CHF: Prognosis and Management

CHF: Prognosis

Poor. 5-year survival around 50%. About 20% survive longer than 8-12 years.
5-year survival rate for Congestive Heart Failure: Half of the patients diagnosed with CHF will be dead within 5 years. (Source: excerpt from NHLBI, Congestive Heart Failure Data Fact Sheet: NHLBI)
Results of a new study published in the March 7 issue of Archives of Internal Medicine suggest that heart failure survival after 6 years in adults 67 years and older on Medicare is very low and may be worse than the prognosis for most types of cancer. (Source: excerpt from Facts About Heart Failure in Older Adults: CDC-OC)
This condition carries a reduced life expectancy. Many forms of heart failure can be controlled with medication, lifestyle change, and correction of any underlying disorder. Heart failure is usually a chronic illness, and it may worsen with infection or other physical stressors.
Estimated mortality rate for Congestive Heart Failure from prevalence and deaths statistics:
Deaths: 50,824 (USA annual deaths calculated from this data: 50,824 deaths (NHLBI 1999); about 260,000 deaths a year (CDC-OC))
Incidence: 4,800,000 (USA prevalence calculated from this data: 4.8 million Americans (NHLBI); 2% age 40-59; 5% age 60-69; 10% over 70's
1.1% (ratio of deaths to prevalence).
Estimated mortality rate for Congestive Heart Failure from incidence and deaths statistics:
Deaths: 50,824 (USA annual deaths calculated from this data: 50,824 deaths (NHLBI 1999); about 260,000 deaths a year (CDC-OC))
Incidence: 400,000 (USA annual incidence calculated from this data: 400,000 new cases annually
12.7% (ratio of deaths to incidence).

Naturally, such forecast issues are by their nature unpredictable.


Management for CHF

Medications
ACE inhibitors such as captopril and enalapril -- these medications open up blood vessels and decrease the work load of the heart.
Diuretics -- there are several types including thiazide, loop diuretics, and potassium-sparing diuretics; they help rid your body of fluid and sodium.
Digitalis glycosides -- increase the ability of the heart muscle to contract properly; prevent heart rhythm disturbances
Angiotensin receptor blockers (ARBs) such as losartan and candesartan which, like ACE inhibitors, reduce the workload of the heart; this class of drug is especially important for those who cannot tolerate ACE inhibitors
Beta-blockers -- this is particularly useful for those with a history of coronary artery disease
Inotropic agents help improve the heart's ability to pump blood. Such drugs include dobutamine and milrinone. They are given intravenously.


Diet Modification

Look for foods that are labeled “low-sodium,” “sodium-free,” “no salt added,” or “unsalted.” Check the total sodium content on food labels. Be especially careful of canned, packaged, and frozen foods. A nutritionist can teach you how to understand these labels. Don’t cook with salt or add salt to what you are eating. Try pepper, garlic, lemon, or other spices for flavor instead. Be careful of packaged spice blends as these often contain salt or salt products (like monosodium glutamate, MSG). Avoid foods that are naturally high in sodium, like anchovies, meats (particularly cured meats, bacon, hot dogs, sausage, bologna, ham, and salami), nuts, olives, pickles, sauerkraut, soy and Worcestershire sauces, tomato and other vegetable juices, and cheese. Take care when eating out. Stick to steamed, grilled, baked, boiled, and broiled foods with no added salt, sauce, or cheese. Use oil and vinegar, rather than bottled dressings, on salads. Eat fresh fruit or sorbet when having dessert.

Other lifestyle modifications
Don’t smoke.
Stay active..exercise. Your doctor can provide a safe and effective exercise plan based on your degree of heart failure and how well you do on tests that check the strength and function of your heart. DO NOT exercise on days that your weight has gone up from fluid retention or you are not feeling well.
Lose weight if you are overweight.
Get enough rest, including after exercise, eating, or other activities.

posted by Chris

causes,signs and symptoms of congestive heart failure

Congestive heart failure/congestive cardiac failure (CCF)/ biventricular cardiac failure

CCF results from the failure of the heart to eject blood effectively, thus it is the most common manifestation of heart failure. It is clinically useful to divide the heart failure into the syndromes of left and right cardiac failure, but it is rare for any part of the heart to fail in isolation.

