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Congested Heart Failure (Exam 3)

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Alfred Jarvis

on 11 June 2015

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Transcript of Congested Heart Failure (Exam 3)

Congested Heart Failure

Heart failure (HF) occurs when the heart muscle is unable to pump effectively, resulting in inadequate cardiac output, myocardial hypertrophy (the enlargement of an organ or tissue from the increase in size of its cells), and pulmonary/systemic congestion. The heart is unable to maintain adequate circulation to meet tissue needs.
HF Overview
The severity of HF is graded on the New York Heart Association's functional classification scale indicating how little, or how much activity it takes to make the client symptomatic (chest pain, or shortness of breath)
Right-sided heart (ventricular) failure results in inadequate right ventricle output and systemic venous congestion (peripheral edema)
Low-output HF can initially occur on either left or right side of the heart
Left-sided heart (ventricular) failure results in inadequate left ventricle (cardiac) output and consequently in inadequate tissue perfusion. Forms include the following:
Assessment - Risk Factors
Left-sided heart (ventricular) failure
Health Promotion & Disease Prevention

Maintain an exercise routine to remain physically active, and consult with the provider before starting an exercise regimen
Exam 3

Systolic blood pressure is elevated in older adults, putting them at risk for coronary artery disease and heart failure
Subjective and Objective Data
Laboratory Tests
Human B-type natriuretic peptides (hBNP): Elevated in heart failure. In clients who have dyspnea, elevated hBNP confirms a diagnosis of heart failure rather than a problem originating in the respiratory system. hBNP levels direct the aggressiveness of treatment interventions.
Diagnostic Procedures
Surgical Interventions
Heart Transplant
Nitroglycerine (Nitrostat) and isosorbide mononitrate (Imdur) prevent coronary artery vasospasm and reduce preload and afterload, decreasing myocardial oxygen demand
Beta-adrengeric blockers (beta-blockers)
Medications such as carvedilol (Coreg) and metoprolol (Lopressor) may be used to improve the condition of the client who has sustained increased levels of sympathetic stimulation and catecholamines. This would include clients who have chronic heart failure.
Patient-Centered Care - Nursing Care

Monitor daily weight and I/O
Herbal medications can stimulate the cardiovascular system. Obtain a list of herbal supplements the client takes, and advise the client of potential contraindications
Diuretics are used to decrease preload
Human B-type natriuretic peptides (hBNP)
hBNPs, such as nesiritide (Natrecor), are used to treat acute heart failure by causing natriuresis (loss of sodium & vasodilation). They are administered IV.
Teamwork & Collaboration
Anticoagulants, such as warfarin (Coumadian), can be prescribed if the client has a history of thrombus formation
Inotropic agents
Inotropic agents, such as digoxin (Lanoxin), dopamine, dobutamine (Dobutrex), and milrinone (Primacor), are used to increase contractility and thereby improve cardiac output
Afterload-reducing agents
Afterload-reducing agents help the heart pump more easily by altering the resistance to contraction
Notes from Class
Stage 1 – beginning
Stage 4 – getting to end of life
Notes from Class
Notes from Class
Antecedents (what causes it) -
Notes from Class

With heart failure patient has a fluid overload and decrease tissue perfusion because the heart cannot contract/pump well enough to meet body demands. They can have confusion because they are not getting enough perfusion to the brain. Also, they can have kidney damage (renal failure) because they are not getting perfusion to the kidneys. Incidence of HF increase with age. Main hallmark of HF is low ejection fraction (EF), so with heart failure you have a low ejection fraction (which is measured in a couple of ways). If the ejection fraction is less than 40% then that is compromised and is low. Measured by, when the patient goes to the cardio-cath lab and gets on a left catheter done (go in with different catheters to look at the vessels of the heart and looking at the degree of blockage that the patient might have in those different vessels or to identify if they have atherosclerosis.
Notes from Class

They also have a procedure done while they are in there called a left ventriculograph - Insert a large amount of dye in (about 30ml), in a sort amount of time. This IV dye can be harmful to the kidneys. When this procedure is performed they look at how well the heart contracts and pumps to move that dye that is pumped in and by doing this they measure the EF. Another way to measure EF is by an echocardiogram (non-invasive ultrasound of the chest). With HF their blood pressure is going to be low, so they won’t be able to tolerate activity too well, get fatigued easily and SOB easily.
Notes from Class

