Transcript
Tami Hendriksz, D.O.Touro University-CaliforniaJoint MSPAS/MPH Program
Objectives – Part 1Recognize the pathophysiology of heart failure. Identify and recognize the compensatory
mechanisms of heart failure. Differentiate the following:
High-output versus low-output heart failure (including common causes of each)
Systolic vs diastolic heart failure Acute vs. chronic heart failure Right-sided vs. Left-sided heart failure Backward versus forward heart failure
Recognize risk factors for heart failure. Identify the etiologies of heart failure.
Objectives – Part 2Identify and recognize modes of prevention of CHF. Recognize the prognosis of heart failure. Recognize the common symptoms and physical exam
findings of CHF. Recognize the diagnostic work-up of CHF and identify lab
results and findings seen on EKG and CXR that are consistent with CHF.
Recognize the role of echocardiography in the diagnosis and management of CHF.
Recognize the pharmacologic and non-pharmacologic treatments in the management of chronic CHF.
Identify the stages of heart failure.Recognize the presentation, work-up and mainstays of
treatment of acute heart failure and pulmonary edema.
Case PresentationChief Complaint: 74-year-old woman with shortness of breath
and swelling.
History: Martha Wilmington, a 74-year-old woman with a history of rheumatic fever while in her twenties, presented to her physician with complaints of increasing shortness of breath ("dyspnea") upon exertion. She also noted that the typical swelling she's had in her ankles for years has started to get worse over the past two months, making it especially difficult to get her shoes on toward the end of the day. In the past week, she's had a decreased appetite, some nausea and vomiting, and tenderness in the right upper quadrant of the abdomen.
On physical examination, Martha's jugular veins were noticeably distended. Auscultation of the heart revealed a low-pitched, rumbling systolic murmur, heard best over the left upper sternal border. In addition, she had an extra, "S3" heart sound.
Heart FailureThe inability of the heart to pump
sufficient blood to meet the metabolic demands of the body
or
The ability to do so only if the cardiac filling pressures are abnormally high
or both
=impaired ability of the ventricle to fill with or eject blood
EpidemiologyPrevalence: estimated at 5-million Americans (75%
> 65 yo)Increases steeply with ageIncidence is increasing (3-4 fold increase from 1971
to 1999)1/5 of hospital admissions in >65yo are due to HF
(most common dx)More Medicare $ on HF Dx and Tx than any other
DxLifetime risk of developing HF after age 40 is 20%Incidence doubles with each successive decade6-9x greater risk of sudden death in patients with
HF
Risk Factors for Heart FailureAny condition that causes myocardial necrosis or
produces chronic pressure or volume overload can induce myocardial dysfunction and heart failure
Valvular heart diseaseCoronary heart diseaseHTNDMDyslipidemiaMetabolic syndrome (abd obesity, dyslipidemia,
elevated BP, glucose intolerance)
Some ReviewHeart normally accepts blood at low filling pressures
during diastolePropels it forward at higher pressures in systoleIn a healthy person, cardiac output is matched to the
body’s total metabolic needThe ability to increase cardiac output during increased
activity is called cardiac reserveCardiac output (CO)=volume of blood ejected from the
ventricle per minute. CO=SV x HREjection Fraction (EF)= the fraction of end-diastolic
volume ejected from the ventricle during each systolic contractionThe fraction of blood pumped out of ventricles with each heart
beat EF=SV/EDV Normal=____
Some ReviewCO=SV x HRSV is determined by preload, afterload and
myocardial contractilityPreload=the stretch on the myocardial fibers before
systoleVolume stretching the heart at the end of diastole
(end-diastolic volume, EDV)Largely determined by the venous return to the heart
Afterload=the force the contracting heart must generate to eject blood from the filled heartAffected by systemic (peripheral) vascular resistance,
and ventricular wall tensionLVEDV=the amount of blood returned to the
heart by the venous system
PathophysiologyThere is no single, simple model that
effectively explains the syndrome of HFCurrently the consensus view integrates
multiple pathophysiologic models to explain the cascade of events leading to this clinical syndromeStructuralFunctional BiologicalHemodynamic
Compensatory MechanismsFall in cardiac output recruits mechanismsto maintain sufficient BP and perfuse theorgans.1. Frank-Starling Mechanism2. Neurohormonal alterations3. Development of ventricular hypertrophy and
remodeling
Frank-Starling Mechanism"Within physiological limits, the force of contraction is directly proportional to the initial length of the muscle fiber".
