Geri Abshire, BSN RN [email protected] Alverno College-MSN 621 May 2007 Click here to start

Geri Abshire, BSN [email protected]

Alverno College-MSN 621May 2007

Click here to start

mailto:[email protected]

Welcome

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Quick ReviewNormal Heart Function

Heart FailurePathophysiology

References

NeurohormonalTherapy

NeurohormonalPathways

Patient Assessment

Introduction

Case Study

Objectives

By the end of this tutorial the learner will Have an increased understanding of

heart failure pathophysiology Understand the neurohormonal

activation process Identify signs and symptoms of right and

left-sided heart failure Understand neurohormonal heart

medication therapy

Heart Failure Statistics There are about 5 million patients with

symptomatic CHF and close to 500,000 new cases every year.

This disorder accounts for 12-15 million office visits and 6.5 million hospital days.

About 300,000 patients die each year of CHF, and in spite of advances in treatment the number of deaths has been increasing steadily.

The total annual inpatient and outpatient costs in the US are at least $40 billion (drugs account for $500 million).

Mann, D, Heart Failure; A Companion to Braunwald’s Heart Disease 2004

Normal Blood Flow Through the Heart

Blood flows from the right atrium to the right ventricle through the tricuspid valve.

The pulmonic valve lies between the right ventricle and the pulmonary artery.

Blood flows from the left atrium to the left ventricle through the mitral valve.

The aortic valve lies between the left ventricle and the aorta.

Copstead, L.E.(1995) Used with permission. www.Wikipedia.com

http://www.wikipedia.com/

Cardiac Cycle The cardiac cycle is composed of a period of

contraction (systole) followed by a period of relaxation (diastole), or one heartbeat.

The cycle begins with ventricular filling, the ventricles are relaxed and blood flows in from the atria through the AV valves. Near the end of ventricular diastole, the atria contract, squeezing more blood through the AV valves in the ventricles.

The ventricles begin to contract immediately following atrial systole causing intraventricular pressure to rise and the AV valves to close. (This produces the S1 sound.) Copstead, L.E.(1995)

Cardiac Cycle With all four cardiac valves closed, ventricular pressure

rises rapidly and the blood within is forcefully compressed.

When ventricular pressure exceeds aortic pressure, the aortic valve is forced open and rapid ejection of blood occurs.

Relaxation phase begins with semilunar valve closure (S2) in response to falling ventricular pressures and ends when the AV valves open to allow for ventricular filling.

Opening of the AV valves signals the beginning of rapid ventricular filling and the start of another cardiac cycle.Copstead, L.E.(1995)

Heart terms to review

Cardiac Output This is the amount of blood that the heart pumps each minute.

Loading conditions The stretch imposed by the blood volume on the cardiac muscle

and the force that the muscle must generate to move the load.

Preload Is the volume of blood stretching the resting heart muscle and is

determined by the venous return to the heart.

Afterload Is the force that the contracting heart must generate to eject blood

from the filled heart.

Porth, C.M., et.al., (2005)

Do You Remember Your Anatomy?Click on the word to move it to the

correct banner on the heart.

http://msjensen.education.umn.edu/Webanatomy/image_database/default.htm: used with permission

Left Atrium

Superior Vena Cava

Mitral Valve

Aorta

Left Ventricle

Right Atrium

Right Ventricle

Bundle of HIS

Inferior Vena Cava

Tricuspid Valve

http://msjensen.education.umn.edu/Webanatomy/image_database/default.htm


What is Heart Failure?

Heart failure is a syndrome that can be caused by a variety of conditions that result in damage to the myocardium and is recognized by a characteristic pattern of haemodynamic, renal, neural, and hormonal responses.

When heart failure develops, the heart is unable to provide adequate amounts of oxygenated blood to meet the needs of peripheral tissue or does so only at abnormally high intracardiac filling pressures.

Greenberg, B., Barnard, D. (2005)

Causes of Heart Failure

Myocardial Infarction (MI) Long standing pressure or volume

overload Myocyte damage caused by a viral

infection Damage caused by replacement of

normal myocardium by infiltrative diseases

Greenberg, B., & Barnard, D. (2005)

Risk Factors of Heart Failure

Hypertension Coronary Disease Valvular Disease MI Diabetes Mellitus Dyslipidemia Atrial Fibrillatin Smoking Physical Inactivity Systemic Inflammation (C-reactive protein)

Greenberg, B., & Barnard, D. (2005

Which conditions can result in damage to the myocardium? (There is more than one right answer)

Unstable Atherosclerotic plaquesRheumatic Heart DiseaseRaynaud’s Disease

Correct! Unstable atherosclerotic plaques rupture causing platelet aggregation and thrombus formation and eventual myocardial infarction.

