Teaching Points::::CHF

[Ace844]

Hi All,

Here's part 4 in my CHF series....

Hope this helps,

ACE844

Cardiomyopathy

Definition

Cardiomyopathy refers to heart muscle disease. The damaged heart does not effectively pump blood. The disease usually progresses to the point where patients develop life-threatening heart failure. In addition, people with cardiomyopathy are more likely to have irregular heartbeats or arrhythmias.

There are two major categories of cardiomyopathy. When the heart muscle is damaged from heart attacks due to coronary artery disease that is called ischemic cardiomyopathy. The less common category of cardiomyopathy is nonischemic. That category includes types of cardiomyopathy that are not related to coronary artery disease.

There are three main types of nonischemic cardiomyopathy:

Dilated

Damaged heart muscles lead to an enlarged, floppy heart. The heart stretches as it tries to compensate for weakened pumping ability.

Hypertrophic

Heart muscle fibers enlarge abnormally. The heart wall thickens, leaving less space for blood in the chambers. Since the heart does not relax correctly between beats, less blood fills the chamber and is pumped from the heart.

Restrictive ? Portions of the heart wall become rigid and lose their flexibility. Thickening often occurs due to abnormal tissue invading the heart muscle.

Hypertrophic Heart :: , http://catalog.nucleusinc.com/generateexhi...TL=9985&A=2

Causes

In many cases, the exact cause is not known. Possible causes include:

Dilated

The cause of the initial damage is often not found but may include:

· Ischemic heart disease, with decreased blood flow to the heart

· Infections, usually viral

· Chronic exposure to toxins, including alcohol and some chemotherapy drugs

· A rare complication of pregnancy or childbirth (probably immune related)

· Rarely, other illnesses, including rheumatoid arthritis, diabetes, or thyroid disease

Hypertrophic

· Inherited: sometimes present at birth but often developing in teens

· With aging: associated with hypertension

Restrictive

usually related to another condition, such as:

· Amyloidosis ? protein fibers collect in the heart muscle

· Sarcoidosis ? small inflammatory masses (granulomas) form in many organs

· Hemochromatosis ? too much iron in the body

Risk Factors

A risk factor is something that increases your chance of getting a disease or condition.

· Family members with cardiomyopathy

· Alcoholism

· Obesity

· Diabetes

· Hypertension

· Coronary artery disease

· Certain drugs

Symptoms

Symptoms vary, depending on the type of cardiomyopathy and its severity. Patients with hypertrophic cardiomyopathy often do not notice any symptoms. Sudden cardiac death may be the first indication of the condition. In dilated cardiomyopathy, it may take years for symptoms to develop. Blood clots may form due to the abnormal pooling of blood in the heart. If a clot moves to another part of the body (embolism), symptoms associated with that organ (the brain, for example) may be the first sign of the heart disease.

Cardiomyopathy ultimately leads to heart failure and the following symptoms:

· Fatigue

· Weakness

· Shortness of breath, often worse when lying down and with exertion

· Cough

· Swelling in feet or legs

· Chest pain

· Irregular heart rhythm

Diagnosis

The doctor will:

· Ask about your symptoms and medical history

· Perform a physical exam

· Listen to your heart with a stethoscope (cardiomyopathies often produce heart murmurs and other abnormal heart sounds)

Tests may include:

Chest X-ray ? to look for heart enlargement

Electrocardiogram ? a test that records the heart's activity by measuring electrical currents through the heart muscle

Echocardiogram? a test that uses high-frequency sound waves (ultrasound) to examine the size, shape, and motion of the heart

Blood Tests ? to check for damage to the heart and other organs, and possibly the underlying cause(s) of the cardiomyopathy

Cardiac Catheterization ? a tube-like instrument inserted into the heart through a vein or artery (usually in the arm or leg) to detect problems with the heart and its blood supply

Heart Biopsy ? removal of a sample of heart tissue for testing

Treatment

No treatment, short of a heart transplant, can reverse the damage already done to the heart muscle. Treatment aims to relieve symptoms and prevent further damage. If a treatable underlying cause is found, treatment will be started to address the problem.

Lifestyle Modification

Changes aim to eliminate anything that contributes to the disease or worsens symptoms:

· Avoid alcohol.

· Lose weight, if you are overweight.

· Eat a low-fat diet to minimize the risk and extent of coronary artery disease.

· Limit salt intake to decrease fluid retention.

· Follow your doctor's advice for exercise. You may need to limit physical activity.

Medications

Medications may include:

· Diuretics ? to eliminate extra fluid

· ACE inhibitors ? to help relax blood vessels, lower blood pressure and decrease the heart's workload

· Digitalis ? to slow and regulate the heart rate, and modestly increase its force of contractions

· Calcium channel blockers ? to lower blood pressure and relax the heart

· Beta blockers ? to slow the heart and limit disease progression

· Anti-arrythmia agents ? to prevent irregular heart rhythms

· Immune system suppressants ? including steroids (depending on underlying cause)

Surgery

Surgical options include:

· A pacemaker may be implanted to improve the heart rate and pattern.

