natriuretic peptide.
Generated from prohormone released from the cardiac myocytes in response to ventricular dialation (remodeling) and or pressure overload.
BNP ALONE classified 74% of pts correctly.
Combined with other methods over 90% accuracy.
Several studies have shown paramedics to be at 50% accuracy. Lets say you are at 75% . Still wanna give Lasix?
AMI : AMI Remember that AMI can cause pulmonary edema and HF.
So do a 12 ld... O2, Nitrates, CPAP and if they can still chew ASA, just dont CPAP it down there!
Q's : Q's Go online and look at capnography for paramedics. Good capnograms that will show both HF and reactive airway diseases.
Also pull up some ECGs. Not uncommon to have different forms of hypertrophy. May be useful in making a stronger case for HF.