Back to the question

Great job! Rheumatic fever is an acute immune-mediated inflammatory diseases that can lead to the development of chronic valvular disorders that produce permanent cardiac dysfunction.


Although this disease causes intense vasospasm of the arteries and arterioles of the fingers and toes, it does not cause damage to the myocardium.


Heart Failure Manifestations

Fluid retention and edema Shortness of breath and other respir

atory manifestations Fatigue and limited exercise toleranc

e Cachexia and malnutrition Cyanosis Elevated BNP levels


Fluid Retention and Edema

Peripheral and portal edema occurs in right-sided heart failure 1 pint of accumulated fluid results in a 1 lb.

weight gain. As a rule, weight gain of > 2 lb in 24 hrs or 5 lb in one week is a sign of worsening heart failure.

Pulmonary edema occurs in left-sided heart failure When the pulmonary capillary filtration

pressure (nl.=10mmHg) exceeds the capillary osmotic pressure (nl.=25mm Hg) there is a shift of fluid from the intravascular into the interstitium of the lung.

© 2007 Microsoft

© 2007 MicrosoftPorth, C.M., et.al., (2005)

Back to CHF S/S

Shortness of Breath and other respiratory manifestations Due to the congestion of the

pulmonary circulation, the following symptoms are left-sided heart failure. Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Cough Cheyne-Stokes respirations


Back to CHF S/S

Fatigue and limited exercise tolerance

Decreased cardiac output from the left ventricle causes fatigue and limb weakness.

These symptoms progress as activity increases during the day.

© 2007 Microsoft


Back to CHF S/S

Cachexia and Malnutrition

Congestion of the liver and gastrointestinal structures from right-sided heart failure impairs digestion and absorption creating a feeling of fullness.

www.daily-diabetic.com

Porth, C.M., et.al., (2005)Back to the CHF S/S

Cyanosis

Cyanosis around the lips and in the peripheral part of the extremities may develop from right and left -sided heart failure. Caused by arterial desaturation resulting from impaired pulmonary

gas exchange Caused by venous desaturation resulting from extensive extraction

of oxygen at the capillary level

Porth, C.M., et.al ., (2005) Back to CHF S/S

Elevated Brain natriuretic peptide (BNP) levels B-type natriuretic peptide is

synthesized and released by ventricular myocytes and fibroblasts in response to myocardial stretching.

Normal lab levels are < 100pg/mL BNP levels in CHF depend on other co-

morbidities. COPD, LVH, obesity, age can all effect the BNP level. (Levels from 100-400pg/mL are questionable for CHF. Values over 500pg/mL are likely due to CHF).Porth, C.M., et.al.,(2005)

Right-sided Heart failure

Occurs when the right side of the heart fails and there is a back up of blood in the systemic venous system

This causes an increase in pressure in which of the following areas?

(Click on the correct answers)

Right atriumRight ventricular end diastolicSystemic venous

Porth, C.M.,et.al., (2005)Porth, C.M.,et.al., (2005)

Right ventricular hypertrophy

Ventricular hypertrophy.svg. www.wikipedia.com LadyofHats. Used under public domain


Left-sided Heart Failure

Impairment of left heart function leads to a decrease in cardiac output, an increase in left atrial and left ventricular end-diastolic pressures and congestion in the pulmonary circulation.

Which of the following manifestations occur with left-sided heart failure?

(Click on the three correct answers)

Chronic dry coughDyspneaRight upper quadrant discomfort Lack of appetite and bloatingParoxysmal nocturnal dyspnea


Adaptive Heart Failure Mechanisms

The net effect of these neurohormonal responses is to:

1. Produce arterial vasoconstriction (to help maintain arterial pressure)

2. Venous constriction (to increase venous pressure)

3. Increased blood volume.

The cardiac reserve is maintained initially through systemic neurohormonal activation of the sympathetic nervous system and the renin-angiotensin-aldosterone mechanism.


How is that done?

