The report deals with the case scenario of Mr. Robert (Bob) Orkins, a 65 year old man with medical history of hypertension, type-2 diabetes, rheumatic fever, mitral stenosis and benign prostatic hyperplasia. He has been taking many medications due to this entire ailment. He is a heavy smoker as well as drinker. He was admitted to hospital after he collapsed suddenly while getting up. After preliminary physical examination and diagnostic test, Dr Kalinic predicts congestive heart failure and wants to confirm it by additional test. With this clinical information related to Bob, this report particularly analyses the pathophysiological relation of congestive heart failure in patient and determines the rationale for additional test ordered by the doctor. As pharmacological therapy has been initiated, the rational for initiating particular medications are evaluated.
Mr. Bob has currently reported symptoms of breathlessness, fatigue and distended abdomen. Following the preliminary observation of Mr. Bob after admission to the hospital when he collapsed in his chair, the physical examination revealed bibasilar crackles, diastolic murmur and edema. Bibasilar crackles or crackling sound from the base of lung is heard when lungs are inflated or deflated. In people with congestive heart failure, this may occur due to pulmonary edema. Due to congestive heart failure, people cannot pump blood efficiently and it leads to increase in blood pressure. The fluid collects in air sacs of lung and hence the crackle sound is heard (Sarnak, 2014). Secondly, diastolic murmurs are related to pulmonary valve regurgitation and mitral or tricuspid valve rumbles. Congestive heart failure is caused due to systolic dysfunction or diastolic dysfunction. Hence due to the observation of the symptoms of in Mr. Bob, Dr. Kalinic suspects that Mr. Bob might be suffering from congestive heart failure.
To further understand the symptoms of Mr. Bob and its relation with congestive heart failure, the understanding about the pathophysiological changes associated with congestive heart failure is important. This will help to relate with Mr. Bob’s preliminary diagnoses and diagnostic results. Congestive heart failure is a chronic condition that has an impact on the pumping power of heart and leads to abnormal circulatory congestion. Patients with congestive heart failure mostly experience symptoms of fatigue, palpitation and shortness of breath even in mild physical activity and this symptom was observed in Mr. Bob too (Anand, 2016). The progression to congestive heart failure occurs in an individual due to compensatory mechanism of altered cardiac rhythm, rennin-angiotensin system activation, sympathetic nervous system activation and myocardial hypertrophy (Segura, Frazier, & Buja, 2014). Symptoms of palpitation is also an indication of irregular heart beat and this is witnessed in patient with congestive heart failure because heart speeds up to compensate for the ability to pump blood normally and this sudden onset of irregular heartbeat (atrial fibrillation) gives the indication to clinician that it is linked to congestive heart failure. Similar symptoms of breathlessness were also seen in Mr.Bob and the pathophysiology behind congestive heart failure explains the reason for presentation of such symptoms (Tanai & Frantz, 2015).
A patient with heart failure has reduced force of contraction due to ventricle overloading. According to Frank Starling Law of the Heart, the force of ventricle contraction is a function of end-diastolic length of cardiac muscle and ventricular end-diastolic volume (Katz & Rolett, 2015). In healthy person, the increased filling in ventricle leads to increased contraction and high cardiac output. However, in patients with congestive heart failure, the ventricle contraction mechanism fails and ventricle becomes loaded with blood. This impairs the heart muscle contraction process and the heart muscles become overstretched in the absence of linking between actin and myosin filaments. Hence ventricular function curve is lowered and stretching leads to cardiac dilatation in patient. This is the reason why patients like Bob experience symptoms of fatigue and breathlessness (Tanai & Frantz, 2015).
When Mr. Bob was admitted to the emergency department, he was sweating profusely and he struggled to breath. Due to this, oxygen therapy was initiated for Mr. Bob at 6Ml/min via facemask. In the preliminary observation, his blood pressure was low and breathing rate was low. It is similar to common symptoms of heart failure such as fatigue, decrease in activity, edema, shortness of breath and cough. Hence, this symptom of breathlessness occurs due to physiological changes in body due to the development of congestive heart failure. Patients with congestive heart failure have reduced cardiac output which affects skeletal muscle blood supply and therefore cause fatigue. Furthermore, interstitial edema due to high left ventricular filling pressure leads to breathlessness. Hence, left ventricular dysfunction has a link with symptoms of breathlessness and fatigue in Mr. Bob (Bekelman et al., 2016).
