Congestive Heart Failure
- causes and risk factors
- signs and symptoms and diagnosis
- pathophysiology
- management of heart failure
- the health care team
- course
- patient education
- community resources
- references
Congestive Heart Failure (CHF) is an extremely common and serious outcome of cardiovascular disease, is the inability of the heart to pump enough blood to meet the needs of the body. It is the most common cause of hospitalization in patients over 65 and is responsible for 9% of deaths.
Over >1% of Canadians and over 4% of seniors have heart failure. Incidence increasing by 4% annually, and people today have a 20% chance of developing HF.
The Case of Mr Faiblicur
- Primary Care
- Specialist Care
- Investigations
- Management
Primary Care
Mr. Faiblicur, a previously healthy 26-year old, visits his family doctor because of some recent concerns.
What physical exams do you do?
History
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Physical Exam
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What's your differential?
Suspecting a problem with Mr. Fablicur's heart, the doctor asks the family practice nurse to do an ECG.
- Q: what does Mr. Faiblicur's ECG show?
- Q: What else do you do before follow-up?
- Q: What is primary care nursing?
return to tab top to continue with The Case of Mr Faiblicur
Specialist Care
Investigations
Management
CASE END
Causes and Risk Factors
CHF can be caused by a variety of underlying conditions and diseases.
Left-sided heart failure is commonly caused by:
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Right-sided heart failure is commonly caused by:
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Other causes of heart failure:
- arrhythmias
- infections
- chronic inflammation, (rheumatoid arthritis)
- congenital heart disease
- dilated cardiomyopathy
(most common ages 20-50)
- idiopathic (most cases of DCM)
- viral myocarditis (coxsackievirus group B, adenovirus)
- alcohol toxicity (direct toxic effects / secondary nutritional deficiencies)
- specific gene mutations (25-35% of cases)
Signs, Symptoms, and Diagnosis
CHF can only be diagnosed clinically, not simply by echocardiogram, CT, catheter, or other modilities.
- history
- physical exam
- lab investigations
- diagnostic imaging
- infants and children
History
DCM presents with slowly progressing signs and symptoms of congestive heart failure, including shortness of breath, easy fatigue, and poor exercise tolerance.
Congestive heart failure can have a profound impact on the way people feel and function, causing:
- easy fatigue
- shortness of breath and tachypnea
- poor exercise capacity
- diaphoresis and pallor (a serious sign - SNS activated to increase cardiac output. Beta-block.)
Left heart failure can lead to pulmonary congestion:
- cough, crackles, pleural effusion
- paroxysmal nocturnal dyspnea
- orthopnea
Advanced CHF can lead to hypoxic encephalopathy, with irritability, restlessness, and loss of attention span, potentially progressing into stupor and coma.
NYHA Classifications
- Class I - no symptoms with ordinary physical activity
- Class II - slight limitation. Comfortable at rest, but ordinary exertion results in palpitations, fatigue, dyspnea, or angina.
- Class III - Comfortable at rest, but marked limitiations otherwise. Likely can't work for a living because of fatigue.
- Class IV - symptoms of cardiac insufficiency at rest or with minimal activity. likely needs institutionalization. Symptoms of cardiac insufficiancy at rest.
Physical Exam
Clinical accuracy rate is 75-80% in cases of acute decompensation.
Cardiovascular
- tachycardia (100-120 is common)
- soft heart sounds (in systolic people)
- S3
Right heart failure can lead to systemic congestion and its symptoms:
- edema (ascites more in older folks, pitting edema in younger)
- weight gain
- elevated jugular venous pressure
- hepatomegaly
- pleural effusions
Lab Investigations
- low O2 sats
- low Na+ (poor prognosticator)
- azotemia (renal hypoperfusion)
BNP - B-type natriuretic peptide
- secreted by ventricles of heart in response to stress or excessive stretching by myocytes
- I heard it causes vasoconstriction and diuresis
- elevated levels in blood can be helpful, but there are false +ves
- pricey
- over 90% when combining clinical impression with BNP
- if its obvious, don't use it. Use in cases of uncertainty
Diagnostic Imaging
ECG
Chest X Ray
Extracardiac effects of left-sided failure are most prominent in the lungs. Increased pressure backs up into pulmonary capillaries and arteries, resulting in pulmonary edema. Perivascular and interstitial transudate forms, particularly in the interlobular septa. This is responsible for Kerley's B lines, or septal lines. Progressive widening of alveolar septa eveltually leads to accumulation of fluid in the alveolar air spaces themselves.
