Rüzgar Miroğlu

Cardiology 2




Cardiology--ECG--





Pharmacological Management of Heart Failure

Treatment of Chronic Heart Failure aims to relieve symptoms, to maintain a euvolemic state (normal fluid level in the circulatory system), and to improve prognosis by delaying progression of heart failure and reducing cardiovascular risk. Drugs used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g.spironolactone).
ACE inhibitor therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.ACE inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy,particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEI therapy.
Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure:
* Loop diuretics (e.g. furosemide) – most commonly used class in CHF, usually for moderate CHF.
* Thiazide diuretics (e.g. hydrochlorothiazide) – may be useful for mild CHF, but typically used in severe CHF in combination with loop diuretics, resulting in a synergistic effect.
* Potassium-sparing diuretics (e.g.Spironolactone) – used first-line use to correct hypokalaemia.
As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, nebivolol and extended-release metoprolol.
Digoxin (a mildly positive inotrope and negative chronotrope), once used as first-line therapy, is now reserved when the adequate control is not achieved with an ACEI, a beta blocker and a loop diuretic.There is no evidence that digoxin reduces mortality in CHF, although some studies suggest a decreased rate in hospital admissions.It is contraindicated in cardiac tamponade and restrictive cardiomyopathy.

 

ECG Cases

Electrocardiography is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes.It is a noninvasive recording produced by an electrocardiographic device.The ECG works mostly by detecting and amplifying the tiny electrical changes on the skin that are caused when the heart muscle “depolarises” during each heart beat. At rest, each heart muscle cell has a charge across its outer wall, or cell membrane. Reducing this charge towards zero is called de-polarisation, which activates the mechanisms in the cell that cause it to contract. During each heartbeat a healthy heart will have an orderly progression of a wave of depolarisation that is triggered by the cells in the sinoatrial node, spreads out through the atrium, passes through “intrinsic conduction pathways” and then spreads all over the ventricles. This is detected as tiny rises and falls in the voltage between two electrodes placed either side of the heart which is displayed as a wavy line either on a screen or on paper. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle.

Complete Guide to ECG

Normal P waves 
Height less than 2.5 mm in lead II 
Width less than 0.11 s in lead II 
Abnormal P waves see in right atrial hypertrophy, left atrial hypertrophy, atrial premature beat, hyperkalaemia

Normal PR interval 
0.12 to 0.20 s (3 – 5 small squares) 
Short PR segment consider Wolff-Parkinson-White syndrome or Lown-Ganong-Levine syndrome (other causes – Duchenne muscular dystrophy, type II glycogen storage disease (Pompe’s), HOCM) 
Long PR interval see first degree heart block and ‘trifasicular’ block

Normal QRS complex 
Less than 0.12 s duration (3 small squares) 
for abnormally wide QRS consider right or left bundle branch block, ventricular rhythm, hyperkalaemia, etc. 
no pathological Q waves

Normal QT interval 
Calculate the corrected QT interval (QTc) by dividing the QT interval by the square root of the preceeding R – R interval. Normal = 0.42 s. 
Causes of long QT interval 
Myocardial infarction, myocarditis, diffuse myocardial disease 
Hypocalcaemia, hypothyrodism 
Subarachnoid haemorrhage, intracerebral haemorrhage 
Drugs (e.g. sotalol, amiodarone) 
Hereditary – Romano Ward syndrome (autosomal dominant) ,Jervill + Lange Nielson syndrome (autosomal recessive) associated with sensorineural deafness

Normal ST segment  – no elevation or depression 
Causes of elevation include acute MI (e.g. anterior, inferior), left bundle branch block, normal variants (e.g. athletic heart, Edeiken pattern, high-take off), acute pericarditis 
cCauses of depression include myocardial ischaemia, digoxin effect, ventricular hypertrophy, acute posterior MI, pulmonary embolus, left bundle branch block

Normal T wave 
Causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and left bundle branch block 
Causes of small, flattened or inverted T waves are numerous and include ischaemia, age, race, hyperventilation, anxiety, drinking iced water, LVH, drugs (e.g. digoxin), pericarditis, PE, intraventricular conduction delay (e.g. RBBB)and electrolyte disturbance.


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Adult Congenital Heart Disease

Congenital heart disease is a type of defect in one or more structures of the heart or blood vessels that occur before birth.

* Congenital heart defects occur while the fetus is developing in the uterus.
* They affect 8 to 10 out of every 1,000 children. Congenital heart defects may produce symptoms at birth, during childhood and sometimes not until adulthood.
* About 500,000 adults in the United States have grown into adulthood with congenital heart disease. This number increases by about 20,000 each year.
 