The failure of systolic and diastolic function or both results in decreased stroke volume and it mainly occurs when the ventricle wall stiffens. Due to this abnormality, heart has to work harder to meet metabolic demands and hence the cardiac output increases in times of physical activity. Furthermore heart rate increases in patient with congestive heart failure and it leads to abnormal heart rhythms which are examined by diagnostic test. Therefore, the preliminary symptoms and observation of Mr. Bob indicates pathophysiology of congestive heart failure and this is the reason why Dr. Kalinic has ordered certain test to confirm the diagnosis and understand different abnormalities of heart in patient (Tanai & Frantz, 2015).
Mr. Bob was also a heavy smoker and drinker and this habit in Mr. Bob might also increase his risk for cardiovascular disease. High consumption of alcohol might block arteries supplying blood to the brain resulting in congestive heart failure due to the inability of the heart to pump blood sufficiently throughout the body. Alcohol consumption increases the blood pressure which is a risk factor for cardiovascular disease. Alcohol intake as well as smoking increase triglycerides levels. Hence, his habit of smoking and alcohol consumption makes him prone to developing the risk factors for congestive heart failure.
As initial physical examination of Mr. Bob revealed bibasilar crackles, diastolic murmur and bilateral oedema above the knees, Mr. Kalinic has suggested additional test to confirm that Mr. Bob is suffering from congestive heart failure. The rational for the following additional test are as follows:
Arterial blood gas analysis (ABG)- ABG test measures the acidity and level of oxygen and carbon dioxide in the blood from artery by parameters of PAO2, PACO2, pH, HCO3 and O2CT. This will help Mr. Kalinic to detect the acid-basic level in blood of Mr. Bob. It helps to detect how lungs can exchange oxygen and carbon dioxide as functional impairment of lungs often affects heart functions of people and leads to symptoms of exertional dyspnea (Park et al., 2015).
Urea and electrolytes- Urea and electrolyte test is done to assess kidney functions and fluid imbalance in patients. The rational for ordering this test for Mr. Bob is that patient with heart failure has low blood flow to the kidney due to heart failure and this test will confirm if Mr. Bob has heart failure or not (Pagana & Pagana, 2013).
Blood glucose level- As Mr. Bob has type 2 diabetes mellitus, this test is important to check elevated blood glucose level as it increases risk of heart failure and it will help to identify underlying cardiac abnormality.
Chest X-ray- Chest X-ray is necessary to identify any pulmonary congestion in patients and identify symptoms of heart failure.
12 lead ECG- 12 lead ECG test is necessary to detect electrical activity of the heart and identify etiological factor related to heart failure. It is a method to approach heart function of patients.
Estimated glomerular filtration rate (eGFR)- It is done to assess the functioning of the kidney and estimate the volume of blood that is filtered by kidneys. It is also a predictor of mortality rate in heart failure.
Full blood examination- Full blood examination is necessary for Mr. Bob to assess any infection that might be a cause of congestive heart failure.
Dr. Kalinic has initiated pharmacological therapy on patient post additional test and the medicines mainly included furosemide (IV), digoxin (PO), enalapril and warfarin. Furthermore, from his previous medication, diltiazem use has been discontinued. Furosemide is a potential diuretic prescribed by doctors to treat accumulation of fluid (edema) caused either by heart failure, kidney failure and nephritic syndrome. Dr. Kalinic has ordered this medicine for Mr. Bob because physical examination of Mr. Bob has revealed pitting oedema above his knees and other test suggests congestive heart failure in patients. The Furosemide drug acts by filtering water and mineral salts out of the blood and into the kidneys. The diuretics functions by blocking the absorption of water and mineral salts from filtered fluid in the kidney tubules and this leads to increase in urine output (diuresis). It is given by IV administration and effect is seen within two hours. This mechanism of action of Furosemide can help relieve symptoms of edema in Mr. Bob. However Mr. Bob needs to be careful while using the drug due to side effects of low blood pressure, dehydration, chest pain and shortness of breath (Ali et al., 2014). The pharmacokinetics of Furosemide drug may get altered by Bob’s underlying condition such as diabetes. As the use of Furosemide my cause hyperglycemia, Mr. Bob should be given the diuretic very cautiously and he should be monitored closely during pharmacotherapy (Zeitlinger, 2016).
