Cardiac Diseases Dr Anil Sabharwal MD
Cardiac Diseases 1. 2. 3. 4. 5. 6. 7.
Disorder of HR, Rhythm & conduction IHD,MI Vascular disease Diseases of heart valves CHD Diseases of myocardium Diseases of pericardium
Heart • Along with brain & lung it is part of tripod of life • Muscular organ,3layers • Wt-300 gm • 4 chambers • Left side of chest
Diseases of HR, Rhythm, conduction • Under resting conditions HR is 60-70/mt • SA node is natural pacemaker • SA node is controlled by autonomic NS-vagus causes inhibition & sympathetic nerves cause↑ HR • Sympathetic stimulation eg exercise, emotional stress, fever, CHF →↑ HR • In diabetes autonomic nerves are damaged so there is little variation in HR
Heart Rate-Bradycardia • Bradycardia :HR<60/mt 1) Sinus bradycardia- ↓automaticity 2) AV block-nodal or idioventricular rhythm
Rhythm disorder-arrythmia • Sinus arrhythmia:-normal,↑ HR during inspiration, ↓HR during expiration • Sinus bradycardia: asymptomatic-no treatment, symptomatic-atropine or pace maker • Sinus tachycardia: anxiety, fever, anemia, CHF, thyrotoxicosis, drugs eg bronchodilator
Atrial tachyarrhythmias • • • •
Atrial ectopic beat Atrial tachycardia Atrial flutter-atrial rate appr 300/mt Atrial fibrillation-irregularly irregular
Supraventricular tachycardia • AV nodal re entry tachycardia (AVNRT) HR-140-220/mt ,re-entry phenomenon, lasts from few seconds to few hours • Atrioventricular re-entry tachycardia & WPW syndrome
Sino atrial Disease-sick sinus syndrome • • • • •
Sinus bradycardia Sinoatrial block PSVT Paroxysmal atrial fibrillation Atrioventricular block
Atrio ventricular or BBB • 1st degree • 2nd degree-Mobitz typeI,Mobitz typeII • 3rd degree • RBBB • LBBB
Ventricular tachyarrythmia • Ventricular ectopic • VT • VF
Heart • Heart acts as 2 separate pumps operating side by side. • LV Systolic pressure is 4 times>right & wall of LV is usually 1cm thicker than right • Coronary circulation: left & right coronary Art. just distal to aortic valve & it’s filling is during diastole.
Heart • Nerve supply-sympathetic & para sympathetic • At rest vagal activity predominates & HR is slow. adrenergic stimulation is associated with exercise, fever, stress→ ↑HR
Atherosclerosis • Atherosclerosis is a progressive inflammatory disorder of arterial wall that is characterized by focal lipid rich deposits called atheroma • Complications of atheroma 1)Impaired perfusion or obstruction 2)Ulceration→thrombus or embolization
Atherosclerosis • In established atherosclerotic plaque macrophages mediate inflammation & smooth muscle cells promote repair. If inflammation predominates plaque becomes unstable →ulceration & throbosis
IHD-Risk Factors • Family H/O CAD-due to shared genetic, environmental &life style factors • Male : Female 4:1 • Age: peak age M-50-60,F 60-70 • Glucose intolerance, insulin resistance • Lipid disorder-cholesterol, triglycerides, apolipo • Hypertension • Cigarette smoking-tobacco use-avoidable cause • Diet: deficient in fresh fruits ,vegetables & PUFA→high risk
Atherosclerosis • • • •
Diabetes Mellitus Physical Inactivity- doubles the risk Obesity-central Alcohol –small amount offer some protection,heavy→HT • Other factors like increased homocystine or hypo estrogenemia
CAD • • • • • •
Stable angina -fixed atheromatous stenosis Unstable angina –unstable plaque MI Heart failure Arrhythmia Sudden death
Diseases of myocardium & pericardium • Acute myocarditis: viral, bacterial, fungal, rickettsial,spirochetal or parasitic agent & toxins, drugs & immunological disorders. • Infectious myocarditis: follows URTI (coxsackie & influenza virus- immuno compromised patients have more chances) • C/F: no symptoms, chest pain, severe CHF • Enzymes ↑ ,CPK-MB, Troponin I & T • ECG: tachycardia, arrhythmias, intra ventricular conduction abnormalities • ECHO: Cardiomegaly & contractile dysfunction. • Treatment-adequate rest, specific antimicrobial