The Renin-Angiotensin-Aldosterone Pathway

For an in-depth review try out this great link. http://faculty.alverno.edu/bowneps

Decreased blood flow to

kidneys

Kidneys secrete RENIN into blood

RENIN reacts with ANGIOTENSINOGEN

A weak vasoconstrictor

Angiotensin I

Angiotensin converting enzyme in

lungs

Adrenal Cortex secretes

Aldosterone into blood

Turns on Na⁺ and K₊ ATPase in kidneys

Angiotensin II

Continue to next slide

A stronger vasoconstrictor

Bowne, P.S., 2004-2007. PATHO Interactive Physiology Tutorials. http://faculty.alverno.edu/bowneps

Caused by low blood pressure

http://faculty.alverno.edu/bowneps


Na₊ and K₊ ATPase in kidneys

2 K₊ secreted from blood into

urine

3 Na₊ reabsorbed from urine into blood

Water follows by osmosis

Increased blood

volume

Increased blood

pressure

Decreased urine

volume

More K₊ in urine

Less K₊ in blood

Restores renal blood flow,

stopping renin

release

Click here to start


Another view of the RAAS

http://www.answers.com/topic/renin-angiotensin-system

When blood flow to the kidneys decreases, what directly turns on the Na⁺/K⁺ ATPase in the kidneys?

a. Angiotensin II

b. Aldosterone

c. Renin

Rethink your answer. Angiotensin II affects the Adrenal Cortex directly to secrete Aldosterone into the blood.


Great job! Aldosterone is secreted by the Adrenal Cortex and turns on the Na⁺/K⁺ ATPase in the kidneys.

Click to the next slide

Incorrect. The kidneys secrete renin, a large enzyme, into the bloodstream when there is a decreased blood flow to the kidneys. Renin acts on circulating Angiotensinogin to produce Angiotensin I (a weak vasoconstrictor).


Acute RAAS Effects

Acute effects of Angiotensin II are good and results in:

Enhanced CardiacOutput

Reduced Left

Ventricular filling

pressures


Chronic RAAS Effects

These neurohormonal changes stimulate expression of proteins and myocyte hypertorphy causing maladaptive cardiac remodeling.

↑Angiotensin II

↑Aldosterone & cytokines

VasoconstrictionNa retention &

volume overload+

Interstitial

Fibrosis

Increased wall stress

Click anywhere on this slide to start


myocyte damage,

decreased contractility,

abnormal hypertrophy

SNS ActivationAdrenergic Receptors

Alphareceptors

Beta receptors

Alpha 1 Alpha 2 Beta 1 Beta 2

Vasoconstriction in blood vessels;

GutKidneys

skin

Skin muscles affected;

hair stands on end and sweat

squeezed out of glands

Pupils dilate

Gut motility

decreases and

digestion stops

Further norepi. release inhibited Broncholes

dilate in lungs

Heart rate

increases and

becomes stronger

Stored fat

released in

adipose tissue

Increased metabolic

rate in many tissues

throughout body

For an in-depth review try out this great link.http://faculty.alverno.edu/bowneps



A B1 heart response from SNS activation

Has a positive inotropic effect on the heart

By increasing the Ca₊ that is available for interaction between the actin and myosin filaments the force of contraction improves.


What happens throughout the body when the Sympathetic Nervous System is turned on? Choose 5 symptoms caused by the activation of the alpha receptors and 5 for the Beta receptors.

Alpha receptors Beta receptorsPupils dilateHeart rate increase

Stored fat released into bloodstream

Bronchioles dilate

Gut motility decrease

Hair on skin stands on end

Stronger heartbeat

Increase metabolic rate

Vasoconstriction in kidneys causing

decreased urine

Pallor, cold skin

Physiology of heart failure

Involves an interaction between two factors: A decrease in the pumping ability of the

heart with a consequent decrease in the cardiac reserve

The adaptive mechanisms that serve to maintain the cardiac output also contribute to the progression of heart failure.


Hemodynamics of Heart Failure

Used with permission. www.Wikipedia.com

Stiff ventricles that fill with less blood

due to fibrous tissue

Enlarging ventricles (shown by red

arrows) pump out less blood

Increased Preload =

↑ end-diastolic ventricular muscle

stretching

Increased Afterload = a decrease in

Ejection Fraction


Increase venous return to the heart

Increased systemic vascular resistance

and


Adaptive Mechanisims

In general, these neurohormonal responses can be viewed as compensatory mechanisms, but they can also aggravate heart failure by increasing ventricular afterload (which depresses stroke volume) and increasing preload to the point where pulmonary or systemic congestion and edema occur.