Another drug digoxin has been prescribed for Mr. Bob to treat mild to moderate congestive heart failure as the drug strengthens heart contraction and irregular heart rhythms. Digoxin is a digitalis compound that inhibits cellular Na+/K+-ATPase. The sodium and potassium ion transport system is important for cell survival as it serves to reduce the concentration gradient across the cell membrane with time. The loss of this ion gradient in the system result in cellular depolarization, decrease in intracellular sodium concentration and accumulation of calcium. The Digoxin increased the sodium ion concentration and accumulates intracellular calcium by inhibiting the Na+/K+-ATPase. This increased contractility and smoothens muscle contraction and vasoconstriction (Ambrosy et al., 2014). Hence due to the cardiotonic effect, this drug has been prescribed for Mr. Bob. Anxiety, dizziness, nausea and headaches are the common side-effect of the drug, however adverse symptoms include fast heartbeat, heart block, blurry vision and irregular heart beat. Mr. Bob should be monitored during the therapy as there are chances of drug-drug interaction as Digoxin interacts with many medications. Hence, it is necessary to review all medications of Mr. Bob while giving this drug (Vamos, Erath, & Hohnloser, 2015).
Warfarin and enalapril is also a part of pharmacological therapy for Mr. Bob. Warfarin is an anti-coagulant agent that blocks multiple coagulation steps by inhibiting the synthesis of Vitamin K dependent coagulation factors. Warfarin therapy reduces the symptoms of left ventricular thrombus and cerebral embolism and to avoid atherothrombotic events in Mr. Bob, Dr. Kalinic has prescribed this drug (Laulicht et al., 2013). There are also chances of interaction of Warfarin with other drugs as it is metabolized by cytochrome P450 isoenzymes and use of drugs prescribed the same enzyme will affect the pharmacokinetic of this drug. In such case Dr. Kalinic have to consider discontinuing some previous medication used by patient. Hence Ditiazem has been discontinued to avoid interaction with other drugs. The efficacy of warfarin is also influenced by alcohol consumption and Mr. Bob will have to avoid alcohol during the therapy (Dechanont et al., 2014).
Secondly, enapril has been ordered for Mr. Bob to treat congestive heart failure. It is a an ACE (Angiotensin Converting Enzyme) inhibitor drug and beneficial effect is seen in patients as inhibits the suppression of rennin-angiotensin-aldosterone system. Due to its ACE inhibition action, it reduces the vasopressor activity and aldosterone secretion. Hence, in combination with digitalis and diuretics, enalapril will help to decrease systemic vascular resistance and increase cardiac output in Mr. Bob. Patient needs to be monitored only for serious side-effects like irregular heart beat and signs of infection. There is chance of drug-drug interaction and other medications should be checked in combination with enalapril (McMurray et al., 2014).
From the analysis of the case scenario of Mr. Robert Orkins, the report gives an idea about the associated symptoms and pathophysiological changes seen in patient with congestive heart failure. Mr. Bob already had past history of certain disease and was taking many medications for it. However, his recent symptoms of breathlessness, fatigue and edema followed by preliminary observation by triage nurse indicated development of congestive heart failure in patients. This was understood due to diastolic murmur, bibasilar crackles and edema in Mr. Bob. As this symptom mainly occurs due to lung function impairment as a result of inefficient pumping of blood, Dr. Kalinic has suggested several additional tests. By the explanation of the pathophysiology of the disease in relation with current symptoms, the rational for each additional test was discussed to confirm the diagnosis. Furthermore, evaluation of pharmacological therapy suggested how different drugs may aid in recovery of patients and reduce the comorbidities associated with the disease. Consideration was also given to possible drug-drug or drug-patient interaction so that Mr. Bob does not suffer any heath risk due to medication use.