= HR x SV (amount of blood pumped by the heart per minute) 4 to 8 L per minute can increase with exercise
Notes from Class

– has to do with contractility; drugs that increase contractility, a drug that increases contractility is called a positive inotropic agent (digoxin), and a drug that decreases contractility is a negative inotropic agent.
Notes from Class

Myocardial infarction (MI)
– whatever vessel is occurs in, causes death of those myocardial cells, and part of that heart vessel is going to die and become necrotic and this necrotic tissue will not have good contractility. Infarction in the right coronary artery this will affect the right ventricle and cause right-sided HF. If you have infarction in the LAD (left anterior descending – coronary artery), which goes around the left ventricle will affect contractility and cause left-sided heart failure. Left ventricular failure can cause right-sided heart failure, which means a patient can have both left and right HF.
Notes from Class

Anything that causes an increase workload on the heart causes increase in heart rate, which causes the heart to work harder and cause a greater workload on the heart and increases blood pressure and using up more oxygen so there is a greater demand of workload on the heart.

HF is the result of an acute or chronic cardiopulmonary problem, such as systemic hypertension (HTN), myocardial infarction (MI), pulmonary HTN, dysrhythmias, valvular heart disease, pericarditis, and cardiomyopathy

Pulmonary edema is a severe, life threatening accumulation of fluid in the alveoli and interstitial spaces of the lung that can result from severe HF

Class I: Client exhibits no symptoms with activity

Class II: Client has symptoms with ordinary exertion

Class III: Client displays symptoms with minimal exertion

Class IV: Client has symptoms at rest

Systolic (when the atrium contracts) heart (ventricular) failure (ejection fraction below 40%, pulmonary and systemic congestion)

Diastolic (the period during which the ventricles are relaxing) heart (ventricular) failure (inadequate relaxation or "stiffening" prevents ventricular filling)
Low-output HF can initially occur on either left or right side of the heart

A common form of HF is high-output failure, in which cardiac output is normal or above normal

Consume a diet low in sodium, along with fluid restrictions, and consult with the provider regarding diet specifications

Refrain from smoking

Follow medication regimen, and follow up with the provider as needed


Coronary artery disease, angina, MI

Valvular disease (mitral and aortic) - disease process involving one or more of the four valves of the heart
Right-sided heart (ventricular) failure

Left-sided heart (ventricular) failure

Right ventricular MI

Pulmonary problems (COPD, pulmonary fibrosis)
Assessment - Risk Factors cont.
High-output heart failure

Increased metabolic needs

Septicemia (fever)



Increased metabolic needs

Coronary artery disease

Infection or inflammation of the heart muscle

Various cancer treatments

Prolonged alcohol use

Assessment - Risk Factors cont.

Certain medications may increase the risk of heart failure or worsen manifestations in the older adult client
Assessment - Risk Factors cont.
Left-sided failure -

Dyspnea, orthopnea (shortness of breath while lying down), nocturnal dyspnea


Displaced apical pulse (hypertrophy)

S3 heart sound (gallop)

Pulmonary congestion (dyspnea, cough, bibasilar crackles)

Frothy sputum (can be blood-tinged)

Altered mental status

Manifestations of organ failure, such as oliguria (decrease in urine output)
Assessment - Risk Factors cont.
Subjective and Objective Data
Right-sided failure -

Jugular vein distention

Ascending dependent edema (legs, ankles, sacrum)

Abdominal distention, ascites

Fatigue, weakness

Nausea, anorexia

Polyuria at rest (nocturnal)

Liver enlargement (hepatomegaly) and tenderness

Weight gain
Assessment - Risk Factors cont.
Subjective and Objective Data
Cardiomyopathy (leading to heart failure) -
Four types

Dilated (most common)


Arrhythmogenic right ventricular


Blood circulation is impaired to the lungs when the cardiac pump is compromised


Fatigue, weakness

Heart failure (left with dilated type, right with restrictive type)

Dysrhythmias (heart block)

S3 gallop

Cardiomegaly (enlarged heart), more severe with dilated type

Angina (hypertrophic type)

The presence of other chronic illnesses (lung disease, kidney failure) can mask the presence of heart failure in older adult clients

A level below 100 pg/mL indicates no heart failure

Levels between 100 to 300 pg/mL suggest heart failure is present

A level above 300 pg/mL indicates mild heart failure

A level above 600 pg/mL indicates moderate heart failure

A level above 900 pg/mL indicates severe heart failure

Assess for shortness of breath and dyspnea on exertion

Administer oxygen as prescribed

Monitor vital signs and hemodynamic pressures

Position the client to maximize ventilation (high-Fowler's)

Check ABGs, electrolytes (especially potassium if on diuretics), SaO2, and chest x-ray findings

Assess for signs of medication toxicity (digoxin toxicity)

Encourage bed rest until the client is stable

Encourage energy conservation by assisting with care and ADLs

Maintain dietary restrictions as prescribd (restricted fluid intake, restricted sodium intake).