Peribronchial cuffing - fluid extravasation around bronchi (online image)
Vascular redistribution (cephalization of flow) - increased flow to the apices of the lung as a result of increased pulmonary venous pressure.
Echocardiography
Ejection fraction is a useful feature.
Infants and Children
cardinal findings
- tachypnea
- tachcardia
- cardiomegaly
other findings
- hepatomegaly
- failure to thrive
- cyanosis, especially during feeding or exertion
Pathophysiology
In many cases, heart failure is preceded by cardiac hypertrophy in an attempt to maintain cardiac output. Progression of anatomical, cellular, and molecular changes leads to left ventricular remodeling.
At the same time, neurohormonal activation of epinephrine/norepinephrine, atrial natriuretic peptide, and the renin-angiotensin-aldosterone system become important drivers of continued heart dysfunction.
The heart is unusally heavy, perhaps 2-3x normal, and is large and flabby. Dilation of all four chambers occurs. Wall can be less than, equal to, or greater than normal. Mural thrombi are common.
Cardiac hypertrophy
We generally believe the heart to be incapable of cell division in adulthood, leaving hypertrophy as the principle means of increasing heart contractility. The Frank-Starling mechanism, along with neurohormonal trophic factors, can increase protein and organelle synthesis, leading to length and size of cardiomyocytes.
Pressure overload tends to result in concentric hypertrophy, with increased wall thickness. Volume overload hypertrophy is characterized by dilation, with increased ventricular diameter but not necessarily increased wall thickness. Decreased capillary density and intercapillary distance, along with increased fibrosis occurs in the face opf increased oxygen demand. This tonic ischemic environment often evolves into cardiac failure.
Numerous transcriptional and morphologic changes occur. Early mediators include c-jun, c-fos, and c-myc and are followed by fetal gene programs. Molecular changes which act to enhance contraction may be less functional or normal, however, and, together with apoptosis, can actually do more harm than good.
CHF also leads to systemic hypoxia and congestion, both which have effects on involved tissues. Liver congestion can lead to hepatomegaly, with centrilobular necrosis or sclerosis possible. Edema of the spleen or large bowel are also possible.
Systolic Heart Failure represents problems with ejection. The heart hypertrophies, and ejection fraction falls below 40%.
Diastolic Heart Failure is difficulty is more with heart filling than ejecting. Less hypertrophy and less mortality, but same hospitalization rates.
Mechanisms designed to increase cardiac output can lead to SNS activity and activation of RAAS, increasing peripheral resistance. EDV and preload increase.
Damage can be done in many ways (make chart)
- LV dysfunction
- neurohormonal activation
- NE/andreochromes
- RAAS
- ADH
- oxidative stress/ inflammation
Management of Heart Failure
Treatments are designed to unload the heart, increase the strength of contraction, and block the SNS effects.
Treatments for DCM are similar to those for other types of CHF. However, given the young age of patients, and high rates of mortality, cardiac transplantation is frequently recommended.
Cause of readmission include volume overload, noncompliance, arrhythmia, ischemia, and others.
- medication
- nutrition
- exercise
- education
- pediatric treatments
Medication
Treatments improving mortality target neurohormonal mediators of heart function. Treatment protocol depends on functional class, ability to come for blood testing, and other reasons.
diuretics, especially loop diuretics and K+ sparing diuretics, unload the heart
- not so many clincial trials
- loop diuretics (ie furosemide) recommended for people with congestive symptoms. Once acute congesiton is dealt with, use lowest dose
- in pts with refractory failure, a 2nd diuretic (thiazides or low-dose metozalone) can be added cautiously
- edema is substantial in gut. absorption drops. don't use oral pills - use IV at first.
