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Download NPLEX Combination Review Cardiovascular Part 2
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NPLEX Combination Review Cardiovascular Part 3 Paul S. Anderson, ND Medical Board Review Services Copyright MBRS Angina Pectoris Clinical syndrome caused by Myocardial ischemia (usually from CAD) Angina Pectoris • Transient precordial pain, brought on by exertion and relieved by rest • Pain may be vague or crushing; may radiate to left shoulder, jaw, throat, teeth, arms • Pain may be worse after meal or in cold weather; may change as collateral circulation builds up • Usually relieved with sublingual nitroglycerin (NTG) within 2-3 min. • EKG often normal with attacks – exercise test may show ST abnormalities that help with diagnosis (ST depression = ischemia) Unstable Angina • More severe form of angina • Same etiology as exertional angina • Variant angina (Prinzmetal’s angina) = angina at rest with ST segment elevation during attack • May occur at same time of day • Felt to be from coronary artery spasm Acute Myocardial Infarction • When insufficient coronary blood supply persists after myocardial energy reserves have been depleted, the myocardial cells become irreversibly ischemic and the process of necrosis termed “myocardial infarction” • Pain not relieved with NTG • Apprehension and sense of “doom” • Most MI’s occur at 9 a.m. on Mondays Five major signs and symptoms of MI • pain or discomfort in the jaw, neck, or back • feeling weak, lightheaded, or faint • chest pain or discomfort • pain or discomfort in the arms or shoulder • and shortness of breath MI • All symptoms typically come and go on a 3-5 minute cycle. • In women the signs may be: – More significant nausea – Back pain (above the kidney area) – No neck or arm pain, often little chest pain – These signs and symptoms cycle on a 3-5 minute rate as well Acute Myocardial Infarction • Abnormal EKG with Q waves • CPK MB fraction elevated • ECHO shows abnormal left ventricular wall motion Heart Failure Congestive Heart Failure • Clinical syndrome in which the heart fails to pump enough blood to meet the body’s need • Leads to – Dyspnea On Exertion – Paroxysmal Nocturnal Dyspnea – Orthopnea Diastolic Heart Failure • Classically, heart failure has been almost synonymous with left ventricular systolic failure (pump failure) • Diastolic dysfunction of the left ventricle occurs when there is impairment of relaxation of the ventricle resulting in delayed filling and increased pulmonary venous pressure • This combined with secondary compensatory tachycardia results in left ventricular volume Adaptive Mechanisms in CHF • Ventricular dilation—will eventually lead to diastolic pressure and pul edema (left failure) and/or systemic edema (right failure) • Reduced blood flow to the kidneys salt and water retention and blood volume with 2º HBP ( afterload) • Sympathetic stimulation increases venous tone, thus shunting blood from the peripheral tissues to the heart causing BP • Tachycardia and increased contractility may precipitate ischemia in pts with CAD Left CHF • Cardinal clinical symptoms are DOE, chronic dry cough and fatigue • Tachycardia, cardiac asthma, productive rust colored sputum, rales, displaced apical impulse, S-3, S-4 gallop rhythms, right sided pleural effusions, reduced carotid pulse • Nocturia due to renal perfusion lying down and exercise intolerance due to blood flow to muscles. • Pallor, tachypnea, restlessness, low BP Right CHF • Fatigue, distended neck veins, pedal edema, ascites, pitting edema, large liver, tricuspid regurgitation murmur and cyanosis; orthopnea and PND. • Diseases that produce these sx include lung disease, pul embolus, volume overload, mitral stenosis. Pulmonary Heart Disease (Cor Pulmonale) • Right ventricular hypertrophy and eventual failure from pulmonary diseases • Causes include: – COPD – Pulmonary fibrosis or emboli – Scleroderma – Primary pulmonary