Drug induced & toxic myocarditis • Emetine, Doxorubicin & other cytotoxic drugs Catecholamines (pheochromocytoma) → inflammation & necrosis→ CHF • Phenohiazine, lithium, chloroquine, antimony & Arsenic compounds→ ECG changes &CHF • Hypersensitivity:sulphonamides,penicillins • Cocaine • Radiation,
Dilated Cardiomyopathy • Causes: idiopathic, alcoholic, postpartum • C/F:CHF, • ECG: low voltage QRS, intraventricular conduction defect • X-ray chest: cardiomegaly • ECHO:LV dilatation, global dysfunction • Treatment-CHF beta blockers, ace inhibitors
Hypertrophic cardiomyopathy • Autosomal dominant • C/F: dyspnea, chest pain, syncope,sudden death during vigorous exercise • ECG:LVH, • ECHO: asymmetric septal hypertrophy,↑ contractility, dynamic LV outflow obstruction • Treatment: beta blocker, calcium channel blocker, ICD (Intra cardiac defibrillator) device • Surgery
Restrictive cardiomyopathy • Impaired diastolic filling because ventricles are stiff .Contractile function are preserved • Causes: Amyloidosis, radiation, myocardial fibrosis, sarcoidosis,hemochromatosis • Diagnosis-echo, CT or MRI
ARF-treatment • Bed rest, Aspirin 0.6-0.9 g 4 hourly, penicillin, erythromycin • Prevention of recurrence-till age of 30
RHD • RF→ rigidity & deformity of valve cusps • Mitral valve alone is affected 50-60 %, combined mitral & aortic 20 % times ,pure aortic valve involvement less common, tricuspid valve affected 10 % along with mitral or aortic involvement • Stenosis or regurgitation or combination • Prophylaxis for SABE for dental extraction or other surgery
Diseases of pericardium • Acute pericarditis-acute inflammation • Causes: infection( viral, bacterial, tubercu losis) autoimmune syndrome, uremia, neoplasm, radiation, drug toxicity, post MI • C/F: chest pain, fever, dyspnea O/E –rub • Lab-↑ TLC, ECG-ST elevation • X-ray-cardiomegaly • Echo-
Pericardial effusion • Collection of fluid in pericardium • Cardiac tamponade-↑ intra pericardial pressure>15 mm Hg→ restriction of venous return & ventricular filling →shock & death • C/F-asymptomatic, pain, dyspnea, • O/E-rub, edema, ascites • X-ray ↑cardiac shadow, • ECG-T wave changes, Low voltage QRS • ECHO • Treatment-Tamponade-emergency removal of fluid
Constrictive Pericarditis • Inflammation→ thick, fibrosed & adherent pericardium which restrict diastolic filling →chronic elevated venous pressures • Causes: tuberculosis, radiation, cardiac surgery, viral pericarditis • C/F dyspnea, fatigue, weakness • O/E: edema, hepatic congestion, ascites • X-ray-cardiomegaly, calcification • ECHO • Treatment-diuretic, surgery
Vascular Diseases • Atherosclerosis-occlusive disease 1)Peripheral 2)Visceral • Acute arterial occlusion-embolus, thrombus • Thromboangitis obliterans • Idiopathic arteritis-of Takayasu (pulse less disease) • Raynaud’s Disease & Raynaud’s phenomenon • Aneurysm • Aortic dissection • Venous Diseases: Varicose veins, Thrombophlebitis
Aneurysm • Weakening of artrial wall from loss of elastin & collagen→ aneurysmal dilatation • Aneurysm of abdominal aorta-cause atherosclerosis-in aorta 25% concomitant occlusive atherosclerosis of lower limbs • Mostly asymptomatic-detected during physical examination or USG. Infra renal aorta is 2cm in diameter in aneurysm it is >4 cm • Severe abdominal or back pain indicate rupture which has highmortality • Treatment-1)Surgical repair,2)Prosthesis • Aneurysm Thoracic aorta- Syphilis, vasculitis, Marfan’s syndrome
Aortic dissection • H/O HT, Marfan’s syndrome • Sudden severe chest pain with radiation to back occasionally migrating to abdomen • It originates at the site of intimal tear then propagates distally • Treatment: treat HT, Surgery
Atherosclerotic Occlusive disease • Atherosclerosis is more at places of stress especially at bifurcations • Symptoms depend on site of occlusion-
