ANP-Atrial Natriuretic Peptide
BNP-B-type Natriuretic Peptide
CHF-Congestive Heart Failure
Itis the opinion of Shaffer and Maurer (2015) that the exclusivepurpose of the heart is to pump blood through the body in order tonourish it. Just like any other human organ, the heart may at timesgive in to disorders or defects that affect its normal functioning.Congestive heart defects are a spectrum of problems with how a heartperforms. Heart failure doesn’t necessarily imply that the heart“fails” or “ceases to work” in the sense of beating as ithappens in cardiac arrest. Instead, it means that the heart has“failed” to function “normally” as in a healthy heart (Yelle& Chaudhry, 2016).
Tocomprehend what really transpires in CHF, it is important to discernhow this organ pumps blood to the body. Wilson (2015) perceptivelystates that the heart is a pumping system that has two autonomouschambers. Each chamber consists of one ventricle and one atrium withthe ventricles being the main pumps. Deoxygenated blood from the bodypasses through the right atrium as it enters the cavities of theheart. From the right chamber, blood is pumped into the lungs toreplace oxygen with carbon dioxide which is then exhaled. Afterblood is “re-nourished,” it is received form the lungs by theleft atrium, moves down to the left ventricle, and then pumped bythis muscular chamber out of the heart and to the whole body. Asblood is flowing through the heart, there are muscular flaps (valves)that open and close to make sure that blood goes in the rightdirection as it is pumped in and out of this organ. Since the hearthas four chambers, it correspondingly has four valves one for eachchamber (Wilson, 2015). And this is how a “healthy” heartperforms its exclusive function of pumping blood through the wholebody.
InCHF, Shaffer and Maurer (2015) observe that the heart does notfunction optimally. As indicated earlier, heart failure can presentitself as a hole in between the right and left chambers of the heart.Also, heart failure can present itself as incompletely formed valvesor missing valves. As in the case of aorticstenosis,the valves may be narrow, causing them to close improperly makingblood leak back into the heart. Per se, CHF is a problem with theheart’s structure and function (Tanai & Frantz, 2015). To thiseffect, CHF directly affect this precious organ in the sense that it“fails” to perform to the level of meeting the metabolicrequirements of the body (Shaffer & Maurer, 2015).
Itis the opinion of Wilson (2015) that congestive heart failure canensue in a myriad of fashions. First, the author notes that heartfailure can occur if heart muscles become too thin and weak. A“weakened” heart cannot pump blood with sufficient vigor toeffectively perfuse to all bodily organs and tissues. In this regard,as Wilson (2015) observes, the heart is said to have “failed.”Second, ineffective valves may occasion irregular blood flow betweenthe different chambers of this organ. In such a scenario, since theblood flow is interrupted right from the source (heart), it reachesthe tissues of the body in insufficient amounts to gratify metabolicneeds. What ensues is an uneven flow of blood throughout the body. Asa result, fluids tend to build up in tissues causing what istherapeutically referred to as congestion (Yelle & Chaudhry,2016). Third, the heart may fail when its muscles become too thick tothe level of becoming stiff. In this situation, the valves of theheart lose elasticity to a point that insufficient blood enters andleaves the chambers of the heart. When the heart pumps the blood, itwill not be adequate to meet the metabolic requirements of bodilytissues (Yelle & Chaudhry, 2016).
Itis the opinion of Tanai and Frantz (2015) that failure in the leftpart of the heart is more common. This is attributed to the fact thatit is the left ventricle that is tasked with the responsibility ofpumping blood through the whole body. Wilson (2015) draws attentionto the fact that CHF can also be occasioned by abnormal diastolic andsystolic contractions. Systolic failure is a propelling complicationwhere the ventricles cannot effectively perform their elementaryfunction of pumping adequate volumes of blood. Diastolic failure isassociated with filling problems. In such a scenario, fluid enteringthe heart is “sucked” back to the veins supplying the organ,causing them to fill and swell (Tanai & Frantz, 2015). In extremecases, fluid may go back into the lungs, causing a sudden and intenseshortness of breath. The authors also note that when the ventriclesof the heart become stiff, they cannot relax properly in betweenheartbeats implying that the heart cannot fill all the chambers withsufficient blood. When there is a failure on the right side of theheart, it is normally attributed to a prolonged failure of the leftside. Since the veins are stiff, blood entering the right ventriclewill back up, causing veins and tissues surrounding the heart swell.This often causes swelling in legs, ankles, feet, and abdomen (Tanai& Frantz, 2015).