End diastolic volume

increases stretching the muscle

fibers

Impairment of ventricular ejection

Increased systemic vascular

resistance

Increase in venous return to the heart


http://msjensen.education.umn.edu/Webanatomy/image_database/default.htm: used with permission



Cardiac Remodeling

It is manifested clinically by changes in cardiac size, shape, and function in response to cardiac injury or increased load.

The importance of remodeling as a pathogenic mechanism is incompletely understood, since factors leading to remodeling could be the major determinants of heart failure prognosis rather than ventricular dilation itself.

www.uptodate.com Cardiac Remodeling: Basic Concepts (2007)

http://www.uptodate.com/

Cardiac Remodeling

The heart undergoes a prototypic series of changes in structure in response to myocardial injury or volume load

Progressive deterioration in both right and left ventricular function of the heart.

Hypertrophy of the Myocardium

Muscle mass &chamber volume

left ventricle

Deposits of fibrous tissue &alterations in

collagen Net effect

and

Increases in


http://www.uptodate.com/

Causes of Cardiac Remodeling Hemodynamic Factors

Pressure overload Volume overload

Neurohormonal Factors Angiotensin II Catecholamines Cytokines (tumor necrosis factor-a) Endothelin

Greenberg, B., & Barnard, D. (2005

Tumor necrosis factor-a

Tumor necrosis factor (TNF, cachexin or cachectin and formally known as tumor necrosis factor alpha) is a cytokine involved in systemic inflammation. TNF causes apoptotic cell death, cellular proliferation, differentiation, inflammation, and viral replication.

http://commons.wikimedia.org/wiki/Image:TNFa_Crystal_Structure.rsh.png#f Used under public domain

Back to the slide


http://commons.wikimedia.org/wiki/Image:TNFa_Crystal_Structure.rsh.png#f

Cellular Changes

Myocyte hypertrophy

Loss of myocytes due to apoptosis or necrosis

Fibroblast proliferation

Fibrosis Electrical Conducti

on delays


Glanzsteifen.jpg http://commons.wikimediaUsed with permission.

Cardiac muscle

Click on

apoptosis

Apoptosis

The apoptotic process is a programmed cell death that is executed in such a way as to safely dispose of cell corpses and fragments.

The process is triggered by another neighboring cell; the dying cell eventually transmits signals that tell the phagocytes, which are a part of the immune system, to engulf it.

http://de.wikipedia.org/wiki/Bild:Apoptose-Mann, D, Heart Failure; A Companion to Braunwald’s Heart Disease 2004

Voltage-gated ion channel

Voltage-dependent calcium channels (VDCC) are a group of voltage-gated ion channels found in excitable cells (neurons, glial cells, muscle cells, etc.) with a permeability to the ion Ca2+, which plays a role in the membrane potential. VDCCs are involved in the release of neurotransmitters and hormones, muscular contraction, excitability of neurons and gene expression.

Synapse llustration2.png


Illustration of the major elements in a prototypical synapse. Synapses allow nerve cells to communicate with one another through axons and dendrites, converting electrical impulses into chemical signals

Electrical Conduction Delays

Calcium signals are critical messengers in excitation contraction coupling and in signal transduction.

There are two voltage gated calcium channels (L-Type for long lasting and T-Type for transient.

Altered Ca₊ handling occurs with cardiac hypertrophy and heart failure causing reduced Ca₊ release which diminishes cardiomyocyte contractile performance.

Synapse llustration2.png

http://www.answers.com/topic/voltage-dependent-calcium-channel

Synaptical transmission (chemical).A : Neuron (Presynaptic) B : Neuron (Postsynaptic)1 Mitochondria 2 Synaptic vesicle full of neurotransmitter 3 Autoreceptor 4 Synaptic cleft 5 Neurotransmitter receptor 6 Calcium Channel 7 Fused vesicle releasing neurotransmitter 8 Neurotransmitter re-uptake pump


Summary of Heart Failure Pathophysiology

Myocardial Injury

Neuroendocrine activation (SNS, RAS)

Direct myocardial effects (remodeling,

LV dysfunction)

Disease progression

Hemodynamic abnormalities

(changes in pressure, volume and flow)

Symptomatology(exercise

intolerance)

MortalityGreenberg, B., & Barnard, D. (2005)

Neurohormonal Therapy

Strategies for the treatment of heart failure have focused on the use of agents that block angiotensin II production and the B-adrenergic system

Feldman, A.M., (2006)

Click here

ACE inhibitors work here to

prevent conversion

Angiotensin Converting Enzyme(ACE) Inhibitors

•Angiotensin II is a powerful vasoconstrictor.