The most common congenital heart disorders affecting adults are:
* Congenital valve defects
* Atrial and ventricular septal defects
* Patent Foramen Ovale
* Anomalous Pulmonary Veins
* Coarctation of the Aorta (CoA)
* Ebstein Anomaly
* Pulmonary Artery Stenosis
* Tetralogy of Fallot (TOF)
* Transposition of the Great Arteries (TGA)
* Patent Ductus Arteriosus (PDA)
* Pulmonary Hypertension
Congenital heart defects may be diagnosed before birth, right after birth, during childhood or not until adulthood. It is possible to have a defect and no symptoms at all. In adults, if symptoms of congenital heart disease are present, they may include:
* shortness of breath
* poor exercise tolerance
Treatment is based on the severity of the congenital heart disease. Some mild heart defects do not require any treatment.Others can be treated with medications, invasive procedures or surgery.

 

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Clinical Features of Infection Endocarditis

Infective endocarditis is an infection of the endocardial surface of the heart. The intracardiac effects of this infection include severe valvular insufficiency and myocardial abscesses. It also produces a wide variety of systemic signs and symptoms through several mechanisms, including both sterile and infected emboli and various immunological phenomena.
The classic clinical presentation and clinical course of Infective endocarditis has been characterized as either acute or subacute. Acute IE frequently involves normal valves. It is a rapidly progressive illness in persons who are healthy or debilitated. Subacute IE typically affects only abnormal valves. Its course, even in untreated patients, may extend over many months.
IE develops most commonly on the mitral valve, closely followed in descending order of frequency by the aortic valve, the combined mitral and aortic valve, the tricuspid valve, and, rarely, the pulmonic valve. Mechanical prosthetic and bioprosthetic valves exhibit equal rates of infection.Congestive heart failure due to aortic valve insufficiency is the most common intracardiac complication of subacute endocarditis.
The complication of arterial embolization is second in frequency to congestive heart failure for both subacute and acute IE. The most common areas of deposition include the coronary arteries, kidneys, brain, and spleen. Infarction at the site of embolization is common.Cerebral emboli occur in 33% of patients. The middle cerebral artery is involved most often.Other neurological embolic damage includes cranial nerve palsies, cerebritis, and mycotic aneurysms caused by weakening of the vessel walls and produced by embolization to the vasa vasorum. Mycotic aneurysms may occur in the abdominal aorta and the splenic, coronary, and pulmonary arteries.
 

 

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Rheumatic fever is an inflammatory disease that occurs following a Group A streptococcal infection.Believed to be caused by antibody cross-reactivity that can involve the heart, joints, skin, and brain, the illness typically develops two to three weeks after a streptococcal infection.This cross-reactivity is a Type II hypersensitivity reaction and is termed molecular mimicry. Acute rheumatic fever commonly appears in children between the ages of 5 and 15.According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection.

 
Major criteria
* Migratory polyarthritis
* Carditis: inflammation of the heart muscle which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
* Subcutaneous nodules: painless, firm collections of collagen fibers over bones or tendons.
* Erythema marginatum
* Sydenham’s chorea (St. Vitus’ dance)
 
Minor criteria
* Fever
* Arthralgia: Joint pain without swelling
* Raised Erythrocyte sedimentation rate or CRP
* Leukocytosis
* ECG showing features of heart block, such as a prolonged PR interval
Supporting evidence of Streptococcal infection: elevated or rising Antistreptolysin O titre.
 
Sydenham’s chorea is a disease characterized by rapid, uncoordinated jerking movements affecting primarily the face, feet and hands.The disease is usually latent, occurring up to 6 months after the acute infection.SC is more common in females than males and most patients are children, below 18 years of age.SC is characterised by the acute onset of motor symptoms, classically chorea, usually affecting all limbs. Other motor symptoms include facial grimacing, hypotonia, loss of fine motor control and a gait disturbance.

 

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Bradycardia Management_Pacemaker syndrome

Pacemaker syndrome is a disease that represents the clinical consequences of suboptimal AV dyssynchrony, regardless of the pacing mode, after the pacemaker plantation.It is an iatrogenic disease—an adverse effect resulting from medical treatment—that is often underdiagnosed.The loss of physiologic timing of atrial and ventricular contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of symptoms production. This altered ventricular contraction will decrease cardiac output, and in turn will lead to systemic hypotensive reflex response with varying symptoms.Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline.
Individuals with a low heart rate prior to pacemaker implantation are more at risk of developing pacemaker syndrome. Normally the first chamber of the heart contracts as the second chamber is relaxed, allowing the ventricle to fill before it contracts and pumps blood out of the heart. When the timing between the two chambers goes out of synchronization, less blood is delivered on each beat. Patients who develop pacemaker syndrome may require adjustment of the pacemaker timing, or another lead fitted to regulate the timing of the chambers separately.
Several risk factors are associated with pacemaker syndrome.
  • In the preimplantation period, two variables are predicted to predispose to the syndrome. First is low sinus rate, and second is a higher programmed lower rate limit.
  • Patients with intact VA conduction are at greater risk for developing pacemaker syndrome.
  • Patients with noncompliant ventricles and diastolic dysfunction_such as hypertensive cardiomyopathy, hypertrophic cardiomyopathy,restrictive cardiomyopathy, and aging, can result in loss of atrial contraction and significantly reduces cardiac output.