Impaired LV function, causes ↓SV, incomplete chamber emptying, and ↑LVEDV, increase stretch↑contractile
force/↑SV of next contraction…to a point
Long term compensation leads to ↑LVEDV
Neurohormonal AlterationsBP=CO x TPR (total peripheral resistance)1. Adrenergic nervous system
Decreased perfusion to baroreceptors realease of norepinephrine
Sympathetic Parasympathetic HR, contractility, vasoconstriction ()
2. Renin-Angiotensin-Aldosterone system A-II constricts arterioles (TPR), stimulates
thirst, increases aldosterone
3. Increased production of ADH Promotes water retention, preload
Ventricular Hypertrophy and RemodelingDevelops over time in response to hemodynamic
burdensSustained wall stress (dilitation or pressure)
stimulates hypertrophy and stiffnessEccentric hypertrophy= synthesis of new sarcomeres
in series, elongation of myocytes, chamber enlarges in proportion to increase in wall thickness. Due to VOLUME overload (MR or AR)
Concentric hypertrophy= synthesis of sarcomeres in parallel with old, myocytes thicken. Wall thickness increases without proportional chamber dilitation. Due to PRESSURE overload (AS, HTN)
A sarcomere is the basic unit of a muscle's cross-striated myofibril
High-output HF vs Low-output HFHigh-output HF=normal myocardial function
but increased demandSevere anemia, hyperthyroidism, AV shunting,
pregnancyTends to be specifically treatable
Low-output HF=impaired pumping ability of the heartIschemic heart disease, cardiomyopathy,
myocarditis, arrhythmia
Systolic HF vs Diastolic HFSystolic HF= decreased pump function and
decreased EFDiastolic HF= impaired ventricular filling
from stiff chamber with normal EF
Forward HF vs Backward HFForward Heart Failure - The inability of the heart
to pump blood at a sufficient rate to meet the oxygen demands of the body at rest or at exerciseInadequate discharge of blood into the arterial system
Backward Heart Failure - The ability of the heart to pump blood at a sufficient rate ONLY when heart filling pressures are abnormally high Back-up of blood in the venous and atrial system behind
the failing ventricleThese are hypotheses to describe the clinical
manifestations of HF
Right HF vs Left HFRight Heart Failure - The inability of the right side of
the heart to adequately pump venous blood into the pulmonary circulationCauses a back-up of fluid in the body, resulting in swelling and
edema (peripheral edema & engorged liver and spleen)Causes = left heart failure, pulmonary HTN, PV stenosis, P
embolismLeft Heart Failure - The inability of the left side of the
heart to pump into the systemic circulationCauses accumulation of fluid in the lungs (pulmonary edema)Causes= MI, cardiomyopathy, AS, MR
Usually if failure has existed for years it affects both sides (biventricular failure)
Right HF
Left HF
Acute HF vs Chronic HFAcute HF= Sudden onset of HF
Often due to massive MI, rupture of cardiac valve leaflet
Symptoms = hypotension and flash pulmonary edemaUsually largely systolic and the sudden reduction in
cardiac output often results in systemic hypotension without peripheral edema
Chronic HF= HF that develops or progresses slowly over timeDilated Cardiomyopathy or multi-valvular HDArterial pressure tends to be well maintained until