Provide emotional support to the client and family

Loop diuretics
, such as
furosemide (Lasix), bumetanide (Bumex)

Thiazide diuretics
, such as
hydrochlorothiazide (Hydrodiuril)

Potassium-sparing diuretics
, such as
spironolactone (Aldactone)
Nursing Considerations -

Administer furosemide IV no faster than 20 mg/min

Loop and thiazide diuretics can cause hypokalemia, and potassium supplementation may be required

Angiotensin-converting enzyme (ACE) inhibitors, such as enalapril (Vasotec), captopril (Capoten)

Angiotensin receptor II blockers, such as losartan (Cozaar)

Calcium channel blockers, such as diltiazem (Cardizem), nifedipine (Procardia)

Phosphodiesterase-3 inhibitors, such as milrinone (Primacor)
These are contraindicated for clients who have renal deficiency
Afterload-reducing agents cont.
Nursing Considerations -

Monitor clients taking ACE inhibitors for hypotension following the initial dose

ACE inhibitors can cause angioedema (swelling of the tongue, throat, and lips), a decreased sense of taste, or a skin rash.

Monitor for increased levels of potassium
Client Education -

Inform the client that this medication can cause a dry cough

Notify the provider if the client observes a rash or has a decreased sense of taste

Notify the provider if swelling of the face or extremities occurs

Remind the client that blood pressure needs to be monitored for 2 hr after the initial dose to detect hypotension
Nursing Considerations -

For a client taking digoxin, take the apical heart rate for 1 min. Hold the medication if apical is less than 60/min, and notify provider

Observe the client for nausea and vomiting

Dopamine, dobutamine, and milrinone are administered via IV. The ECG, blood pressure, and urine output must be closely monitored
Inotropic agents cont.
Client Education -
Teach clients who are self-administering digoxin to:

Count pulse for 1 min before taking the medication. If the pulse rate is irregular or the pulse rate is outside of the limitations set by the provider (usually less than 60/min or greater than 100/min), instruct the client to hold the dose and contact the provider

Take the digoxin dose at the same time each day

Do not take digoxin at the same time as antacids. Separate the two medications by at least 2 hr

Report signs of toxicity, including fatigue, muscle weakness, confusion, and loss of appetite

Regularly have digoxin and potassium levels check
Nursing Considerations -

Monitor BP, pulse, activity tolerance and orthopnea

Check orthostatic blood pressure readings
Client Education -

Instruct the client to weigh daily

Advise the client to regularly check BP

Tell the client to follow the provider's instructions on increasing medication dosage
Nursing Considerations -

Vasodilators are given to treat angina and help control blood pressure

Use cautiously with other antihypertensive medications

Vasodilators can cause orthostatic hypotension
Client Education -

Remind the client that a headache is a common side effect of this medicaiton

Encourage the client to sit and lie down slowly
Nursing Considerations -

hBNPs can cause hypotension, as well as a number of cardiac effects, including ventricular tachycardia and bradycardia

BNP levels will increase while on this medication

ECG, blood pressure, & other parameters should be monitored
Client Education -

The client can be asymptomatic with a low blood pressure

Remind the client to sit and lie down slowly
Nursing Considerations -

Assess for contraindications (active bleeding, peptic ulcer disease, history of cerebrovascular accident, recent trauma)

Monitor bleeding times - PT, aPTT, INR, and CBC
Client Education -

Remind the client of the risk for bruising and bleeding while on this medication

Remind the client to have blood monitored routinely to check bleeding times
Notes from Class
Risk factors for CHF –
Notes from Class
Notes from Class
Left Sided vs Right sided HF

Eventually heart gets too weak and goes into cardiomyopathy and then into acute cardiogenic shock because nothing is getting perfused (brain[ lose LOC], kidneys [renal failure], Distal extremities [cyanotic – get cold and pale and start turning bluish]) when they get to the end stage