hypertension – Alveolar hypoxia from any cause Cor Pulmonale • Chronic cough, exertional dyspnea, wheezing, fatigue, weakness, cyanosis, clubbing epigastric pulsations, distended neck veins, hepatomegaly, polycythemia • CXR shows RVH • PFTs show underlying lung disease • ECHO shows right ventricular disease Disturbances of Rate and Rhythm Normal Sinus Rhythm • Impulses originate in SA node • Regular rate of 60-100/min in adults • Each P followed by QRS Normal Sinus Rhythm Sinus Arrhythmia • Similar to normal sinus rhythm • Effect of respiration changes the frequency the SA node discharges. Sinus Bradycardia • Similar to NSR except the rate is < 60/min in adults • Physiological bradycardia occurs in healthy individuals (usually athletes) with vagal tone Sinus Bradycardia Sinus Tachycardia • Impulses originate in SA node at rate of 100-160/min in adults • QRS follows each P wave Atrial Premature Beat (APB) • Impulse is discharged prematurely by an irritable focus in the atria • The further from the SA node the ectopic focus is, the more abnormal will be the P configuration • PR is variable, but QRS is normal Atrial Premature Beat (APB) Atrial Tachycardia aka Supraventricular Tachycardia SVT • Impulses originate in an atrial pacemaker at rate of 140-250/min • QRS is usually narrow • At very rapid rates, only every 2nd P may be followed by QRS (2:1 block) • Vagal stimulation can terminate the AT • Common, occurs in young people with no known heart disease Atrial Tachycardia Atrial Flutter • Impulses originate in an atrial pacemaker at rate of 240-340/min, but some are blocked at the AV node • Atrial activity is represented by saw tooth-like deflections (Flutter waves) • Symptoms of palpitations, sweating weakness, dizziness, syncope • Vagal stimulation has no effect Atrial Fibrillation • Impulses originate in multifocal atrial pacemaker at rate of 300-600/min, but only some are conducted to the ventricles • Many patients are asymptomatic • Since there is a deficit in radial and precordial pulse, apical pulse should be taken in patients • Pulse is irregular, irregular • Vagal stimulation has no effect on ventricular rate Atrial Fibrillation Premature Ventricular Contractions (PVC) • QRS is wide (> 0.12 sec), not preceded by P wave • Etiology is an irritable focus in the left or right ventricle that fires prematurely and the impulse is spread to the opposite ventricle with delay producing a bizarre QRS complex • PVCs are forerunners of ventricular tachycardia if they are frequent (> 5/min) • May feel palpitations or be asymptomatic Premature Ventricular Contractions Ventricular Tachycardia • By definition, VT consists of at least three consecutive QRS complexes originating from the ventricles and recurring at a rapid rate (over 120 beats/min). Ventricular Tachycardia • Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute and wide QRS complexes • P waves are frequently hidden or may appear as notches at various points on the QRS-T complexes, but at a slower rate • Vagal stimulation has no effect Ventricular Tachycardia Ventricular Fibrillation • Multiple sites in the ventricle fire impulses in an uncoordinated fashion • Ventricular fibrillation is a terminal arrhythmia, uniformly requiring rapid initiation of emergency measures Sick Sinus Syndrome • Sick-sinus syndrome is a general term used to indicate abnormalities of cardiac impulse formation and intraatrial and AV conduction that may be manifested by various combinations of brady- and tachyarrhythmias • CAD is the most common cause • Symptoms include none, light headedness, fatigue, syncope, confusion, CHF or angina Heart Block • Often the presenting sign of heart block is SYNCOPE. First Degree AV Block • Impulses originate in SA node • First-degree AV block is defined as a PR interval in excess of 0.2 s at normal heart rates • QRS follows each P wave Second Degree AV Block • Second-degree AV block is characterized by intermittent failure of conduction from atria