very late in the course, but there is often accumulation of peripheral edema
Causes of HFSystolic DysfunctionImpaired contractility
MITransient myocardial ischemiaChronic volume overload
Mitral Regurge or Aortic Regurge
Dilated cardiomyopathyIncreased Afterload (pressure overload)
Aortic StenosisUncontrolled HTN
Causes of HFDiastolic DysfunctionImpaired Ventricular Relaxation
LV hypertrophyHypertrophic cardiomyopathyRestrictive cardiomyopathyTransient myocardial ischemia
Obstruction of LV fillingMitral StenosisPericardial constriction/tamponade
Most Common Underlying Causes of HFIschemic Heart Disease (75%)CardiomyopathiesValvular diseasesHTNCongenital heart disease
Precipitating CausesAcute disturbance that places an additional load on amyocardium that is chronically excessively burdened
InfectionArrhythmiasPhysical, dietary, fluid, environmental, emotional excessesMIPulmonary EmbolismAnemiaThyrotoxicosis PregnancyAggravation of HTNRheumatic and viral myocarditis Infective endocarditis
Clinical PresentationLeft-Sided HFDyspnea (DOE or at rest)Dulled Mental StatusNocturiaFatigue/weaknessOrthopneaParoxysmal Nocturnal DyspneaNocturnal coughHemoptysis
Clinical PresentationRight-sided failureAbdominal discomfort (RUQ)Nausea, anorexiaPeripheral edemaUnexpected weight gain
Left HF
Right HF
Directed HistoryOnset, Progression, Provoking, Palliative,
Quality, TimingPMH: pulmonary dz (copd, asthma), DM,
lipids, CAD/PVD, RF, MI, HTN, congenital, valvular disease
FH: MI, strokes, PAD, sudden cardiac death, myopathy, need for pacemaker, cardiomyopathy
SH: Exercise, smoke, drink, diet, stressMeds: CARDIOTOXINS
Directed PhysicalVitals: BP(sitting and standing), Wt, BMI, RR, HRGen: cachexia (if severe), dusky, diaphoreticNeck: JVDLungs: pulmonary rales, coarse rhonchi and
wheezing. Pleural effusions (both R and L)Heart: PMI, louder P2, S3, S4, MR. Right
ventricular heave, TRAbdomen: Hepatomegaly, RUQ tendernessPV: pulsus alternans, peripheral edema
Clinical Presentation
Symptoms Physical Findings
Left-Sided Dyspnea (DOE)
Orthopnea
PND
Fatigue
Diaphoresis
Tachycardia
Tachypnea
Pulmonary rales
Loud P2
S3 gallop (+/- S4)
Right-Sided Peripheral edema
RUQ pain
JVD
Hepatomegaly
Peripheral edema
Laboratory TestingCBCUACMP (Mg and Ca) Liver EnzymesFasting Glucose, HgAICLipidsTSH(BNP)
Diagnostic StudiesECG: LAE, LVH, ST-T changes, RVH, active
ischemia, old MI, arrhythmias (AF, VT)CXR: Cardiomegaly, cephalization, pleural
effusions, Kerley B lines, batwing or butterfly pattern
Echocardiogram with Doppler: to determine LVEF, wall motion abnormalities, chamber size, & valve fxn. Differentiates systolic from diastolic HF.
Stress testing/Cardiac Cath: in selected pts. Can assess wall abnormalities, valve fxn and EF
cardiomegaly
cephalization
http://www.mypacs.net/cgi-bin/repos/mpv3_repo/wrm/repo-view.pl?cx_subject=1666444&cx_image_only_mode=off&cx_repo=mpv4_repo
Echocardiogramhttp://www.heartfailure.org/eng_site/hf_test_ecg.asp
Two-dimensional echocardiogram showing a four-chambers view of the heart in a patient with systolic dysfunction. Note dilated LV. (LV = left ventricle; RV = right ventricle; RA = right atrium; LA = left atrium)
Two-dimensional echocardiogram showing a four-chambers view of the heart in a patient with diastolic dysfunction. Note the normal LV size with hypertrophy.