Most commonly, there is a pre-existing Left heart failure followed by Right heart failure.

Left heart failure

Causes include:
*ischaemic heart disease: causing infarction of the heart walls, such as the myocardium hence the ventricles cannot contract efficiently thus reducing cardiac output.
*systemic hypertension: the heart has to pump harder to overcome the arterial pressure thus increases the afterload resulting in hypertrophy of the heart thus leading to CCF.
*mitral and aortic valve disease: incompetent valves leads to the heart having to pump harder, leading to hypertrophy of heart. i.e in mitral regurgitation, there is excessive preload
*Cardiomyopathy: can cause dilation and failure of the heart

Symptoms
*Fatigue (due to inadequate systemic perfusion, or lack of sleep because of paroxysmal dyspnoea)
*exertional dyspnoea ( breathlessness)
orthopnoea ( shortness of breath when lying down due to fluid in the chest cavity. this is relieved by sitting up.)
*paroxysmal nocturnal dyspnoea ( sudden breathlessness at night)
*wheeze
*nocturnal cough with or without pink sputum

Signs
*LV third or fourth heart sound ( S3 and S4)
*Tachycardia
*Crackles are heard at lung bases( pulmonary oedema)
*Peripheral cyanosis ( due to insufficient cardiac output leading to poor circulation in the peripheries)








Right heart failure

Causes include:
*left heart failure and others


symptoms
*fatigue
*peripheral oedema (the left ventricle is pumping more blood than the right heart can handle on return thus there is an accumulation of fluid in the peripheries)
*nausea
*anorexia
*pulsation in neck and face (raised right heart pressure)


signs
*jugular venous distension
*ascites ( development of abdominal fluid, systemic oedema)




Other causes of CCF also include

Drugs
beta blockers causing inadequate heart rate
negatively inotropic ( decrease heart contractility) drugs
excessive alcohol intake resulting in high BP leading to cardiomyopathy

Congenital defects in cardiac structure

Heart sounds

Hi all,

I remember some of you requested posting the heart sounds up here, but it's not possible on blogger. So, if anyone wants the sounds, bring ur thumb drives or whatever and I can pass them to ya.

See you Friday.

Addendum: ECG changes in left ventrocular hypertrophy

ECG changes in left ventricular hypertrophy
If there is left ventricular hypertrophy then this will result in :
~a tall R wave (greater than 25mm in V5 or V6), or R plus S greater than 35 mm (1)
~a deep S in V1 or V2
~if there is significant left ventricular 'strain' then there are also inverted T waves in V5 and V6 and possible ST depression
~left axis deviation may also be present
~QRS may be slightly prolonged
Source: http://www.gpnotebook.co.uk/cache/241893382.htm

Treatment and Prognosis

Aortic Stenosis – Treatment and Prognosis

Treatment is usually aimed at improving cardiac output and controlling abnormal heart rhythms (dysrhythmias)

Monitoring:
- for asymptomatic or mild cases
- Symptomatic patients – physical exam every 6-12 months, ECG every 1-3 years
- Echocardiography is performed periodically to monitor heart and valve function, helps doctors determine when to schedule surgery

Medications:
- to prevent heart failure (diuretics, digoxins)
- b-blockers (propranolol)
- calcium channel blokers (diltiazem)
- treating angina is often difficult because drugs used to treat angina (nitroglycerin) in people with CAD worsens the angina in people with AS

Hospitalization – for moderate to severe cases

Lifestyle patterns such as maintaining physical activity while avoiding hard physical exercise, control of weight and avoidance of smoking