to ventricles and is further subdivided into type I (Wenckebach phenomenon) and Möbitz type II second-degree block Second Degree AV Block Type I (Wenckebach) • Impulses originating in SA node are conducted through AV node at progressively slower speed. • A blocked P wave occurs after 2-5 conducted P waves and then repeats itself (PR interval becomes progressively longer until the QRS is dropped) Second Degree AV Block Type II (Mobitz) • In type II second-degree AV block, appropriately timed P waves fail to conduct, but there is not a pattern of progressive PR lengthening. • Prognosis is not good Third Degree (Complete) AV Block • Impulses originate in SA node, but none are conducted through the AV jct. • In third-degree (complete) AV block, the atrial and ventricular rates are regular but dissociated • Maneuvers by the patient, such as arm movement, standing up, or marching in place, may increase the sinus rate (P waves) without corresponding changes in the ventricular escape rate, confirming loss of AV conduction. Bundle Branch Block (BBB) • Impulses originate in SA node, spread through atria, but are blocked through the right or left branches of the bundle of His • Wide QRS • LBBB is more ominous than RBBB Wolff-Parkinson-White Syndrome (WPW) • Impulses originate in SA node, spread over atria, but bypass the AV jct. through an accessory bundle with premature activation of the ventricles Vasculitis • Large-Vessel Vasculitis – Giant Cell Arteritis – Takayasu's Disease • Medium-Vessel Vasculitis – Polyarteritis Nodosa – Kawasaki's Disease • Small-Vessel Vasculitis – ANCA Associated Small Vessel Vasculitis – Non-ANCA Small Vessel Vasculitis Small Vessel Vasculitis • Symptoms – – – – – – – – – • Fever Weight loss Malaise Myalgias and arthralgias Dyspnea Cough (Hemoptysis may be present) Diarrhea Nausea or Vomiting Abdominal Pain Signs – Dermatologic findings • • – Palpable Purpura (duration longer than 24 hours) Urticaria Pulmonary findings • • Interstitial Lung Disease Pulmonary hemorrhage – Neurologic findings – Gastrointestinal findings • • – Fecal blood positive Differential Diagnosis • • • • • • Peripheral Neuropathy Embolic disease Sepsis Lymphoma Leukemia Myelodysplastic condition Labs – – – – – – – – – – – – Antineutrophil Cytoplasmic Antibodies (ANCA) Complete Blood Count (CBC) Normocytic Anemia Thrombocytosis Chemistry profile (e.g. Chem8) Renal Function tests may show renal insufficiency Liver Function Tests Increased liver enzymes Fecal Occult Blood Urinalysis (Glomerulonephritis) Hematuria Proteinuria Murmurs: • S-1 (T/M) ---Systole--- S-2 (A/P)---Diastole---S-1 • Systolic Murmurs: “Big Deal” – May be normal variants – May indicate pathology • (Midsystolic) Aortic / Pulmonic Stenosis • (Pansystolic - Holosystolic) Mitral/Tricuspid Regurgitation, Ventricular Septal Defect • Diastolic Murmurs: BIG DEAL – (Almost) Always indicate heart disease! • (Diastolic Rumble)Mitral Stenosis • (Decrescendo – Immediate Diastolic Murmur)Aortic Regurgitation Cardiac Murmurs • The types of valvular heart disease can be distinguished by the type of murmur heard on auscultation • Stenotic lesions of the aortic and pulmonary valve have an ejection murmur; they are systolic in timing, have a crescendo component and do not completely fill systole until late ( 12 12 ) Aortic Stenosis (AS) • Most frequent etiology for AS is senile calcific stenosis; second is calcification of a congenital (bicuspid) valve; third is rheumatic heart dis. • Sx include syncope, angina, SOB, CHF • Signs include ejection murmur at right 2nd ICS, weak and delayed peripheral pulses • Diagnosis is by ECHO Aortic Insufficiency • SOB, palpitations, angina • Signs include a diastolic murmur that is “blowing” and soft, elevated systolic BP and low diastolic BP • CXR shows signs of CHF and/or cardiomegaly Mitral Stenosis (MS) • Usual etiology for pathology is postrheumatic heart disease • SOB, DOE, PND, which are all part of CHF • Murmur is diastolic