Left-sided failure – causes pulmonary signs and symptoms

Right-side failure – causes edema, abdominal ascites (fluid in the abdomen), abdominal s/s, GI distress
Interrelated concepts –

pain (all the extra fluid), ascites in the abdomen causes?, brain not getting good perfusion = confusion, mobility because the heart cannot meet the bodies demands (pt have difficulty getting up and walking short distances [bed to bathroom), end stage even at rest, sitting in chair not doing anything and short of breath and on oxygen. Smoking not good for these patients = takes away oxygen they need. No cure for the end stages, either go on a left ventricular assistive device until they can get on the list for a heart transplant and most result in death

Ventricular hypertrophy (either right or left, but usually is the left) caused by increased myocardial oxygen demand caused by elevated or uncontrolled high blood pressure or from a heart attack and the vessel was obstructed (say the right coronary artery was obstructed and infarcted the right coronary artery which affects the right ventricle and go into a right sided heart failure).

CHF can be acute (medications can potentially help) or chronic (progressively getting worse through the years, especially if the person is not doing any type of smoking cessation, taking medications as they should or not doing cardiac rehab. So, it progressively gets worse until they get to the end stage (stage 4) and will be put on some type of left ventricular assistive device and put on the list for a heart transplant (will end up dying without replacement).

= amount of blood pumped out of the left ventricular in one contraction with each heart beat

– the amount of resistance that the left ventricular has to work against to get the blood pumped out (so if the blood pressure is elevated the left ventricle has a lot to work against and some drugs decrease afterload and decrease cardiac output)

– the amount of pump that the heart has (so HF pt’s do not have good heart pumping action)

– the end diastolic ventricular volume (the volume of the blood in the ventricle at the end of diastole)

Preload and CO can be measured by certain catheters (HR or certain surgeries done)

: HF develops when the heart is unable to keep up with the body’s demand for oxygen and nutrients.

is the primary cause of HF, from the plaque build-up in the inner lining of the coronary arteries, the heart has to work harder, and over time from working harder it develops heart failure

– disease of the myocardium and can induce cellular necrosis and fibrosis (the thickening and scarring of connective tissue, usually as a result of injury), so the myocardium will not have good contractility (causes – infections, drugs, certain chemotherapy agents, mitral valve prolapse [keeps from blood from going forward and backs up = increase workload on the heart], congenital heart defects)

Ventricular hypertrophy
– over time if the left ventricle has to work really hard to get the blood pumped out into the aorta and has to work against a great resistance over time causes ventricular hypertrophy and eventually leads to left ventricular failure and left-side HF and can lead to right-side heart failure

Increase SNS
– will increase HR and BP and contractility and causes greater workload on the heart .So, increase myocardial work and increase oxygen demand. Blood pressure medications work to decrease the oxygen demands on the heart.

RAA system
– increases preload and afterload and can cause pulmonary congestion. So, ACE inhibitors those are drugs that used in the RAA system

Coronary artery disease
- because of all the plaque build-up (atherosclerosis) and its defused (might not just be in one vessel) = increase workload on the heart and eventually over time can lead to heart failure (or a blockage in the right coronary artery) or cause an MI and lead to HF.

– increases workload on the heart

Family History
– genetics = more at risk for developing HF

– chemotherapy agents can cause HF

= increases oxygen demands of the heart and causes vasoconstriction so the heart has to work harder (if you smoke and have the end stage of HF you need to stop). Chewing tobacco too (because it is nicotine or second hand smoke being exposed all the time)
Risk factors for CHF –


Alcohol abuse

Diabetes linked to coronary artery disease (more at risk for having coronary artery disease, more atherosclerosis)

Left sided failure
– pulmonary signs and symptoms, pulmonary congestion (occurs because the left ventricle cannot pump effectively to get the blood out into the aorta and into the systemic circulation). Increase left ventricular volume and increases the volume of blood in the left atrium, which backs up into the pulmonary circulation. Common Signs and symptoms in these patients = fatigue and activity intolerance, pulmonary s/s, SOB, auscultated crackles, orthopneic (not being able to breath well without sitting up), at night they have to sleep on two to three pillows (cannot lay flat), dyspnea, cyanosis, abnormal heart sound upon auscultation. A lot of SOB and will eventually need supplemental oxygen (just sitting will become SOB as it progresses)