Surgery

Two main surgical procedures:

· Aortic valve replacement
- surgically replaced with artificial valve (preferably before the left ventrical is irreversibly damaged)
- pulmonary autograft/Ross operation (person’s own pulmonary valve used)
- high risk patients – poor candidates
- best treatment for adults of all ages

· Balloon valvuloplasty (less invasive)
- catheter is inserted into blood vessel (artery) in groin and threaded up to heart
- tip of catheter is placed inside the aortic valve and balloon is inflated – stretch and widen the valve – improve blood flow to heart
- usually limited to those with congenital AS usually in children. However later when children are fully grown, the valve usually must be replaced.
- In adults, stenosis usually always recurs after balloon valvuloplasty; so among adults this procedure is used for frail older people who cannot tolerate surgery.

While balloon valvuloplasty has not yet been proven to be successful, aortic valve replacement has an excellent prognosis

Although AS is curable by surgery, there may be continued risk for arrhythymias which may sometimes cause sudden death

Without surgery, probable outcome is poor if there are signs of angina or heart failure

Person with AS should not participate in strenuous activities such as competitive sports

http://health.allrefer.com/health/aortic-stenosis-prognosis.html
http://merck.com/mmhe/sec03ch028/ch028f.html
http://www.provet.co.uk/health/diseases/aortic%20stenosis.htm#i
http://www.nlm.nih.gov/medlineplus/ency/article/00178.htm

~Shantz

Link of the Day

Yello,

This is the Link of the Day (reminiscent of last year's MUSO discussion board, eh?). I daresay, this may even be the Link of the Week! ;)

http://www.blaufuss.org

You need flash player for the tutorials. Relevant to PCL 2 are the heart sounds tutorials and quiz, and relevant to PCL 1 is the ECG thingy.

Have fun.

anatomy of the heart

Anatomy of the heart

Blood flow

Superior and inferior vena cava > right atrium > tricuspid valve> right ventricle> pulmonary valve>pulmonary arteries> lungs> pulmonary veins> left atrium>mitral valve > left ventricle> aortic valve> aorta> body

Right atrium (RA)
• forms the right border of the heart
• deoxygenated blood enters R.A through 1 of 3 vessels
• superior and inferior vena cava: deliver blood to the heart from the body
• coronary sinus: returns blood from the walls of the heart itself
• superior vena cava: enters the upper posterior portion of the RA
• inferior vena cava and coronary sinus: enter by lower posterior portion of RA
• blood exits the RA into RV via right atrioventricular orifice during ventral diastole
• the tricuspid valve between RA and RV closes during ventricular systole
• note that there are also numerous openings of the smallest cardiac veins on the walls of RA for drainage of blood from the myocardium into the RA

Tricuspid valve
• right atrioventricular orifice is closed during ventricular contraction by the tricuspid valve to prevent the back flow of blood
• the contraction of the papillary muscles attached to the valve cusps by the chordae tendinae prevent the cusps from being everted back into the RA during ventricular systole

Right ventricle (RV)
• most anterior surface of heart
• in relation to RA, RV is located in front of and to the left of the right atrioventricular orifice
• blood entering RV from RA moves in a horizontal and forward direction
• 3 papillary muscles( derived from trabeculae carneae on RV wall) have only one end attached to ventricular surface while the other end serves as the point of attachment for tendon-like fibrous cords called chordae tendinae which connect to the free edges of the cusps of the tricuspid valve

Pulmonary valve
• 3 semi lunar cusps
• Each cusp form a pocket-like sinus, after ventricular contraction, the recoil of blood fills the pulmonary sinuses and forces the cusps close hence preventing blood from flowing back into the RV


Left atrium
• LA receives 4 pulmonary veins
• Interatrial septum is part of the anterior wall of LA
• Thin area in the septum is the valve of the foramen ovale (if not closed properly at birth, causes a “hole in the heart”)