Sowhat are the causes of CHF? According to Morton and Fontaine (2013),most people that suffer from this condition either have, orpreviously had another heart ailment. It is these pre-existingcardiac disorders that damage or weaken the heart, predisposing anindividual to the development of CHF. This does not suggest that aheart has to be weakened in order to fail. As previously indicated,the heart can also fail when it becomes too stiff. Even so, the mostcommon ailments known to damage the muscles of the heart are highblood pressure and coronary artery disease (Morton & Fontaine,2013).
Coronaryartery disease, according to the authors, is the most common cause ofheart failure. With the passage of time, the arteries that supply theheart with blood may get narrow following the deposition of fat(atherosclerosis) along arterial walls. This deposition of fat iswhat causes a reduction in the volume of blood that flows into theheart (Shaffer & Maurer, 2015). In a hypertensive individual, theheart is pumping blood at a higher pressure than an individual whoseblood pressure is within the standard range. Since the pressure iselevated, the heart is forced to work harder than it should to makesure that blood circulates through the whole body. Overtime, themuscles of the heart become thicker and stiffer to compensate for theincreased pressure and additional work. Eventually, the arterialmuscles supplying the heart become too stiff to effectively supplythe heart with the adequate volume of blood (Wilson, 2015).
Aboveand beyond these diseases, Yelle and Chaudhry (2016) observe that aninflammation of the muscles of the heart, as in the case ofmyocarditis,can occasion a left-sided failure of the heart. Moreover, heartdefects that individuals are born with can predispose them to thedevelopment of congestive heart failure. These spectrums of disordersare known as congenital heart defects, and they may be causativefactors in the progression of congestive heart failure (Wilson,2015). Furthermore, damages to heart muscles (cardiomyopathy) caninduce heart failure along with anomalous heart rhythms. Cardiacarrhythmia can make a heart beat too fast, making the organ workharder. With time, the heart may weaken, resulting in CHF. Morton andFontaine (2013) perceptively state that a slow heart can lead tocongestive heart failure. Beating mildly, the heart will not be ableto pump enough blood out to the body causing congestion in lungs andother organs of the body.
Bearingin mind that CHF gets its name from the congestion of bodily fluids,the first eye-catching symptom of the condition is edema (swelling)in different parts of the body like the abdomen (ascites),legs, feet, and ankles (Tanai & Frantz, 2015). In some patients,this might appear as a sudden gain in weight, attributed to theexcessive retention of fluid. Second, since fluid builds up in thelungs when it is backing up, the second notable symptom of CHF isdyspnea (sudden, severe shortness of breath), especially when anextraneous task is being undertaken. This often causes generallethargy and reduced ability to exercise. Other general symptoms ofCHF may include (but not limited to): irregular or rapid heartbeat,lack of appetite, chest pain, increased need to urinate at night,decreases alertness, and persistent wheezing or coughing with brownor beige blood-tinged mucus (Wilson, 2015).
Fora medical professional to effectively diagnose CHF, he/she will haveto closely scrutinize an individual’s medical history, perform aphysical assessment, and review the symptoms for a cross-check. Whendiagnosing congestive heart failure, physicians also check for themanifestation of risk factors such as hypertension or coronary arterydisease (Morton & Fontaine, 2013). Using a stethoscope, medicalspecialists “listen” to the lungs for signs of congestion. Also,the authors note that the stethoscope can detect any anomalies in themanner the heart is beating.
Moreover,doctors and nurses also examine the chest and abdomen using x-rayimaging. In CHF, fluid buildup may be visible in the lungs or chestcavity (Yelle & Chaudhry, 2016). To diagnose congestive heartfailure, medical specialists also administer electrocardiogram (ECG)tests to record the activities of the heart through sensors attachedon the skin. These tests record any anomalies of the heart as wavesthat are often displayed on a specialized monitor. Above and beyondthe ECG, physicians administer tests that include: MRI (magneticresonance imaging), CT (cardiac tomography) scan, coronary angiogram,myocardial biopsy, and echocardiogram (Morton & Fontaine, 2013).