Right sided failure
– blood backs up to the right ventricle to the right atrium and then out into the systemic and backs up into jugular veins (JVD), and backs up into the abdominal cavity (ascites), nausea/vomiting/anorexia, do not have an appetite (not eating = weightloss), nocturia, weight gain from all the fluid, JVD even when standing up.
Notes from Class
Notes from Class
Notes from Class
Notes from Class
Notes from Class
Notes from Class
Notes from Class

– look how they are breathing, edema (fluid overload), crackles of lungs, are they gaining weight over a short period of time (2-3 lbs), echocardiogram and look for the decreased EF (less than 40 = significant), or cath lab (ventriculography done – good estimate for EF), chest x-ray (shows enlarged heart)

– BNP (B-type Natriuretic Peptide - blood test, key diagnostic indicator of HF) BNP is a substances secreted from the ventricles in response to changes in pressures that occur when heart failure develops and worsens. So, the levels of BNP increases when the heart failure symptoms worsen, as the heart failure progresses the BNP levels will go up (pretty high 800-900, want it to be less than 100). Heart failure can progressively get worse, if they haven’t been taking their medications or have not been decreasing sodium intake and get fluid overload and end up in the hospital (first in the hospital their BNP level will be elevated, but after treatment BNP level will go down). BNP is important in diagnosing heart failure.

MI can cause heart failure

Stage A –
At risk for developing heart failure with no structural heart disease (means they have good pumping action)

Stage B –
Have structural heart disease but no signs of heart failure.

Stage C –
Have structural heart disease and current or previous symptoms of heart failure

Stage D –
Refractory heart failure –have symptoms at rest despite treatment (they have symptoms with activities and at rest. Will be on hospice care at this stage [at end of life], will be giving infusion drugs [positive inotropic drugs and diuretics] and will need a heart transplant to stay alive (before heart transplant they will need some type of mechanical support)
Drug Therapy –

ACE inhibitor
– block the action of the protein that causes the blood vessels to narrow and allows the blood vessels to relax and widen and lower blood pressure and makes it easier to pump the blood. Also, they help release water and sodium, which helps relieve the BP as well. Side effects: can raise potassium levels (monitor electrolytes), specifically monitor them if on potassium supplement, do not take if pregnant or have kidney problems (can worsen this condition), one main side effects is that can cause a irritating dry hacking cough (once taken off can go away). Prevents conversion of angio 1 to forming into 2 (vasoconstrictor). End in the letters PRIL

– Angiotensin 2 receptor blockers – Diovan (valsartan), Cozaar (losartan) block the effects of angiotensin 2 at the receptors site (blocks the affects at the receptor site). Contraindicated in pregnancy and lactation and watch for hyperkalemia (monitor potassium).

– coreg (carvedilol) end in LOL - reduce the SNS response, lower HR and BP, reduce CO. Side effects, depression, erectile dysfunction in men, fatigue (because they lower CO). give low doses of coreg and slowly increase. Also, metoprolol is used a lot

– Lasix and Bumex (both loop diuretic, which are very potent) action is in the loop of henle, potassium excreting, and will diuresis the patient, need potassium supplementation, monitor urine output, if given IV put a foley catheter (put in before giving the med or else they will need to go to the bathroom right away, but they ‘re fatigued) usually given for severe HF.

Positive inotropes
– increase contractility of the heart (Digoxin) also referred to as cardiac glycoside. Pt at risk for becoming digoxin toxic if their potassium is low (if they double up on doses). Also, if potassium low, hypokalemia = increased risk for digoxin toxicity) Put them on potassium supplement if on Digoxin. Side effects (severe bradycardia – hold the medicine if apical pulse less than 60). Other side effects – dizziness, seeing halo around objects, yellow colored light (visual disturbances), and GI distress (may not be notice at first that it is due to digoxin toxicity) (n/v) and can cause low HR, do not want to eat or cannot tolerate meals. Do not double on medications if you forget to take them “trying to catch up.” Given IV initially and given a loading dose to get them to a therapy level. Make sure they’re getting the right dose (0.125 mg vs 0.25 mg).
Circulatory assistance devices –

IABP (intra-aortic balloon pump)
– basically augments coronary perfusion, helps get the blood pumped through the heart. Works to increase CO. These people on this machine, their heart is weak and enlarged and do not have good contractility. So, the organs, brain, kidneys, are not getting good perfusion. The balloon comes in different sizes a big one 30 to 40 cc. Inserted in the femoral artery up into the aorta. Sets the pumps at different settings, but set to inflate during diastole and deflate during systole and works to increase CO. Watch for blood clots (especially if turned off and then turned back on) have patient on a blood thinner. May be on a balloon pump for some time period, then go to a ventricular assistive device, then a heart transplant.

mechanical pump device used to support the heart function and blood flow in people with weakened hearts. Tube that carries blood out of the heart into the pump and another tube that carries blood from the pump to the blood vessels and delivers it to the rest of the body.