- thaizides don't work well by themselves. why?
- together with beta blockers, are standard therapy
- provide ~20-25% improvement in many regards - hypertrophy, hospitalizations, stroke
- contra: hypokalemia, severe renal insufficiency, severe hypotension
- long term mortality benefit - up to 12 years
- reduce TPR and therefore preload and afterload
- decrease aldosterone leading to lowered preload
- decreased NE release
- decreased bradykinin breakdown
- decreased ventricular remodeling
- ARBs can be considered as an alternative in pts with AMI with acute HF or LVEF <40%
- can be used in addition to ACEIs and further drops in negative outcomes
- additional cost, effort, side effects
cardiac glycosides - digoxin
- increased contractility, leading to increased CO
- anti-arrhythmic
- Na/H exchange inhibitor
- neutral effect on mortality, improves exercise, symptoms, hospitalizations
- reserved for pts with many symptoms
beta blockers (carvedilol, bisoprolol, metoprolol tartrate): block SNS activity
- metoprolol blocks signs and symptoms of CHF; decreases HR
- carvedilol (a nonselective SNS antagonist) reduces signs and symptoms, slows progression, and decreases mortality
- β1 antagonism decreases HR
- α1 antagonism blocks vasoconstriction and decreases afterload
- perhaps bb's lower concentration of recpetors
- airplane headphones analogy
- side effects: hypotension, fluid retention, braducardia/heart block
reduce mortality by 30-40%,most pronounced in sickest patients.
we think it antagonizes toxic neurohormonal effects, but we don't know
as bb's reduce HR and contractility, too much too soon can decrease EF and make them very sick. Therefore, titrate slowly upwards to avoid initial deterioiration and to then build clincial beenfits.
vasodilators, ie nitroglycerin, used acutely
ionotropic agents, ie dobutamine, used acutely.
low dose dopamine: vasodilator in renal beds, allowing diuretics to penetrate
Aldosterone Blockers
ie spironolactone
- reserve for pts who have failed other treatments
minimal impact on BP, but major effect on creatinine and potassium
learn more about this...
nitrates + hydralazines
- strict vasodilator
- use in in people unable to tolerate ACEis and ARBs
- appear particulary useful in black folks
anticoagulation
- only use in ppl with arrhythmias or people with clots
Avoid:
- Ca2+ channel blockers
- NSAIDs
- some antipsychotics
- corticosteroids
Nutrition
Exercise
Regular mild exercise promotes efficient blood flow.
Education
people with heart failure often have complex comorbidities and can't learn well.
5% of pts with CHF can explain what CHF is (get ref for this!)
Many therapies aren't taken.
- aggressive risk factor reduction
- lifestyle
- fluid/salt vigilance
Pediatric Treatments
fix underlying cause
medication
- reduce preload: diuretics
- inotropics: digoxin, dopamine, dobutamine
- reduce afterload: ACE inhibitors
nutrition
anemia
measure success by growth
The Health Care Team
HF clinics cut adverse outcomes.
The Capital Health Heart Function clinic is located in the Halifax Infirmary.
They see 8-10 patients per day, some coming in almost weekly to get stabilized and on the right track.
There is a lot of telephone management.
NPs can titrate drugs up and change the dose.
They have a good means of communicating with GP, though means of national database (?)
Consequences and Course
Clean this up...
Prognostic value best indicated by plasma NE levels with CHF
Increased heart mass predisposes to sudden death.
Complications
- arrhythmias
- pulmonary edema
- depression
Avg age for admission is 75
Within 1 year 10-20% mortality rate (50% sudden).
25-40% total hospitalization rate
lost days
9.5 dealths/100 hosp pts over 65
readmissions are over 30% within 1 year
People with DCM can quickly fall into a decompensated function state. In the end stage, ejection fractions are often less than 25%.
Secondary mitral regurgitation, arrhythmias, and emboli are common.
Mortality is high, with only 25-50% of people alive after 5 years.
Patient Education
Resources and References
Jaarsma T. 2005. Interprofessional team approach to patients with heart failure. Heart. 91:832-838.