1) Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs due to issues with how the heart fills or empties.
2) Common causes include heart attacks, high blood pressure, and heart valve problems.
3) The renin-angiotensin system helps regulate blood pressure and fluid levels in the body and is activated in heart failure. Drugs that block this system such as ACE inhibitors are used to treat heart failure.
This Presentation provides a general introduction to Cardiac Pharmacology, list of various Cardiac disorders and Drugs used to treat Cardiac disorders. An assignment for the subject, Advanced Pharmacology - I, 1st year M.Pharm, 1st semester.
Association and prevalence of different comorbidities in hypertension and management with focus guidelines with benefits & choice of different antihypertensives in different comorbidities.
Cardiovascular pharmacology
Cardiovascular (=Circulatory) system – heart and blood vessels
Arteries – transport blood to tissues
Capillaries – sites of exchange, fluid O2, CO2, nutrients etc.
Venules – collect blood from capillaries
Veins – transport blood back to heart
Blood moves within vessels – higher pressure to lower pressure
Resistance to flow depends on vessel diameter, length and viscosity of blood
Brief description of drugs which are used to alter cardiac action potential in arrythmic patients. It focuses on understanding of action potentials in short descriptions as possible.
This Presentation provides a general introduction to Cardiac Pharmacology, list of various Cardiac disorders and Drugs used to treat Cardiac disorders. An assignment for the subject, Advanced Pharmacology - I, 1st year M.Pharm, 1st semester.
Association and prevalence of different comorbidities in hypertension and management with focus guidelines with benefits & choice of different antihypertensives in different comorbidities.
Cardiovascular pharmacology
Cardiovascular (=Circulatory) system – heart and blood vessels
Arteries – transport blood to tissues
Capillaries – sites of exchange, fluid O2, CO2, nutrients etc.
Venules – collect blood from capillaries
Veins – transport blood back to heart
Blood moves within vessels – higher pressure to lower pressure
Resistance to flow depends on vessel diameter, length and viscosity of blood
Brief description of drugs which are used to alter cardiac action potential in arrythmic patients. It focuses on understanding of action potentials in short descriptions as possible.
Comparative effectives of angiotensin-converting enzyme inhibitors and/or angiotensin II receptor blockers added to standard medical therapy for treating patients with stable ischemic heart disease and preserved left ventricular systolic function.
HYPERTENSION- THE LATEST MANAGEMENT
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
Comparative effectives of angiotensin-converting enzyme inhibitors and/or angiotensin II receptor blockers added to standard medical therapy for treating patients with stable ischemic heart disease and preserved left ventricular systolic function.
HYPERTENSION- THE LATEST MANAGEMENT
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
A 30-year-old man presented to the emergency department with palpitations and tachycardia.He had been experiencing sore throat, fevers, andmyalgias for the past day.He became
alarmed when he awoke from sleep with strong palpitations and a heart rate greater
than 200/min documented on his smartwatch.Hehad similar symptoms1 year ago andwas diagnosed with and treated for supraventricular tachycardia (SVT). A subsequent outpatient
echocardiogram revealed a structurally normal heart; results of a follow-up electrocardiogram (ECG) were also normal
2. Introduction Heart failure (HF) is a complex, progressive disorder in which the heart is unable to pump sufficient blood to meet the needs of the body. Its cardinal symptoms are dyspnea, fatigue, and fluid retention. HF is due to an impaired ability of the heart to adequately fill with and/or eject blood. It is often accompanied by abnormal increases in blood volume and interstitial fluid, hence the term congestive HF because symptoms include dyspnea from pulmonary congestion in left HF, and peripheral edema in right HF.
3. Underlying causes of HF include arteriosclerotic, myocardial infarction, hypertensive, valvular heart disease, dilated cardiomyopathy, and congenital heart disease. Left systolic dysfunction secondary to coronary artery disease is the most common cause of HF, accounting for nearly 70 percent of all cases. The number of newly diagnosed patients with HF is increasing, because more individuals now survive acute myocardial infarction.
4. Role of physiologic compensatory mechanisms in the progression of HF Chronic activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis is associated with remodeling of cardiac tissue, characterized by loss of myocytes, hypertrophy, and fibrosis. The geometry of the heart becomes less elliptical and more spherical, interfering with its ability to efficiently function as a pump. This prompts additional neurohumoral activation, creating a vicious cycle that, if left untreated, leads to death.