Heart transplant
– pt needs to be on antirejectant meds

Vasotec (ACE inhibitor)

KCL (potassium chloride)
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Summary p1 -
Summary p2 -
Summary p3 -
Summary p4 -
Summary p5 -
Summary p6 -
Summary p7 -
Summary p8 -
Summary p9 -
Summary p10 -
Heart Failure (aka Congestive Heart Failure):


Coronary Artery Disease (CAD), prior MI

Chronic HTN

- Dilated



- Restrictive
- Ischemic

Valvular and congenital heart disease

Pulmonary diseases
Left-Sided Heart Failure (LHF)
Causes -

Left Ventricle Infarct, cardiomyopathy
Symptoms -

dyspnea, cough, fluid accumulation in lungs
Signs -

S3 gallop, tachycardia, inspiratory rales beginning at lung bases, expiratory wheezes due to bronchospasms (misdiagnosed with asthma)
Laboratory Findings:

ABGs reveal hypoxemia, chest x-rays shows pulmonary edema or pleural effusions
Right-Sided Heart Failure (RHF) -
Causes -

LHF, right ventricle infarct, pulmonary or tricuspid valve disease, pulmonary HTN, COPD, PE
Symptoms -

dyspnea on exertion, fatigue, weight gain, fluid retention
Signs -

Increased central venous pressure (CVP), jugular venous distention (JVD) >3-4 cm, hepatomegaly, ascites, peripheral or sacral edema, pleural and pericardial effusions are also not common
Right-Sided Failure Laboratory Tests

Liver function shows hepatic congestion

Increased liver enzymes, increase PT, INR

Hyponatremia (fluid restriction only if Na+ <132 mg/dL

Increased BUN/creatinine = decrease renal perfusion
Sodium and volume homeostasis

As CO decreases, renal perfusion decreases

This activates the renin-angiotensin system

This causes fluid retention
Pharmacologic Management
Angiotensin converting enzyme (ACE) inhibitors
- Captopril
- Enalapril
- Fosinopril
- Quinapril
- Ramipril
- Perindopril
- Benazepril
ACE Inhibitors end in "P.R.I.L"
Loop diuretics
- Furosemide
- Bumetanide
- Torsemide
Loop diuretics ending in "I.D.E"?

- Thiazide-related drug: metolazone

Aldosterone antagonists
- Spironolactone
- Epleronone

- Digoxin
- Dobutamine

Phosphodiesterase Inhibitors
- Milrinone

Natriuretic peptides
- Nesiritide

Beta blockers
- Metoprolol
- Carvedilol
- Bisoprolol
Ending in "L.O.L"

Angiotensin II receptor blockers
- Losartan
- Candesartan
- Valsartan
Ending in "S.A.R.T.A.N.?"

- Nitrates: isosorbide dinitrate
- Hydralazine
- Nitroprusside
- Prazosin

Dopamine agonist
- Dopamine

- Morphine

- Warfarin
- Aspirin
Summary p11 -
Nursing Management

Regular exercise strongly encourage - improves function of skeletal muscle more than changes in myocardial funciton
Diet -

Limit sodium intake

Fluid restriction only if Na+ <132 mg/dL

Avoid excessive fluids (because of congestion)

Avoid alcohol - depresses myocardial contractility

If CAD, low cholesterol, low fat, low Na+

Cessation of smoking
Additional Information
Additional Information
Additional Information
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Description -

The heart pumps blood through the arteries and veins.

With congestive heart failure, the pumping force of the heart is reduced.

Left sided heart failure results in fluid backing up into the lungs causing breathing problems

Congestive heart failure (CHF) can have many causes with the most common being high blood pressure (hypertension), heart attacks, viral heart infections (myocarditis), congenital heart defects, and valvular heart disease.