 

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Mitral valve prolapse (MVP)

Mitral valve prolapse (MVP) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. Prolapsed mitral valves are classified into several subtypes, based on leaflet thickness, concavity, and type of connection to the mitral annulus. Subtypes can be described as classic, nonclassic, symmetric, asymmetric, flail, or non-flail.In its nonclassic form, MVP carries a low risk of complications. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, congestive heart failure, and in rare circumstances cardiac arrest, usually resulting in sudden death.MVP may occur with greater frequency in individuals with Ehlers-Danlos Syndrome and Marfan syndrome.Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common.

patients with MVP experience heart palpitations, atrial fibrillation, or syncope, though the prevalence of these symptoms does not differ significantly from the general population.
Echocardiography is the most useful method of diagnosing a prolapsed mitral valve. Two- and three-dimensional echocardiography are particularly valuable as they allow visualization of the mitral leaflets relative to the mitral annulus.Thickening of the mitral leaflets more than 5 mm and leaflet displacement more than2 mm indicates classic mitral valve prolapse.
Individuals with MVP are at higher risk of infective endocarditis.American Heart Association recommended prescribing antibiotics before invasive procedures, including those in dental surgery.

 

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Cardiac dysrhythmia

Cardiac dysrhythmia is a term for any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. Arrhythmias can be life-threatening medical emergencies that can result in cardiac arrest and sudden death.

 

Atrial Arrhythmia – Premature Atrial Contractions (PACs),Multifocal atrial tachycardia,Atrial flutter,Atrial fibrillation.
Junctional arrhythmias -Supraventricular tachycardia (SVT),AV nodal reentrant tachycardia is the most common cause of Paroxysmal Supra-ventricular Tachycardia (PSVT),Junctional rhythm,Junctional tachycardia.
Ventricular arrhythmias – Premature Ventricular Contractions (PVC),Ventricular fibrillation,Polymorphic ventricular tachycardia etc.
Heart blocks
  • First degree heart block, which manifests as PR prolongation
  • Second degree heart block
  • Type 1 Second degree heart block, also known as Mobitz I or Wenckebach
  • Type 2 Second degree heart block, also known as Mobitz II
  • Third degree heart block, also known as complete heart block
The method of cardiac rhythm management depends firstly on whether or not the affected person is stable or unstable. Treatments may include physical maneuvers, Antiarrhythmic drugs, electricity conversion, or electro or cryo cautery.Defibrillation or cardioversion may be accomplished by an implantable cardioverter-defibrillator (ICD).Electrical treatment of dysrhythmia also includes cardiac pacing. Temporary pacing may be necessary for reversible causes of very slow heartbeats, or bradycardia.A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover.

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Cardiac cycle is the all events related to the flow or blood pressure that occurs from the beginning of one heartbeat to the beginning of the next.Each beat of the heart involves five major stages: The first, “late diastole”, is when the semilunar valves close, the atrioventricular (AV) valves open, and the whole heart is relaxed. The second, “atrial systole”, is when the atrium contracts, the AV valves open, and blood flows from atrium to the ventricle.The third, “isovolumic ventricular contraction”, is when the ventricles begin to contract, the AV and semilunar valves close, and there is no change in volume. The fourth, “ventricular ejection”, is when the ventricles are empty and contracting, and the semilunar valves are open. During the fifth stage, “Isovolumic ventricular relaxation”, pressure decreases, no blood enters the ventricles, the ventricles stop contracting and begin to relax, and the semilunar valves close due to the pressure of blood in the aorta.
The cardiac cycle is coordinated by a series of electrical impulses that are produced by specialized heart cells found within the sino-atrial node and the atrioventricular node.
 

 

 

Atrial systole is the contraction of the myocardia of the left and right atria.Normally, both atria contract at the same time.70% of the blood flows passively down to the ventricles, so the atria do not have to contract a great amount.Electrical systole of the atria begins with the onset of the P wave on the ECG.Ventricular systole is the contraction of the myocardia of the left and right ventricles.Cardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing.Together they are known as complete cardiac diastole.

 

 
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