Framingham Criteria for Diagnosis of Congestive Heart Failure
To establish a clinical diagnosis of congestive heart failure by these criteria, at least one major and two minor criteria are required.
MAJOR CRITERIAParoxysmal nocturnal
dyspneaNeck vein distentionRalesCardiomegalyAcute pulmonary edemaS3 gallop Increased venous pressure
(>16 cmH2O)Positive hepatojugular
reflux
MINOR CRITERIAExtremity edemaNight coughDyspnea on exertionHepatomegalyPleural effusionVital capacity reduced by one-third
from normalTachycardia ( 120 bpm)
MAJOR OR MINORWeight loss 4.5 kg over 5 days'
treatment
Stages of Heart Failure
Acute Cardiogenic Pulmonary Edema
Results from severe L-sided HFElevated capillary hydrostatic
pressure leads to rapid accumulation of fluid within the interstitium and alveolar spaces of the lung
Often with hypoxemiaDue to sudden insult to
previously Asx pt OR precipitating event in chronic compensated HF
Acute Cardiogenic Pulmonary EdemaSevere dyspneaAnxietyHypoxemiaTachycardiaTachypneaCold, clammy skinCoughing “frothy” sputumRales +/- wheezingTx: lasix, morphine, nitrates, oxygen,
position
Goals of Therapy1. Identification and correction of the
underlying condition causing HF2. Elimination of the precipitating cause of
symptoms3. Management of HF symptoms
a) Treatment of pulmonary and systemic vascular congestion
b) Measures to increase CO
4. Modulation of the neurohormonal response
5. Improvement of long-term survival
A Winning HandThe Hand You’re Dealt
- Know your type of heart failureAn ACE Up Your Sleeve
- Take your medicinePlaying Your Cards Right
- Eat a healthy dietThe High Stakes
- Record a log of daily weightsDon’t Gamble With Your Health
- Report early signs of worseningStack the Deck
- Keep regular doctor visits
http://www.afmc.org/HTML/consumer/health_info/hfailures.aspx
Diastolic HF ManagementEstimated 1/2 of patients with HF have
preserved LVEFCorrect underlying causeReduce volume overload (cautious
diuretics)Slow HRReduce afterload
Non-Pharmacologic ManagementLifestyle Modification
Weight reductionSmoking cessationETOH avoidanceCardiotoxin avoidanceExerciseNa/Fluid restriction
Daily WeightsControl metabolic syndrome
Medications to Avoid in HFMost antiarrhythmics (save amiodarone)NSAIDS and COX-2 inhibitors
Can increase blood pressure and interfere with blood-pressure-lowering drugs
Antacids with added sodiumThiazolidinediones (glitazones)
Can result in dangerous levels of fluid retention Certain Chemo agents
CardiotoxicHormone replacement therapy & OCPs
Can raise blood pressureStimulants (Adderall, methylphenidate, cocaine, meth)
Elevate blood pressure and increase heart rateSildenafil (Viagra)
Can increase blood to heart and increase exercise tolerance
Caution when using it with other medications (such as nitrates)
Pharmacologic ManagementACE-InhibitorsARBsBeta-blockersDiureticsHydralazineNitratesInotropic agentsAldosterone Antagonists
Advanced Nonpharmacologic Interventions
Implantable Cardioverter-Defibrillators (ICDs): survival in LVEF <35%
Cardiac Resynchronization Therapy (CRT) via Biventricular Pacemaker: symptomatic HF with widened QRS complex
Ventricular assist devices: short but significant prolongation of survival in patients who had end-stage heart failure and were ineligible for transplantation
Percutaneous coronary interventionCoronary artery bypass grafting (CABG)Cardiac Transplantation: severe LV dysfunction,
refractory to maximal medical mgmt. Hospice
Ventricular Assist Devices
Biventricular Pacemaker
Implantable Cardioverter-Defibrillator
PrognosisSymptomatic HF confers a 1-year
mortality of 45%<50 % of patients are living 5 yrs after
their initial dx & <25 % are alive at 10 years
Worse prognosis than the majority of cancers
Prognosis
PreventionTreatment of HTN (with focus on systolic
pressure) reduces incidence of HF by 50%Effective even in pts >75 yrs old
Reduce risk of first or recurrent MIsControl DM, hypertension, dyslipidemia
In post-MI patients and/or those with reduced LVEFAdd beta blockers and ACEI – delays
progression of LV dysfunction & HF
Case PresentationChief Complaint: 74-year-old woman with shortness of breath
and swelling.