Patients with known CHF can experience worsening symptoms if they eat too much salt, stop taking their medications or have another coexisting illness such as pneumonia

Right sided heart failure produces fluid in the legs (edema) and the abdomen (ascites).
Symptoms -

Shortness of breath, especially if lying flat (orthopnea)

Swollen legs (edema)

Shortness of breath with exercise.

Distended abdomen (ascites)

Awaking suddenly gasping for air (paroxysmal nocturnal dyspnea)
Tests -

A history and physical exam will be performed. The goal is to identify the cause of the heart failure and reverse the adverse effects. Once the cause is identified the extent of the disease can be assessed by performing X-rays, blood tests and an echocardiogram.

Complete blood count (CBC), Comprehensive metabolic panel (CMP), EKG, Troponin, X-ray
Treatment -
Therapy depends on the extent of the disease and the severity of the symptoms.
Treatment includes:

Controlling the blood pressure and reducing the work of the heart with blood pressure medications

Increasing the urine output with diuretics

Maximizing oxygen with supplemental oxygen
Reversing the cause of CHF exacerbation is essential to recovery.
For severe cases that do not improve with standard medications, heart transplant may be recommended
Expected Duration -

Heart failure often is a lifelong condition. However, if that cause is treatable, heart failure can go away
Prevention -

To avoid heart failure, prevent the various forms of heart disease that precipitate the illness.

To prevent coronary heart disease, eat a healthy, balanced diet, control blood pressure and cholesterol levels, maintain a normal body weight, exercise regularly and do not smoke. Limit alcohol use to one to two drinks per day. Some types of heart failure cannot be prevented
When to call a Doctor -
Call a doctor if any of the following symptoms, particularly if already have been diagnosed with some form of heart disease:

Significant fatigue

Difficulty breathing

Swelling of the ankles and legs

Swelling of abdomen

Episodes of breathlessness
3D Medical Animation Congestive Heart Failure Animation
Congestive Heart Failure Medical Animation
Additional Information
Congestive Heart Failure
Additional Information
Treatment of CHF (Congestive Heart Failure) in the ED
Additional Information
Cardiology - Cardiac Output
Additional Information
Cardiology - Coronary Blood Supply
Additional Information
Cardiology - Relationship of conduction system, ventricular contraction and ECG
Additional Information
Cardiology - Heart Physiology I (Cardiac Myocyte and Membrane Potential)
Additional Information
Cardiology - Heart Physiology II (Muscle contraction and Pacemaker activity)
Additional Information
Renin Angiotensin Aldosterone System - MADE EASY
Additional Information
Renin-Angiotensin-Aldosterone System
Additional Information
GFR 1 - Control of GFR
Additional Information
Part I - Regulation of Blood Pressure (Hormones)
Additional Information

Part II - Regulation of Blood Pressure (Hormones)

4. Aldosterone = increase Na+ and CI- retention (increase water retention) K+ excretion
1. Renin (from kidneys) = Renin hormone combines with the liver hormone angiotensinogen that is broken into angiotensin I
2. Angiotensin I = converted (in the lungs) into Angiotensin II (ACE starts here)
3. Angiotensin II = helps the production of aldosterone in the adrenal cortex (kidneys), which increases in ADH secretion (keep more water around),
• Stimulation of Simulation of SNS (fight-or-flight),
• Secretion of K+, and also cause Vasocronstriction
• And **Stimulates Aldosterone Secretion**
Concept Map
angioneurotic edema

cardiac edema
a manifestation of congestive heart failure, due to increased venous and capillary pressures and often associated with renal sodium retention.

cytotoxic edema
cerebral edema caused by hypoxic injury to brain tissue and decreased functioning of the cellular sodium pump so that the cellular elements accumulate fluid.

dependent edema
edema in lower or dependent parts of the body.
edema neonato´rum a disease of premature and feeble infants resembling sclerema, marked by spreading edema with cold, livid skin.

pitting edema
that in which pressure leaves a persistent depression in the tissues.

pulmonary edema
diffuse edema in pulmonary tissues and air spaces due to changes in hydrostatic forces in capillaries or to increased capillary permeability, with intense dyspnea.

vasogenic edema
cerebral edema in the area around tumors, often due to increased permeability of capillary endothelial cells.
Types of Edemas (FYI)
generalized edema
that affects peripheral tissues and several organs. For instance, heart failure can cause pulmonary edema, ascites (fluid collection around the abdominal organs), pleural effusions (fluid in the lungs) as well as peripheral edema (swelling in the lower limbs).
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