Tanaiand Frantz (2015) observe that as CHF is developing, there are manycompensatory processes that are instituted in order to maintain aconsistent cardiac output. One such mechanism can be explained byFrank-Starling’slaw of the heart. This law describes how an optimal stretch ofcardiac muscles (sarcomeres) substantially increases contractility,and in so doing, linking cardiac ejection to cardiac filling (strokevolume) (Wilson, 2015). According to Starling’slaw,an increase in the length of cardiac muscles increases contractilitywhich is essential for harmonizing the preload (venous return) andthe afterload (stroke volume). An increase in preload dilates theventricles, stretching the myocardium. This increases the contractileforce of the cardiac muscles, increasing the stroke volume. Theventricles, in this case, can house increased venous returns owing toa more vigorous contractile force that ejects greater volumes ofblood from the heart preserving forward cardiac output (Morton &Fontaine, 2013).
Thepathophysiology of CHF can also be explained by the diastolic andsystolic functions of the heart. Normal diastolic functions of theheart are determined by two major factors: myocardial relaxation andelasticity of the left ventricle. In this regard, ventricular fillingis impaired when there are structural changes that affect therelaxation of the myocardium in early diastole. This causes anelevated level of pulmonary venous pressure and left-arterialpressure that eventually leads to pulmonary congestion. In order togenerate enough systolic pressures to pump an excessive afterload outof the heart and to the whole body, wall stress is often increased inCHF.
Inresponse to a sustained increase in cardiac pressure, hypertrophy ofventricular myocytesis stimulated. The purpose of the increase in the volume and mass ofventricular myocytesis to sustain the force of contraction so as to counteract the forceexerted on ventricular walls. In extreme cases, the ventricularmuscle fibers may dilate out of proportion, resulting in rapiddeterioration of ventricular functions. In a heart that is failing,the increase in myocardial volume is the assurance of myocardialremodeling. Hypertrophy is a sign of dying myocytes(Shaffer & Maurer, 2015). As more of them die, the remainingmyocytesexperience an amplified work load. The progenitor cells, in charge ofreplenishing the dead myocytes,eventually become ineffective with the progression of myocardialfailure which means that the underlying pathologic process isbasically hastening.
However,Wilson (2015) notes that the pathophysiology of CHF is not limited tostructural abnormality and failures it also entails the activationof neuro-hormonal mechanisms. In the beginning of congestive heartfailure, these mechanisms help to maintain a near normal perfusion ofvital organs. For instance, RAAS leads to the activation ofAngiotensin II. Research indicates that cardiac Angiotensin IIincreases total peripheral resistance in order to maintain thepressure of the blood within a normal range. Also, Angiotensin IIleads to an increased rate of myocyte apoptosis (Yelle &Chaudhry, 2016). In this regard, Angiotensin II mediates myocardialhypertrophy that can promote the complete loss of myocardialfunctions. The RAAS also produces aldosterone that is responsible forincreasing systolic volume by increasing sodium absorption andretention. This increases preload, which in turn increases thesystolic volume (Tanai & Frantz, 2015).
What’smore, the RAAS secretes ADH that after sensing a significant decreasein cardiac output, promotes the retention of water in the distalcollecting tubules so as to increase the volume of preload (Tanai &Frantz, 2015). In addition to the RAAS, the adrenergic nervous systemis also activated. Chemoreflexactivation of the adrenergic system induces the production andrelease of norepinephrine and epinephrine. This results in anincreased sympathetic outflow towards the heart, while decreasing theeffects of the parasympathetic system. Norepinephrine and epinephrinecause an increased heart rate, which causes a direct increase incardiac output (Tanai & Frantz, 2015). Also, these chemicalcompounds cause peripheral vasoconstriction, thereby increasingvascular pressure for the maintenance of blood pressure within normalparameters. In response to low cardiac output, the atria and theventricles produce ANP and BNP. Both these peptides promotenatriuresis and vasodilation, processes that attempt to decrease thevolume of blood so that the heart does not work too hard to itthrough the whole body.