History: Martha Wilmington, a 74-year-old woman with a history of rheumatic fever while in her twenties, presented to her physician with complaints of increasing shortness of breath ("dyspnea") upon exertion. She also noted that the typical swelling she's had in her ankles for years has started to get worse over the past two months, making it especially difficult to get her shoes on toward the end of the day. In the past week, she's had a decreased appetite, some nausea and vomiting, and tenderness in the right upper quadrant of the abdomen.
On physical examination, Martha's jugular veins were noticeably distended. Auscultation of the heart revealed a low-pitched, rumbling systolic murmur, heard best over the left upper sternal border. In addition, she had an extra, "S3" heart sound.
Case Questions 1. What is causing this murmur? A low-pitched, rumbling murmur is usually due to a stenotic (i.e. narrowed) valve. The
left, upper sternal border is where the closing sound of the pulmonic valve is heard the best. Since Martha's murmur is heard best in this area, it is most likely due to pulmonic valve stenosis.
2. What is causing her "S3" heart sound? The "S3" heart sound is an extra sound heard early in ventricular diastole in
individuals with congestive heart failure, corresponding to the time when there is rapid filling of the ventricle with blood. One theory regarding its cause is that ventricular wall tension is increased in congestive heart failure, causing atrial blood to be forced against a relatively non-compliant ventricular wall during diastole, creating the "S3" heart sound.
3. Is her history of rheumatic fever relevant to her current symptoms? Explain. Her history of rheumatic fever may or may not be relevant to her current symptoms.
Rheumatic fever is thought to be caused by a hypersensitivity response to an infection by Streptococcus pyogenes. Certain bacterial antigens appear to be cross-reactive with antigens from human heart tissue. Hence, an immune response to the bacterium may cause unwanted destruction of human heart tissue, including the pericardium, myocardium, and endocardium. Destruction of the myocardium can, itself, lead to congestive heart failure. Destruction of the endocardium can involve the valves, though by far the most commonly affected are the valves in the left side of the heart (i.e. the mitral and / or aortic valves). Since it is Martha's pulmonic valve that is stenotic, it may be unrelated to her prior history of rheumatic fever.
Case Questions 4. A chest X-ray reveals a cardiac silhouette that is normal in diameter. Does this rule out a
possible problem with Martha's heart? Explain. A "normal" cardiac silhouette does not rule out a problem with Martha's heart. Her pulmonic
stenosis creates more resistance to the outflow of blood from the right ventricle into the pulmonary artery. Over time, the right ventricle will undergo concentric hypertrophy in an attempt to generate stronger contractions to overcome this resistance to flow. In concentric hypertrophy, the thickness of the wall increases, but the overall diameter of the ventricle does not change much. Since Martha's ventricular diameter hasn't changed much, the silhouette appearance of her heart on a chest X-ray will not be enlarged.
5. You examine Martha's abdomen and find that she has an enlarged liver ("hepatomegaly") and a moderate degree of ascites (water in the peritoneal cavity). Explain these findings.