•Chronic activation leads to maladaptive cardiac remodeling.

•Synthesis of medications that diminish angiotensin II levels might prove beneficial in patients with heart failure.

Angiotensin I

Kidneys secrete Renin into

blood

Angiotensin II

Angiotensin converting enzyme in

lungs

Feldman, A.M., Heart Failure Pharmacologic Management (2006)

FDA Approved ACE Inhibitors

Benazepril (Lotensin) Captopril (Capoten) Enalapril (Vasotec) Fosinopril (Monopril) Lisinopril (Prinivil) Moexipril (Aceon) Quiapril (Accupril) Ramipril (Altace) Trandolapril (Mavik)

Adverse Effects Hypotension Hyperkalemia Dry cough Acute renal failur

e Angioedema

FeldmanFeldman, A.M., Heart Failure Pharmacologic Management (2006)

Who should receive ACE Inhibitors?

ACE inhibitors should be used when: When there is any degree of

symptomatic heart failure Asymptomatic patients with left

ventricular (LV) dysfunction In patients at risk for developing LV

dysfunction


Contraindications of ACE Inhibitors Angioedema Hypersensitivity (cough that’s intolerable)

Symptomatic hypotension Worsening renal function

Warn patients against use of nonsteroidal anti-inflammatory drugs as they can block favorable results of ACEI’s and can enhance its adverse effects.


Click here

Beta Blockers• Chronic adrenergic signaling occurs as a compensatory mechanism in the failing human heart.

•Increased cardiac myocyte apoptosis appears to be exclusively mediated by the B1 receptor.

• An effective therapeutic strategy would be to inhibit B receptor signaling.

Sympathetic nervous system

Epi

Epi

E

E

E

NE

NEE

Secretes acetylcholine (Ach)

B1A1 Beta blockers

inhibit B receptor signaling

Myocyte apoptosis

Contractile dysfunction

Hypertrophy


FDA Approved Beta Blockers

Adverse EffectsAV blockBronchospasmDizzinessHypotensionBradycardiaHypersensitivity

Metoprolol Bucindolol Bisoprolol Carvedilol Nebivolol


Who should receive Beta Blockers?Beta blockers should be used when: In the presence of ACE inhibitor

therapy. Symptomatic left ventricular (LV)

systolic function. Post-infarct time period (even with

normal LV systolic function).


Contraindications for Beta blockers Sinus node or conduction system

disease with bradycardia True reactive airway disease (COPD,

asthma, etc.) Abrupt discontinuation of Beta

blockers Cardiogenic shock Pulmonary edema


Other medications

Diuretics Digitalis Aldosterone inhibitors Angiotensin Receptor Blocker’s


Case Study #1

GB is a 54 year old black female who presented to the office for an initial exam. She reports shortness of breath and leg swelling. She has been experiencing nausea, vomiting and abdominal bloating over the past several weeks.

Case Study #1PMHx:Dyslipidemia

Severe Asthma (FEV1<80%)

Social:

Occasional smokerDenies alcohol

Caffeine, 1 cup/day

Minimal exercise

Married

Family Hx:

Premature heart disease

Medications:

Pantoprazole 40mg every day

ROS:

Dyspnea, bloating sensation

PE:

B/P 110/70, HR 74 Wt156. Lungs clear, Jugular vein distension (JVD) to jaw, ascites, edema +1 lower extremities, decreased urine output

Which is a risk factor for heart failure?

Choose all that apply Dyslipidemia Asthma 1 cup caffeine/day Family history of premature heart dis

ease

YEA! Dyslipidemia is a risk factor for heart disease and heart failure. Remember, this is a high ratio of total cholesterol to high-density lipoprotein cholesterol.

Click here for another choice

No, asthma is not a risk factor for heart failure.

Click here for another

choice

Caffeine, although constricts your blood vessels and increases your heart rate and blood pressure, is not a risk factor for heart failure.

Click here for

another choice

Correct, genetics is a risk factor for heart failure.

Click to get to next slide

Does GB have right or left-sided heart failure?

Click on the correct answer

Right-sided heart failure!

Left-sided heart failure!

Correct! Right –sided heart failure occurs when there is back up of blood in the venous system causing symptoms of abdominal bloating, ankle swelling and jugular vein distension.