CongestiveHeart Failure Recommended Treatment Strategies
Accordingto the American Heart Association (2015), there is an extensive scopeof interventional approaches that are available to supportindividuals with CHF in order to improve and prolong their lives.Efficacious treatment of CHF entails strategies comprised of:
Non –pharmacological strategies.
Best practice pharmacotherapy.
Surgical processes and supportive devices.
Post discharge congestive heart failure management.
Accordingto AHA (2015), the non-pharmacological management of congestive heartfailure is as important as prescribing appropriate medicines. Thereis evidence supporting the benefits of non-pharmacological approachesin the management of people with this disorder. As such, a physicalactivity program is recommended as a non-pharmacological solutionstrategy for patients with systolic and diastolic heart failure.Moreover, being overweight increases demands upon the heart in termsof daily living and during physical activity (AHA, 2015).
Secondly,dietary intervention is yet another important non-pharmacologicalintervention in the management of this cardiac condition. It isimportant for a patient suffering from CHF to indulge in healthydietary practices like reducing the consumption of saturated fats(AHA, 2015). The sedentary lifestyle of an individual can predisposethem to the development of congestive heart failure, like in the caseof smoking and drinking. Furthermore, psychosocial support ofpatients with congestive heart failure may help reduce stress anddepression which positively deter the rate of progression of theailment (AHA, 2015).
Pharmacotherapyis needed for the treatment of symptomatic CHF. To this effect, thereis a wide variety of drugs that are used in practice. ACE inhibitorsare used to block the activation of the RAAS system that producesAngiotensin II, which is responsible for cell apoptosis (AHA, 2015).Also, Beta blockers are used because of their beneficial effects ofinhibiting the chronic activation of a chain of neuro-hormonalreactions responsive to low cardiac output. The most commonly usedbeta blockers in the treatment of CHF include: carvedilol,metoprolol, and bisoporolol (AHA, 2015). Diuretics are also used tomanage CHF because they increase urine sodium excretion, therebydecreasing the physical signs of fluid retention (edema). What’smore, Angiotensin II inhibitors have proven to provide benefits inthe treatment of CHF because these classes of drugs prevent theprogression of myocyteapoptosis (AHA, 2015).
Similarly,aldosterone antagonists are used for their benefit in the preventionof cardiac muscles hypertrophy, cardiac fibrosis, and arrythmogenesis(AHA, 2015). Examples of drugs in this category includespironolactone and eplerenone. The blockade of aldosterone receptorsin the heart can help reduce the progression of congestive heartfailure. Calcium channel clockers are still another class of drugsused to manage this cardiac condition. These drugs, includingverapamil and amlodipine, are used because of their anti-ischemic andvasodilator effects (AHA, 2015). Digoxin, as an effective drug,inhibits the enzyme sodium-potassium ATPase which is responsible forthe retention of blood sodium. Hence, this drug acts by inhibitingthe retention of sodium in the blood: reducing the level of fluid“congestion.” Patients suffering from CHF are also given ironsupplements since anemia worsens the symptoms of the condition due toan insufficient number of red blood cells to deliver oxygen to thewhole body. Hence, congestive patients are sometimes placed on ironsupplements medication to decrease odds of the occurrence of cardiacischemic effects (AHA, 2015).
Basically,surgical procedures in the treatment of CHF are aimed atreconstructing the ventricles of the heart (AHA, 2015). In thisregard, surgeries like left ventricle aneurysmectomy, surgicalventricular reconstruction, and coronary revascularization areperformed on the hearts of patients suffering from this cardiaccondition. In some extreme cases of congestive heart failure, cardiactransplantation is performed on patients with acute refractoryconditions. Sometimes, instead of cardiac transplantation, assistivedevices are surgically inserted to assist the heart work at anoptimal rate (AHA, 2015).