Mitral valve also known as bi-cuspid valve
• has two cusps
• the bases of these cusps are secured to a fibrous ring surrounding the opening between LA and LV( left atrioventricular orifice)
• the coordinated action of the chordae tendinae and papillary muscle (same as in RA and RV) keep the valve closed

Left ventricle
• lies anterior to LA
• forms the apex of heart
• blood enters LV in a forward direction to the apex
• has the thickest layer of myocardium
• the papillary muscle found in LV are larger than those in RV

Aortic valve
• opening from the LV into aorta is closed by aortic valve
• 3 semilunar cusps: right, left and posterior
• The right and left coronary arteries originate from the right and left cusps

Stenosis: a narrowing of the orifice, caused by the valve’s inability to open fully

The Cardiac Cycle - PCL 2

The cardiac cycle describes the events that occur during one beat of the heart.



The cycle can be divided into 5 stages in general.

Stage 1 (Atrial Systole)

The cardiac cycle starts when the SA node initiates atrial systole, causing the atria to contract and to pump blood into the ventricles. This contributes only the final 20% of ventricular filling as most of the ventricles have been filled passively due to venous pressure at the end of the previous cardiac cycle.

Stage 2 (Isovolumetric Contraction of the Ventricles)

Electrical impulses subsequently reaches the ventricles, intiating ventricular systole and causing the ventricles to contract. This increases the ventricular pressure to a level above the atrial pressure and causes the AV valves to close. The closing of the AV valves produces S1, the 1st heart sound. At the same time, the semilunar valves remain closed as pressure in the pulmonary artery and the aorta are still higher than the ventricular pressure. The ventricles are hence sealed and their volumes are constant.

Stage 3 (Ventricular Ejection)

As the ventricles continue to contract, the ventricular pressure increases until it is higher than the pressure in the aorta and pulmonary artery. This opens the semilunar valves, ejecting blood into the aorta and pulmonary artery respectively. Subsequently, ventricular contraction stops and ventricular pressure starts to fall. The ejection of blood out of the ventricles also contribute to the fall in ventricular pressure.

Stage 4 (Isovolumetric Relaxation of the Ventricles)

The ventricles then start to relax causing a further fall in ventricular pressure. Eventually, ventricular pressure falls below the aortic and pulmonary arterial pressure and the semilunar valves close. This gives rise to S2 or the 2nd heart sound. Concurrently, the AV valves remain closed as the atrial pressure is still lower than the ventricular pressure. Once again, the ventricles are sealed and are of constant volumes.

Stage 5 (Passive Ventricular Filling)

As the ventricles continue to relax, ventricular pressure falls below atrial pressure(which has been increasing concurrently due to venous return to the heart)and the AV valves open. Blood flows from the atria into the ventricles without the atria contracting. At this point in time, the whole heart is relaxed.

Stage 5 marks the end of a cardiac cycle and a new cycle begins when the SA node initiates Atrial Systole again.

Note: Stages 5 and 6 shown in the diagram above have been grouped together as Stage 5 in my explanation. The term diastasis refers to the last stage of diastole in the heart, just before atrial systole is initiated.

Contributed by John Lee

Heart Sounds & Heart Murmurs

Note: A bit wordy, but I've tried to make it as clear as possible, and also highlighted key points, if that's helpful.

Heart Sounds (aka Heartbeats)

First Heart Sound (S₁)

S₁ is the sound which marks the approximate beginning of systole, and is created when the increase in intraventricular pressure during contraction exceeds the pressure within the atria, causing a sudden closing of the tricuspid and mitral, or AV valves. The ventricles continue to contract throughout systole, forcing blood through the aortic and pulmonary, or semilunar valves.

Second Heart Sound (S₂)

At the end of systole, the ventricles begin to relax, the pressures within the heart become less than that in the aorta and pulmonary artery, and a brief back flow of blood causes the semilunar valves to snap shut, producing S₂.