Ali, Y., Parekh, A. M., Rao, R. K., & Baig, M. R. (2014). Furosemide Induced Electrolyte Imbalance: A Real Danger of Overdiuresis in Patients with Heart Failure. Journal of International Translational Medicine, 2(4), 482-484.
Ambrosy, A. P., Butler, J., Ahmed, A., Vaduganathan, M., van Veldhuisen, D. J., Colucci, W. S., & Gheorghiade, M. (2014). The use of digoxin in patients with worsening chronic heart failure: reconsidering an old drug to reduce hospital admissions. Journal of the American College of Cardiology, 63(18), 1823-1832.
Anand, I. S. (2016). High-Output Heart Failure Revisited. Journal of the American College of Cardiology, 68(5), 483.
Bekelman, D. B., Allen, L. A., Peterson, J., Hattler, B., Havranek, E. P., Fairclough, D. L., … & Meek, P. M. (2016). Rationale and study design of a patient-centered intervention to improve health status in chronic heart failure: The Collaborative Care to Alleviate Symptoms and Adjust to Illness (CASA) randomized trial. Contemporary clinical trials, 51, 1-7.
Dechanont, S., Maphanta, S., Butthum, B., & Kongkaew, C. (2014). Hospital admissions/visits associated with drug–drug interactions: a systematic review and meta?analysis. Pharmacoepidemiology and drug safety, 23(5), 489-497.
Katz, A. M., & Rolett, E. L. (2015). Heart failure: when form fails to follow function. European heart journal, ehv548.
Laulicht, B., Bakhru, S., Jiang, X., Chen, L., Pan, D., Grosso, M., … & Steiner, S. (2013). Antidote for new oral anticoagulants: mechanism of action and binding specificity of PER977. J Thromb Haemost, 11(suppl 2), 1322.
McMurray, J. J., Packer, M., Desai, A. S., Gong, J., Lefkowitz, M. P., Rizkala, A. R., … & Zile, M. R. (2014). Angiotensin–neprilysin inhibition versus enalapril in heart failure. New England Journal of Medicine, 371(11), 993-1004.
Pagana, K. D., & Pagana, T. J. (2013). Mosby’s manual of diagnostic and laboratory tests. Elsevier Health Sciences.
Park, J. J., Choi, D. J., Yoon, C. H., Oh, I. Y., Lee, J. H., Ahn, S., … & Cho, M. C. (2015). The prognostic value of arterial blood gas analysis in high?risk acute heart failure patients: an analysis of the Korean Heart Failure (KorHF) registry. European journal of heart failure, 17(6), 601-611.
Roerecke, M., & Rehm, J. (2014). Alcohol consumption, drinking patterns, and ischemic heart disease: a narrative review of meta-analyses and a systematic review and meta-analysis of the impact of heavy drinking occasions on risk for moderate drinkers. BMC medicine, 12(1), 182.
Sarnak, M. J. (2014). Attending rounds: a patient with heart failure and worsening kidney function. Clinical Journal of the American Society of Nephrology, CJN-11601113.
Segura, A. M., Frazier, O. H., & Buja, L. M. (2014). Fibrosis and heart failure. Heart failure reviews, 19(2), 173-185.
Tanai, E., & Frantz, S. (2015). Pathophysiology of heart failure. Comprehensive Physiology.
Vamos, M., Erath, J. W., & Hohnloser, S. H. (2015). Digoxin-associated mortality: a systematic review and meta-analysis of the literature. European heart journal, 36(28), 1831-1838.
Zeitlinger, M. (2016). Drug Interactions. In Clinical Pharmacology: Current Topics and Case Studies (pp. 265-292). Springer International Publishing.