Post-discharge management programs
Theseinterventional programs entail both pharmacological andnon-pharmacological management of congestive heart failure (AHA,2015). Generally, this is done to prevent the factors that contributeto poor patient outcome from making the cardiac condition worse.Interventions in this management strategy include adherence toprescribed pharmacological treatment, disseminating adequateknowledge of underlying illnesses and the prescribed treatment,patient care, patient counseling, encouraging individualized care,and the application of non-pharmacological strategies whereapplicable (AHA, 2015).
Eventhough palliative care is typically offered to patients withdegenerative neurological disorders, patients with congestive heartfailure can also be beneficiaries of this process. Palliative care isbest delivered by allied health, nursing, coordinated medicalspecialists, the community, and social services work. This alsoincludes working with family members to provide support to peoplesuffering from congestive heart failure. Just like any otherinterventional strategy, palliative care entails the employment ofpharmacotherapy and non-pharmacological strategies in the managementof this cardiac condition (AHA, 2015). This is normally done toensure an all-rounded patient management in terms of pharmacologicaland non-pharmacological interventional approaches.
Rolesof Nursing Practitioner
Inpractice, the engagement of a nursing practitioner in the treatmentof CHF is inevitable (Morton & Fontaine, 2013). Generally, it isthe role of a nursing practitioner to employ advanced proficiency innursing skills in the assessment, planning, and coordinating the careof one patient or a group of patients that suffer from CHF (Shaffer &Maurer, 2015). A nursing practitioner is in a perfect position toimprove the health of a patient because he/she has the ability andproficiency to cater to the needs of a patient in terms ofpharmacological and non-pharmacological interventional strategies.Also, it is the role of a nurse to disseminate vital informationrelated to the ailment, on top of providing information that canpromote self-care among patients (Yelle & Chaudhry, 2016). It isthe role of a nursing practitioner to educate, assist, and supportthe patient and family to understand the seriousness of the conditionand the possible consequences of living with the chronic nature ofCHF (Morton & Fontaine, 2013). Furthermore, it is the role of anurse to work with allied health, family members, and the generalcommunity to make sure that the supportive needs of patientssuffering from congestive heart failure are adequately gratified.This entails the role of a nurse involving the patient and theirfamilies in the treatment plan (Wilson, 2015).
CHFis one of the most prevalent ailments of the heart. Research showsthat individuals that suffer from congestive heart failure eitherhave, or had a cardiac complication. These pre-existing cardiacconditions are responsible for the predisposition of many individualsto the development of CHF. Such diseases include coronary arterydisease and high blood pressure. Being a “congestive” disease,this condition manifests itself as edema, irregular heartbeats andshortness of breath, prolonged wheezing coughs, reduced energy, anddecreased urination. To diagnose CHF, medical specialists administertest on a patient to cross-check for the real symptoms of congestion.The tests include physical examinations, CT scans, MRI imaging, andelectrocardiogram (ECG). If someone is diagnosed with congestiveheart failure, there are treatment inventions aimed at restoring thecardiac output. Interventional approaches generally entailpharmacological and non-pharmacological approaches that includesurgery and the inclusion of assistive devises into the heart. All inall, CHF is a manageable disorder because research has proven thatappropriately applied intervention approaches often have a positiveimpact on the lives of patients.
AmericanHeart Association. (2015). 2015 AHA/ACCF Guideline for the Managementof Heart Failure. Retrieved September 16, 2016, fromhttp://circ.ahajournals.org/content/128/16/e240
Morton,P. G., & Fontaine, D. K. (2013). Criticalcare nursing: A holistic approach.Philadelphia: Wolters Kluwer Health/Lippincott Williams &Wilkins.
Shaffer,J. A., & Maurer, M. S. (2015). Multiple Chronic Conditions andHeart Failure∗.JACC:Heart Failure,3(7),551-553. doi:10.1016/j.jchf.2015.04.005
Tanai,E., & Frantz, S. (2015). Pathophysiology of Heart Failure.ComprehensivePhysiology,187-214. doi:10.1002/cphy.c140055
Wilson,E. C. (2015). Heartattack and congestive heart failure: 20 simple lifestyle changes toprevent and reverse heart disease.S.l.: CreateSpace.
Yelle,D., & Chaudhry, S. (2016). Congestive Heart failure. RetrievedSeptember 16, 2016, from http://www.pathophys.org/heartfailure/