The 2nd heart sound tends to become softer as the aortic stenosis becomes more severe. This is a result of the increasing calcification of the valve preventing it from "snapping" shut and producing a sharp, loud sound.

Note to help in understanding the splitting of heart sounds:

Although S₁ and S₂ are considered to be discrete sounds, notice that each is created by the near-instantaneous closing of two separate valves.

During S₁, the closing of the mitral valve slightly precedes the closing of the tricuspid valve, while in S₂, the aortic valve closes just before the pulmonary valve.

Remember that the pressure during systole in the left ventricle is much greater than in the right, and hence, you can predict that the mitral valve closes before the tricuspid in S₁.

Similarly, because the pressure at the start of diastole in the aorta is much higher than in the pulmonary artery, the aortic valve closes first in S₂.

Knowing the order of valve closure makes understanding the different reasons for splitting of heart sounds easier.

Third Heart Sound (S₃)

Shortly after S₂, the closing of the semilunar valves, the AV valves open and diastole begins. Diastole is itself further divided into several stages, the first being that of rapid filling, where 80% of the blood stored in the atria during systole is transferred to the ventricles.

At the end of this stage, about 140-160 ms after S₂, an S₃ may be heard if the volume which has been transferred is abnormally large, as in mitral regurgitation.

It can be thought of as a sound which is generated when the ventricle is forced to dilate beyond its normal range because the atrium has overloaded volume.

An S₃ is usually heard best with the bell of the stethoscope placed at the apex while the patient is in the left lateral decubitus (i.e. lying down) position. The presence of an S₃ is usually normal in children and young adults, but pathologic in those over the age of 40.

Fourth Heart Sound (S₄)

The late stage of diastole is marked by atrial contraction, or kick, where the final 20% of the atrial output is delivered to the ventricles.

If the ventricle is stiff and non-compliant, as in ventricular hypertrophy due to long-standing hypertension (increases in left ventricular pressure), the pressure wave generated as the atria contract produces an S₄.

It is heard best with the bell of the stethoscope at the apex.

Heart Murmurs

Produced as a result of turbulent flow of blood, turbulence sufficient to produce audible noise. They are usually heard as a whooshing sound. The term murmur only refers to a sound believed to originating within blood flow though or near the heart.

Systolic Ejection Murmur in relation to Aortic Stenosis

Systolic Ejection Murmur is a sign of aortic stenosis, detected by auscultation.

Aortic valve stenosis causes significant turbulence to blood flowing during contraction of the left ventricle resulting in a loud murmur; Systolic ejection murmur occurs during ejection of blood through the ventricular outflow tracts into the great arteries.

The loudness of the murmur does not, however, correlate with the severity of stenosis. Patients with mild stenosis can have loud murmurs, while patients with severe stenosis and heart failure may not pump enough blood to cause much of a murmur.

Other causes of heart murmurs

Innocent heart murmurs: caused by blood flowing through the chambers and valves of the heart or the blood vessels near the heart. Situations that cause innocent heart murmurs are,

• Anxiety
• Stress
• Fever
• Pregnancy
• Anemia and thyrotoxicosis (the murmur is not pathologic itself, but indicates the underlying disease process)
• Children also frequently have innocent murmurs which are not due to underlying structural abnormalities.

Note: Just as a murmur can be caused by normal flow through a stenotic valve, it may also be created by high flow through a normal valve.

Pathologic heart murmurs: caused by structural abnormalities of the heart. Situations that cause pathologic heart murmurs are,

• Regurgitation through the mitral valve (however, about 20% of cases of mitral regurgitation, though obvious using echocardiography, do not produce an audible murmur)
• Regurgitation through the aortic valve
• Stenosis of the aortic valve
• Other audible murmurs are associated with abnormal openings between the left ventricle and right heart (septal defects) or from the aortic or pulmonary arteries back into a lower pressure heart chamber.

Note: Regurgitation through the tricuspid or pulmonic valves essentially never produces audible murmurs.