Martha's hepatomegaly and moderate ascites are caused by increased systemic venous pressure. Since there is resistance to the flow of blood out of the right ventricle into the pulmonary artery, hydrostatic pressure rises in Martha's right ventricle, right atrium, and central systemic veins (this is why her jugular veins appear distended). This build-up of hydrostatic pressure is reflected backwards into her more peripheral systemic veins - - thus pressure rises in the inferior vena cava and hepatic vein of the liver. Elevated venous pressure in the hepatic sinusoids forces water from the bloodstream into the interstitial spaces of the liver, causing the liver to become swollen. A similar build-up of systemic venous pressure forces water from the bloodstream out into the peritoneal cavity, causing "ascites."
6. Examination of her ankles reveals significant "pitting edema." Explain this finding. The pitting edema in Martha's ankles is also caused by an elevated systemic venous pressure.
Fluid escaping from the peripheral capillaries into the interstitial spaces of her legs causes them to become edematous. This condition is aggravated when Martha spends several hours of the day standing, and is alleviated to some extent when Martha lies down with her feet above heart level.
Case Questions7. She is advised to wear support stockings. Why would this help her?Support stockings will place an external pressure on Martha's
lower legs, forcing some of the excess interstitial fluid into the lymphatic and blood vessels. One must be careful, however, when advising patients to wear support stockings. The stockings should place even pressure around the entire lower legs, and should not have restrictive bands of elastic at the top. Furthermore, if the patient has atherosclerosis and blockage of arteries supplying the legs, such support stockings may actually limit arterial blood flow into the legs, and thus should not be used.
8. Which term more accurately describes the stress placed upon Martha's heart -- increased pre-load or increased afterload?
Increased afterload
9. What is the general term describing Martha's condition?Right-sided congestive heart failure, which classically causes
systemic edema. Compare this with left-sided congestive heart failure, which causes pulmonary edema.
Case Questions 10. How might Martha's body compensate for the above condition?
The increased afterload placed upon Martha's right ventricle decreases her right ventricular stroke volume (i.e. decreases the volume of blood pumped out of the ventricles per contraction). To maintain an adequate cardiac output (i.e. volume of blood pumped out of the heart in one minute) to meet Martha's metabolic needs, she must either (A) increase the strength of contraction (i.e. increased contractility), and / or (B) increase the heart rate (i.e. the number of contractions per minute). In either case, Martha's sympathetic nervous system coordinates the response via the baroreceptor reflex. Furthermore, since Martha's cardiac output is likely to be below that required to meet her metabolic needs, the sympathetic nervous system stimulates systemic arteriolar vasoconstriction to the "less vital" organs (e.g. those of digestion and urination) while more blood is preferentially diverted to the "more vital" organs (e.g. the heart and brain).
Over the long term, Martha's right ventricle will undergo concentric hypertrophy as mentioned in #4. This will allow the right ventricle to increase its strength of contraction, but there are limits to how well this mechanism works. For example, as Martha's right ventricular wall thickens, the innermost portion of it receives relatively less blood, limiting its contractile strength.
Reduced cardiac output will diminish blood flow to the kidneys, triggering the renin-angiotensin-aldosterone (R-A-A) axis. During this response, the hormone renin is released from the juxtaglomerular ("granular") cells of the nephrons and enzymatically converts the liver protein angiotensinogen into angiotensin I. Angiotensin I, in turn, is converted into angiotensin II by ACE (i.e. angiotensin-converting enzyme). Angiotensin II has multiple effects, most of which serve to increase the systemic arterial pressure. Angiotensin II directly causes widespread systemic arteriolar vasoconstriction (hence, its name), which increases the total peripheral resistance to blood flow, and thus also the blood pressure. It also triggers the hypothalamic release of ADH (antidiuretic hormone), a hormone that stimulates the kidneys to conserve water and produce smaller volumes of very concentrated urine, ultimately increasing total blood volume and blood pressure. Perhaps most importantly, angiotensin II stimulates the release of the hormone aldosterone from the adrenal cortex. Aldosterone stimulates tubular reabsorption of sodium ions (in exchange for hydrogen and potassium ions) in the distal renal tubules of the kidneys. The movement of sodium ions from the renal tubules back into the bloodstream is followed by the osmotic movement of water, thus increasing the systemic blood volume and blood pressure.