Click here for

next slide

Think again! Look at all the s/s of GB, clear lungs, JVD, nausea, vomiting, and abdominal bloating, and ankle swelling. In this case, with clear lungs, her shortness of breath is caused by an enlarged liver and other abdominal organs that are pushing up on her diaphragm making it difficult for her to breath.

Click here to

try again

Which statement is true?

An increase in GB’s systemic vascular resistance caused an increase in her afterload leading to s/s of right-sided heart failure.

An increase in GB’s venous return to the heart caused an increase in her preload leading to s/s of right-sided heart failure.

This is not correct. The increase in systemic vascular resistance would make it harder for the left ventricle to pump blood out of the heart causing an increase in afterload.

Back to the

question

YEA! Great job! Increased venous return to the heart

increases end diastolic pressure in the ventricle causing cardiac muscle stretching and an increase in preload.

Which neurohormonal response created the preload? Renin-angiotensin-adlosterone

system

Sympathetic nervous system

Both the Renin-angiotension-aldosterone system and the sympathetic nervous system

You are partially correct. The aldosterone secreted from the adrenal gland turns on the Na⁺/K₊ ATPase which directly increased blood volume which increases the venous blood return to the heart.

Back to the

question

You are partially correct. The SNS alpha receptors do cause vasoconstriction to occur in the blood vessels of the gut, kidneys and skin which will increase venous blood return to the heart.

Back to the

question

Correct! You are putting it all together.

The Na/K ATPase is turned on during the renin-angiotensin-aldosterone sysstem causing increased blood volume and the SNS causes vasoconstriction to the blood vessels of the gut, kidneys and skin to increase venous blood return to the heart.

Would GB benefit from ACE or Beta blocker medications?

Choose one

ACE Inhibitor medication

Beta blocker medication

Both ACE inhibitors and Beta blockers

ACE inhibitor is the correct medication to use. Great job!

Click here for

next slide

Although a beta blocker is usually needed, this is not the right answer for GB. Try again.

Back to the

question

Severe Asthma

Click here to find GB’s medical history that could

contraindicate the use of beta blockers.

Usually this would be the correct answer. Think back. What does GB have in her medical history that could cause beta blockers to be contraindicated?

Back to the

question

Congratulations! You have completed the CHF tutorial. I hope you enjoyed it.

References


Colucci, W.S., (2007) . Pathophysiology of heart failure: Left ventricular pressure-volume relationships. Accessed through www.uptodate.com.

Demers, C., Mody, A., Teo, K., McKelvie, S. (2005). ACE Inhibitors in Heart Failure; what more do we need to know? American Journal Cardiovascular Drugs, 5 (6) 351-359.

Feldman, A.M., (2006). Heart Failure Pharmacologic Management. Malden, Ma: Blakewell Publishing.

Fuentes, V.L., (2007). Advances in Treatment of Heart Failure. WSAVA Congress. Accessed through http://www.vin.com/proceedings/Proceedings.plx?CID

Girod, S., Becker, A., Cardiac cell image accessed through http://commons.wikimedia . Retrieved April 23, 2007.

Greenberg, B.H., Barnard, D.D., (2005). Contemporary Diagnosis and Management of Heart Failure (3rd edition). Newtown, PA: Handbooks in Health Care Co.

References

Hebert, P.R., Foody, J.M., Hennekens, C.H. (2003). The Role of Inhibitors, Blockers, and Genetic Polymorphisms in the Treatment and Prevention of Heart Failure. Current Vascular Pharmacology.

Jensen, M., 1998-2006. WebAnatomy. http://msjensen.education.umn.edu/webanatomy/

Mann, D., et.al., (2004). Heart Failure; A Companion to Braunwald’s HEART DISEASE. Philadelphia, PA: Saunders.

Porth, C.M.,et.al., (2005). Pathophysiology; Concepts of Altered Health States (7th edition). Philadelphia, PA: Lippincott Williams and Wilkins

Sawyer, D., Colucci, W. (2004). Atlas of Heart Disease: Failure . Retrieved Apoptosis image April 23, 2007. http://de.wikipedia.org/wiki/Bild:Apoptose-german.png

Sheffield, S., 2000-6. GetBodySmart. ConceptCreators, Inc. http://www/getbodysmart.com/

www.wikpedia.com Heart images retrieved April 2, 2007.

Documents

Geri Abshire, BSN RN [email protected] Alverno College-MSN 621 May 2007 Click here to start