Sources:

http://www.medicinenet.com/aortic_stenosis/page4.htm#5whatmight
http://www.uni-duesseldorf.de/WWW/MedFak/Herz-Kreislauf-Physiologie/lehre/sounds/html/murmur_overview.html

Psychosocial Aspects

Psychosocial Aspects
Economics – medication and treatment (drugs to control heart failure, physical exam
and ECG)
– financial issues for surgery/balloon valvuloplasty
– might not be working anymore (65 years old)

Emotional – Khairul
 feel depress
 a burden to his wife and family
 could cause him to feel stressed (increases BP which becomes a risk
factor)
– Jamila
 feel depress
 regret that she married him
 blame him for not going for a check up earlier

Social support/motivation – lack of energy affects social life as well as marriage
– needs support and motivation from his wife and family
– lifestyle changes
(eg. controlling his diet, start exercising)

Exercise/Work – might not be able to do strenuous activities depending on the
severity of his condition
(eg. might not be able to do gardening – could then affect his wife)

Personality Factors – his own believes and determination to get well, to change
certain lifestyles


(Posted by: Vivian)

Aortic Stenosis

How does Aortic Stenosis related to pain and tightness on the chest?
• In 4% of patient with AS, the 1st symptom is sudden death, usually during strenuous exertion
• It is probably due to heart rhythm abnormalities secondary to inadequate blood flow through the narrowed aortic valve
• Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass).However, the coronary arteries that supply myocardium doesn’t become longer or bigger, so the muscle might become ischemic.
• Thus, the lack of oxygen in the heart muscle causes chest pain and possible abnormal heart rhythm


Chest pain (Angina)
• Chest pain is often described by patient as pressure below the breast bone brought on by on exertion and relieved by rest
• Chest pain is the 1st symptom in 1/3 patients and eventually occurs in 1/2 of patients with AS
• The thickened heart muscle must pump against the high pressure to push blood through the narrowing aortic valve
• This increased heart muscle oxygen demand in excess of the supply delivered in the blood, causing chest pain (angina)

Lawrence
(Part time Chairman of PCL group D) :P

Aortic Stenosis: Causes & Risk Factors

Causes:

-Progressive wear and tear of a bicuspid valve present since birth (congenital defect). It is the most common cause of AS in patients under 65. Over time, excessive wear and tear leads to calcification, scarring, and reduced mobility of the valve leaflets.
-Wear and tear of the aortic valve in the elderly.Protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Valve leaflet mobility is reduced by calcification, turbulence across the valve increases, causing scarring, thickening, and stenosis of the valve.
-Scarring of the aortic valve due to rheumatic fever as a child or young adult. Rheumatic fever is a condition resulting from untreated infection by group A streptococcal bacteria. Damage to valve leaflets from rheumatic fever causes increased turbulence across the valve and more damage. The narrowing from rheumatic fever occurs from the fusion (melting together) of the edges (commissures) of the valve leaflets.


Risk Factors:

-3 times more common in men than women
-Age (affects the elderly)

IX of Aortic Stenosis

Abridged Notes
(http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/(Pages)/Aortic_stenosis?OpenDocument )
Aortic stenosis is diagnosed using a number of tests including:
~ Physical examination including listening to the heart with a stethoscope.
~ Chest x-ray.
~ Electrocardiogram (ECG) to monitor the heart rate and pick up any unusual rhythms and to assess thickening of the left ventricle.
~ Echocardiograph (ultrasound scan) of the heart to assess the functioning of the aortic valve and of the left ventricle.
~ Cardiac catheterisation (a slender tube is inserted into a blood vessel of the groin and threaded up to the heart).
~ Left ventriculography, which includes using a dye so that the heart shows up more clearly on x-ray.
~ Coronary arteriography to assess whether there is coronary artery disease in addition to the recognised aortic valve disease

For more details, see Comment.