Occlusive disease of iliac arteries 1)Intermittent claudication-pain & weakness of lower limbs C/F on walking & relieved after taking rest 2) rest pain means serious disease 3) Impotence O/E: absent peripheral pulses, bruit may be heard over aorta, Systolic BP normally higher in leg is higher in brachial artery & difference is more during exercise Investigation: 1)Doppler,2)aortography,3)MRI Treatment:1)stop smoking 2)Grafting 3)Thromboendarterectomy
Occlusive Cerebrovascular disease • TIA-sudden onset of neurological deficit which resolves completely in 24 hours • Stroke-neurological deficit beyond 24 hours • C/F contra lateral weakness or sensory changes, speech alteration or visual changes
Aneurysm-Thoracic aorta • Causes:
Valvular Heart Disease • • • • • • • •
Mitral Stenosis Mitral valve size-4-6 cm2, <1cm-critical MS Mitral Stenosis- cause RHD C/F-dyspnea, orthopnea, PND-symptoms ↑by any stress like fever, pregnancy O/E-S1-↑,Opening snap, diastolic murmur ECG-LA abnormality, AF ECHO confirms diagnosis & assess severity Treatment-
Mitral Regurgitation • Causes: RHD,MVP,SABE,PMD,AMI • C/F-DOE & Fatigue, MVP-chest pain, palpitation • O/E-S1↓,Pan systolic murmur, LV enlargement
Aortic stenosis • • • • • •
Causes: Congenital, Bicuspid aortic valve, RHD Usually no symptom till 50,DOE,Angina, syncope O/E Harsh systolic murmur ECG-LVH X-ray calcific valve Echo
Aortic Regurgitation • Causes: Bicuspid, RHD, SABE, trauma • C/F-Palpitation, dyspnea, angina • O/E collapsing pulse, bounding pulses,early diastolic murmur • ECG-LVH,T↓, • Chest X-ray-cardiomegaly, • ECHO:
Congenital Heart Disease • CHD-child is born with heart disease .It may or may not manifest at birth. E.g ASD, bicuspid aortic valve • congenital heart disease complicates approximately 1% of all live births. It occurs in about 4% of offspring of women with congenital heart disease. .
Fetal Circulation • In fetus oxygenated blood comes through umblical vein to IVC (Through ductus venosus)→ RA→LA( through foramen ovale), LV →Aorta • Venous blood from SVC ,partially mixed with oxygenated blood in RA→RV→ Pulm A → descending aorta through ductus arteriosus • Aortic isthmus is a constriction in aorta which lies in the aortic arch before the junction with the ductus arteriosus & limits the flow of oxygen rich blood to descending aorta. This means that less oxygen rich blood is supplied to organs which take up function after birth ie GIT, Kidney
Changes at birth • Lungs expand with air pulm vascular resistance ↓ & pulmonary flow starts LA pressure becomes >LA pr,so foramen ovale closes. Umblical A & veins close .In nnext few days ductus arteriosus closes under influence of prostaglandins & aortic isthmus closes
Incidence CHD VSD ASD PDA PS Co Aorta AS TOF TGA Others
20% 10% 10% 7% 7% 6% 6% 4% 20%
CHD-Causes • Maternal infection, drugs, toxins • Rubella→ PDA, PS, AS, ASD Alcohol→ VSD Dilantin→ PS, AS,Coarctation of Aorta, PDA Lithium→Ebstein anomaly, Tricuspid atresia Genetic & Chromosomal factors Down’s syndrome (Trisomy 21) ASD
Clinical Features • • • • • • • • •
Birth & Neonatal period Cyanosis Heart failure Infancy & Childhood Cyanosis CHF Arrhythmia Murmur Failure to Thrive
Clinical Features • • • • • •
Adolescence & adulthood CHF Murmur Arrhythmia Cyanosis-shunt reversal Hypertension (Co arctation)
• Central Cyanosis-of cardiac origin occurs when de saturated blood enters the systemic circulation without passing through lungs (R→L shunt). • In neonate cause-TGA, • In older children VSD with severe PS(TOF) or with pulm vascular disease (Eisenmenger syndrome) • Clubbing-prolonged cyanosis→clubbing
• Early diagnosis important because treatment is available or many CHD
Congenital Heart Disease • ETIOLOGY AND PREVENTION • Congenital cardiovascular malformations are generally the result of aberrant embryonic development of a normal structure, fetal development. Malformations are due to complex multifactorial genetic and environmental causes.