As can be seen, the R-A-A axis increases total blood volume and thus increases the pre-load placed upon Martha's right ventricle. This increase in pre-load will increase the strength of right ventricular contraction via the Frank-Starling relationship in the heart, though there are limits to the effectiveness of this heightened R-A-A axis (see answer #12).
CaseQuestions 11. Martha is started on a medication called digoxin. Why was she
given this medication, and how does it work?
Digoxin is a digitalis derivative that slows the heart rate (i.e. it is a negative chronotropic drug) and increases the contractility (i.e. it is a positive inotropic drug) of Martha's failing right ventricle, making it a more efficient pump. By blocking the Na+/K+ ATPase pump in the cardiac contractile cell membrane, digoxin increases intracellular Na+ concentration. This, in turn, decreases the tendency of the cell membrane Na+/Ca+2 ion exchanger to move Na+ ions into the contractile cell and Ca+2 ions out of the contractile cell. The net effect of digoxin is thus to increase the concentration of Ca+2 ions in contractile cells. Cytoplasmic Ca+2 directly and indirectly helps to initiate the sliding filament mechanism of muscle contraction in contractile cells. It directly does so by binding to troponin C and uncovering the myosin globular head binding sites on actin proteins. It indirectly does so by stimulating release of additional Ca+2 ions from the sarcoplasmic reticulum into the cytoplasm. In the end, the higher the cytoplasmic Ca+2 ion concentration, the stronger and more long-lasting the ventricular contraction.
CaseQuestions 12. Two weeks after starting digoxin, Martha returns to the physician's office
for a follow-up visit. On physical examination, she still has significant hepatomegaly and pitting edema, and is significantly hypertensive (i.e. she has high blood pressure). Her physician prescribes a diuretic called furosemide (or "Lasix"). Why was she given this medication, and how does it work?
The activation of the R-A-A axis (as described in #10 above) may initially be a useful response, helping to increase the pre-load and thus the stroke volume of the right ventricle via the Frank-Starling relationship of the heart. However, continued increases in pre-load will only increase the stroke volume up to a certain point, beyond which any further increase in blood volume can exacerbate the systemic edema and congestive heart failure. At this point, it is useful to treat Martha's systemic edema with furosemide ("Lasix"), a loop diuretic which blocks the active transport of sodium ions from the loop of Henle back into the bloodstream. Since less sodium is reabsorbed, less water follows by osmosis. This will increase Martha's urinary output and help her to excrete some of the excess sodium and water from her interstitial fluid. Martha's high blood pressure places an increased workload ("afterload") on her heart. Her physician may prescribe an "ACE inhibitor" medication (e.g. captopril, enalopril) to block the conversion of angiotensin I to angiotensin II. This will effectively slow down the R-A-A axis and significantly reduce her systemic arterial blood pressure, allowing her ventricles to function more efficiently.
References• SA Hunt, et al. ACC/AHA 2005 Guideline Update for the
Diagnosis and Management of Chronic Heart Failure in the Adult: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society. Circulation. 2005;112:e154-e235. http://circ.ahajournals.org/cgi/content/full/112/12/e154
• L Goldman & DA Ausiello. Cecil Textbook of Medicine, 23rd ed. Saunders, 2007. Chapters 57 & 58.
• National Institutes of Health Website on Heart Failure. http://www.nhlbi.nih.gov/health/dci/Diseases/Hf/HF_WhatIs.html. Accessed May 11, 2010.
• I Dumetru. Heart Failure. Emedicine article. Updated January 22, 2010. http://emedicine.medscape.com/article/163062-overview. Accessed May 12, 2010.
• McGraw Hill. Anatomy & Physiology Case Studies. http://www.mhhe.com/biosci/ap/ap_casestudies/cases/ap_case16.html. Accessed May 10, 2011.
•
top related