5. Renin-Angiotensin System HF leads to activation of the renin-angiotensin system What is the renin-angiotensin system ?
7. Angiotensin-converting enzyme inhibitors These drugs block the enzyme that cleaves angiotensin I to form the potent vasoconstrictor angiotensin II. ACE inhibitors should not be used in pregnant women, because they are fetotoxic.
8. Adverse effects These include postural hypotension, renal insufficiency, hyperkalemia, angioedema, and a persistent dry cough. The potential for symptomatic hypotension with ACE inhibitor therapy requires careful monitoring. ACE inhibitors should not be used in pregnant women, because they are fetotoxic.
9. Angiotensin-receptor blockers Angiotensin-receptor blockers (ARBs) are nonpeptide, orally active compounds that are extremely potent competitive antagonists of the angiotensin type 1 receptor. ARBs have the advantage of more complete blockade of angiotensin action, because ACE inhibitors inhibit only one enzyme. ARBs are a substitute for ACE inhibitors in those patients who cannot tolerate the ACE inhibitors.
10. Physiology of Muscle Contraction The myocardium, like smooth and skeletal muscle, responds to stimulation by depolarization of the membrane, which is followed by shortening of the contractile proteins and ends with relaxation and return to the resting state. However, unlike skeletal muscle, which shows graded contractions depending on the number of muscle cells that are stimulated, the cardiac muscle cells are interconnected in groups that respond to stimuli as a unit, contracting together whenever a single cell is stimulated.
11. Action potential Cardiac muscle cells are electrically excitable. However, unlike the cells of other muscles and nerves, the cells of cardiac muscle show a spontaneous, intrinsic rhythm generated by specialized pacemakerm cells located in the sinoatrial and atrioventricular nodes. The cardiac cells also have an unusually long action potential, which can be divided into five phases.
13. Cardiac contraction The contractile machinery of the myocardial cell is essentially the same as that in striated muscle. The force of contraction of the cardiac muscle is directly related to the concentration of free (unbound) cytosoliccalcium. Therefore, agents that increase these calcium levels (or that increase the sensitivity of the contractile machinery to calcium) result in an increased force of contraction (inotropic effect). The inotropic agents increase the contractility of the heart by directly or indirectly altering the mechanisms that control the concentration of intracellular calcium.
14. Ion movements during the contraction of cardiac muscle. ATPase = adenosine triphosphatase
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16. In biology, depolarization is a change in a cell's membrane potential, making it more positive, or less negative. Membrane potential is the difference in voltage (or electrical potential difference) between the interior and exterior of a cell (Vinterior − Vexterior).
17. Goals of pharmacologic intervention in HF The goals are to alleviate symptoms, slow disease progression, and improve survival. Accordingly, six classes of drugs have been shown to be effective: 1) inhibitors of the renin-angiotensin system, 2) β-adrenoreceptor blockers 3) diuretics 4) inotropic agents 5) direct vasodilators 6) aldosterone antagonists
18. Symptoms of heart failure Common symptoms of heart failure include breathlessness, tiredness, and swollen feet and ankles. Other symptoms depend on which side of your heart is most affected.
19. Left-sided heart failure affects the lungs and ability to breathe. Symptoms include breathlessness when exercising and/or when lying flat, extreme tiredness, wheezing and a cough with a pink froth, usually occurring at night. Right-sided heart failure affects the fluid balance in the body. Symptoms include swollen ankles, feeling sick, extreme tiredness and weight gain
20. The electrical conduction of the heart The normal electrical conduction of the heart allows electrical propagation to be transmitted from the Sinoatrial Node (SA) through both atria and forward to the Atrioventricular Node (AV). Normal/baseline physiology allows further propagation from the AV node to the Ventricle or Purkinje Fibers and respective bundle branches and subdivisions/fascicles. Both the SA and AV nodes stimulate the Myocardium.
21. Anatomy of heart conduction system 1. Sinoatrial node (SA)2. Atrioventricular node (AV)3. Bundle of His4. Left bundle branch5. left posterior fascicle6. left-anterior fascicle7. Left ventricle8. Ventricular septum9. Right ventricle10. Right bundle branch
22. All the wave of electrical activity across the heart muscles can be measured by the electrocardiogram (ECG). Function of this conduction system is to keep the heart beating in regular and synchronized manner – thus maintaining cardiac output.