• Pulmonary Hypertension . Increases in pulmonary arterial pressure result from elevation of pulmonary blood flow and/or resistance, the latter due sometimes to an increase in vascular tone but usually the result of obstructive, obliterative structural changes within the pulmonary vascular bed. • Eisenmenger syndrome is applied to patients with a large communication between the two circulations at the aortopulmonary, ventricular, or atrial levels and bidirectional or predominantly right-to-left shunts because of highresistance and obstructive pulmonary hypertension.
PATHOPHYSIOLOGY • Functionally normal, congenitally bicuspid aortic valve may thicken and calcify with time, resulting in significant aortic stenosis; • A well-tolerated left-to-right shunt of an atrial septal defect may not result in cardiac decompensation,fourth or fifth decade.
Persistent Ductus Arteriosus • If ductus fails to close after birth→PDA • Aortic pressure >pulmonary pressure→ continuous flow of blood →(arterovenous shunt)continuous or machinery murmur • 50 % of CO recirculates thro lungs→↑work load on heart • CHF,dyspnea,palpitation,tachycardia • Treatment: 1) PG inhibitor-indomethacin, ibuprofen may induce closure2)device closure
Coarctation of aorta • • • • • •
C/F-Important cause of CHF in newborn Headache due to HT Cramps in legs-due to ↓circulation in legs Radio femoral delay Systolic murmur due to associated bicuspid valve Complications: LVF, Dissection of aorta, cerebral hemorrhage • X-ray chest notching of ribs, 3 sign • Treatment: Surgical
ASD
Erythrocytosis The chronic hypoxemia in cyanotic congenital heart disease results in erythrocytosis due to increased erythropoietin production
• INFECTIVE ENDOCARDITIS • Routine antimicrobial prophylaxis is recommended for most patients with congenital heart disease It is recommended for all dental procedures, gastrointestinal and genitourinary surgery, and diagnostic procedures such as proctosigmoidoscopy and cystoscopy. Prophylaxis includes both chemotherapeutic (antimicrobial) and nonchemotherapeutic (hygienic) measures. Meticulous dental and skin care is required.
Teratogenic factors
ACYANOTIC CONGENITAL HEART DISEASE ASD
• • • • • • • • • •
F>M
The sinus venosus Ostium primum Ostium secundum –most common Flow:LA→RA→RV→pulm. Circulation C/F :asymptomatic, Recurrent URTI, often detected on routine examination Wide fixed splitting of 2nd heart sound ,systolic murmur over pulm valve Chest x-ray-cardiomegaly ECG –RBB,rSR pattern ECHO Treatment 1)Device closure,2)Surgical
• Patients with atrial septal defect are usually asymptomatic in early life, • Beyond the fourth decade, a significant number of patients develop atrial arrhythmias, pulmonary arterial hypertension, bidirectional and then rightto-left shunting of blood, and cardiac failure.
• Electrocardiogram shows right axis deviation and an rSr¢ pattern in the right precordial leads Varying degrees of RV and RA hypertrophy may occur with each type of defect, depending on the height of the pulmonary artery pressure. • Chest roentgenograms reveal enlargement of the RA and RV, dilatation of the pulmonary artery and its branches, and increased pulmonary vascular marking.
VSD Ventricular septum has –membranous & muscular portion Most VSD are peri membranous C/F-flow LV→RV→ pan systolic murmur Small defect loud murmur, large defect soft murmur CHF Treatment:surgical closure
TOF PS Overriding of aorta VSD RVH C/F-cyanosis ,clubbing, polycythemia, systolic murmur Fallot’s spell -↑cyanosis after crying→ attack or feeding→ apnoea & unconsciousness • ECG-RVH,X ray-boot shape • Treatment-surgical correction • • • • • •
Other causes of cyanoticCHD • Tricuspid atresia- absent tricuspid orifice,VSD • Pulmonary atresia • TGA • Ebstein anamoly –TV is dysplastic & displaced into RV