· For patients with hypertrophic disease, doctors may remove part of the thickened wall separating the heart's chambers. Surgery may be needed to replace a heart valve.

· A heart transplant may be possible for otherwise healthy patients who do not respond to medical treatment. Candidates often wait a long time for a new heart. Those waiting may temporarily receive a ventricular assist device, which is a mechanical pump that assumes some or most of the heart's pumping function.

Prevention

Aggressively treating hypertension, coronary artery diseases, and their risk factors is the best way to prevent most cases of cardiomyopathy. Other less common causes, however, are not preventable. People with a family history of the disease should ask the doctor about screening tests, especially before starting an intense exercise program.

RESOURCES:

American Heart Association

http://www.americanheart.org

The Cardiomyopathy Association

http://www.cardiomyopathy.org/homepage.htm

References:

Braunwald E, Zipes DP, Libby P, et al. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, PA: W. B. Saunders Company; 2001.

Cecil RL, Goldman L, Bennett JC. Cecil Textbook of Medicine, 21st ed. Philadelphia, PA: W. B. Saunders Company; 2000.

Dambro MR. Griffith's 5-Minute Clinical Consult, 2001 ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.

National Heart, Lung, and Blood Institute website. Available at: http://www.nhlbi.nih.gov/. Accessed October 13, 2005.

Primary Care Medicine, 4th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2000

[Ace844]

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder characterized by unexplained left ventricular hypertrophy (increased muscle thickness), myocyte disarray (disorganized cardiac cells) and fibrosis (see Figure A, below). It is the most common heritable cardiovascular disorder with an estimated prevalence of 1/1000 in the general population. Genetic studies have defined HCM as a disease of the sarcomere, with more than 250 mutations identified in 10 different components of the contractile apparatus of the heart. Although associated with an increased risk for progressive heart failure and sudden death, the complexity and diversity of HCM impose significant challenges to clinical management.

Figure A: Microscopic picture of a heart with HCM showing myocyte disarray and fibrosis (blue) Figure B: Normal heart histology

echocardiogram of a heart with HCM.

Diagnosis, Management and Treatment of Hypertrophic Cardiomyopathy (HCM)

An integrative approach is essential for optimal management of patients and families with hypertrophic cardiomyopathy, with particular attention to unique features of this disorder:

· Genotypic analysis to allow for definitive diagnosis

· Comprehensive evaluation of affected individuals (cardiac imaging, exercise testing, surveillance for dysrhythmias)

· Family screening

· Stratification regarding risk for sudden cardiac death

· Implantable Cardioverter Defibrillator and pacemaker therapy

· Alcohol septal ablation for treatment of refractory obstructive HCM

· Surgical septal myomectomy/myotomy for treatment of refractory obstructive HCM

· Management of end-stage heart failure, including cardiac transplantation

Learn More About Hypertrophic Cardiomyopathy:

· http://www.brighamandwomens.org/cvcenter/S...enetics/HCM.pdf

· [video width=400 height=350:be943aa488]http://www.brighamandwomens.org/cvcenter/HCMHeartvideo.asp[/video:be943aa488]

In case you can't get the video here is the link:: http://www.brighamandwomens.org/cvcenter/HCMHeartvideo.asp

Hope this helps,

ACE844

[Ace844]

(Prehospital Emergency Care

Publisher: Taylor & Francis Health Sciences @ part of the Taylor & Francis Group

Issue: Volume 10, Number 1 / January-March 2006

Pages: 41 - 45

URL: Linking Options

DOI: 10.1080/10903120500366938

Do Medications Affect Vital Signs in the Prehospital Treatment of Acute Decompensated Heart Failure?

Karl A. Sporer A1, A2, Jeff A. Tabas A1, A2, Roland K. Tam A4, Karen L. Sellers A1, A2, Jon Rosenson A1, Chris W. Barton A1, A2, Mark J. Pletcher A1, A3

A1 Department of Medicine, University of California, San Francisco, San Francisco, California

A2 Department of Emergency Services, San Francisco General Hospital, San Francisco, California

A3 Department of Epidemiology and Biostatistics, Albert Einstein School of Medicine, New York, New York

A4 Albert Einstein School of Medicine, New York, New York)

Abstract:

Introduction. Prehospital treatment of patients with acute decompensated heart failure (ADHF) has been shown to decrease mortality and morbidity. Vital sign changes have been proposed as clinical endpoints in the evaluation of prehospital treatment for this condition. Objective. To examine the effect of prehospital treatments on vital signs among patients with ADHF. Methods. Records of an urban emergency medical services system from September 1, 2002, through September 1, 2003, were queried for patients who had a paramedic impression of shortness of breath or respiratory distress and had received nitroglycerin and/or furosemide. Demographics, initial and repeat vital signs (blood pressure, heart rate, respiratory rate, and oxygen saturation), and medications and doses were collected. Results. Three hundred nineteen patients were included; the average age was 77 (±12) years and 47% were male. Treatments administered to these patients included nitroglycerin, 296 (93%); furosemide, 194 (61%); albuterol, 189 (59%); aspirin, 57 (18%); morphine, 20 (6%); and prehospital intubation, 15 (5%). Patients were initially hypertensive [mean ± standard deviation of systolic blood pressure (SBP) was 167 ±37 mm Hg], tachycardic (heart rate 106 ± 24 beats/min), tachypneic (respiratory rate 33 ± 7 breaths/min), and hypoxic (pulse oximetry 88% ± 9.5%). After treatment, mean changes included decreases (95% confidence interval) in (SBP), -10.6 mm Hg (-14.1 to -7.1), heart rate, -2.3 beats/min (-4.0 to -0.7), and respiratory rate, -3.0 (-3.6 to -2.3), and an increase in oxygen saturation, +8.2 (7.1 to 9.3). Changes in blood pressure and oxygen saturation after treatment correlated with initial values. There was no independent association of either nitroglycerin, furosemide, albuterol, or morphine with improvement in vital signs. Conclusion. Prehospital patients with ADHF are a heterogeneous group of patients with significant variability in vital signs. The change in systolic blood pressure or oxygen saturation after treatment depends greatly on the patient's starting point. There was no association of either nitroglycerin or other medications with the improvement in vital signs.

[whit72]

I was just wondering is it completely possible to diagnose CHF in the field?

I know the clinical signs & symptoms, presentation, etc.

What I can determine through interview when possible:

Onset

Meds

PMH

presence of C/P

presence of Nausea/vomiting

presece of productive cough

What I can determine through assessment:

LOC

Hypertension

heart rate/regular or irregular

Pulses alternans

Lung sounds Rales/Rhonci/wheezing

The presence of edema both pulmonary and peripheral

Ancillary muscle use

JVD

Temp/diaphoresis: in this situation I find difficult to determine the difference

presence of productive cough

Although my treatment is not going to differ much between the usual subject CHF/COPD/pneumonia

Is there more I should be looking for?

[AZCEP]

Two of the easiest are the hepatojugular reflex and the Valsalva maneuver.

The Valsalva will give you a response when you are taking a blood pressure. Have the patient bear down, or exhale against a closed glottis, the blood pressure will drop, then when they stop, their blood pressure should overshoot where it was to begin with. If CHF is present, the blood pressure won't be able to make the big jump past the original.

The hepatojugular reflex is a piece of cake to assess. Have the patient recline to about 45 degrees on the gurney, if they are able. Find the liver, palpate with moderate pressure, and watch the jugular veins. When they jump out at you, this is a positive.

[ERDoc]

Medical cases are 90% history and 10% PE. You should be able to narrow down your differential from the history and help to confirm it with your physical exam. CHF will also cause dyspnea on exertion, paroxysmal nocturnal dyspnea and othropnea. Ask them how many pillows they sleep on. Ask if they able to walk as far as they used to with getting sob. Ask if there has been any weight gain. They are just a few examples. If you have one of those really cool ambulances with a full stocked lab you can order up a BNP.

[whit72]

AZCP wrote:

The hepatojugular reflex is a piece of cake to assess. Have the patient recline to about 45 degrees on the gurney, if they are able. Find the liver, palpate with moderate pressure, and watch the jugular veins. When they jump out at you, this is a positive.

Excellent thank you. Is this present with all CHFers or just a percentage?

ERDOC wrote:

CHF will also cause dyspnea on exertion, paroxysmal nocturnal dyspnea and othropnea. Ask them how many pillows they sleep on. Ask if they able to walk as far as they used to with getting sob. Ask if there has been any weight gain.[/

A few more good questions to ask. Thanks appreciated.

No we don't have one of those cool ambulances. I am thankful when I can keep it running for a whole 24, without having to tape something together or back on to it.

Question for all:

Have you had much experience with Pulses alternans or alternating pulses, and if so how frequent is it in CHFers? I have witnessed it maybe in 50% of the cases.

[whit72]

Actually two questions:

hepatojugular reflex is this present in all CHF pt's or just in a acute crises?

Removed the other I found the answer.

Thanks

[AZCEP]

I'm not giving you the answer on this one. I did that once, and you learned nothing, so you will have to find it for yourself.

That is, if your ego will allow you to realize that you don't know something.

[whit72]

Thats big of you.

Where did I state I knew everything?

Thats your perrogative.