with an opening snap (due to stiff, thickened valves) followed by a low pitched rumbling sound best heard at the apex or left sternal border. ( 2-3 ) Mitral Stenosis (MS) • EKG may show notched P waves indicating left atrial enlargement • Diagnosis is by ECHO and cardiac cath • Indications for surgery include sx, presence of transvalvular gradient, measured by catheter, of > 4 mm Hg. Mitral Regurgitation • Symptoms of dyspnea, fatigue, left ventricular failure • Left ventricle eventually becomes compromised leading to cardiac dilatation • Murmur is pansystoloic, max at apex and radiating to axilla, blowing in quality with prominent 3rd heart sound • Echo Tricuspid Stenosis (TS) • Most frequent etiology is congenital, RHD, neoplasms • Right atrium is , atrial fib is frequent • EKG shows atrial fib and right atrial • Dx can be made by Echo Tricuspid Regurgitation (TR) • Most frequent etiology for TR is physiologic, as a reflection from left sided heart disease; endocarditis, especially in drug addicts (60% are due to Staph aureus) • Murmur low pitched, blowing, pansystolic, worse with inspiration and heard along left sternal border Endocarditis • Infective endocarditis is a microbial infection of the endocardium, usually a subacute bacterial endocarditis (SBE) • Most pts have underlying organic heart dis (abnormal valves, septal defects);High incidence seen in IV drug users • Nonspecific symptoms of cough, dyspnea, arthralgia, diarrhea, pallor, splenomegaly, abd./flank pain from emboli • Petechiae on palate or conjunctiva or in nail beds, splinter hemorrhages • 90% have heart murmurs and a changing murmur with leukocytosis is common Endocarditis • Blood cultures are the definitive diagnostic procedure; may be falsely negative in 5% • Echo confirms the vegetations Myocarditis: Inflammation of the myocardium • Etiology usually caused by infection (viral, most common); toxins, drugs, radiation, immunologic reactions. Often follows a URI • Typically present with heart failure following a febrile illness or with heart failure alone • Symptoms: – fatigue, dyspnea, palpitation, precordial pain through the first few weeks of the infection Hypertension Essential Hypertension • No known cause • There is a natural progression of the disease suggesting early in blood volume and cardiac output might cause resistance • This could be mediated by enhanced sympathetic activity or by circulating levels of angiotensin II Secondary Hypertension • • • • • • • • Renal artery stenosis Chronic renal disease Primary hyper-aldosteronism Hyper or hypo thyroidism Pheochromocytoma Pre-eclampsia Aortic coarctation BCP use Disease of the Aorta Aneurysms • Local dilation of the aorta resulting from weakness of the wall with distention • Most common etiology is atheroma; more recently evidence of Chlamydia pneumoniae has been found • 90% of aortic aneurysms are abdominal • Best noninvasive method is ultrasound (98% accurate on determining size) Rupture rate of aneurysm at 5 yrs Size of aneurysm % rupture rate 7 cm or greater 75% 6-7 cm 35% 5-6 cm (less than 5 cm) 25% (insufficient data) Signs and Symptoms of AAA • Aneurysms < 5 cm are usu asymptomatic • Pain in abdomen or low back • Pulsatile mass (many thin patients will have a pulsatile mass that is normal) • Tenderness over the pulsatile mass • Bruit over the mass (also can be heard in normals) Aortic Dissection • Occurs in ascending aorta; caused by a break in the intima allowing blood to flow in a plane between the media and adventitia • Pain is severe, chest or neck; may radiate to back and later to abdomen • Peripheral pulses and BP may be unequal • Syncope, hemiplegia or paralysis of the lower extremities may occur • CT and transesophageal echocardiography Inflammatory Pericarditis • Most cases are idiopathic or have a viral etiology • Patients typically complain of sharp central chest pain that worsens with recumbency and is relieved by leaning forward • Pain may be pleuritic in nature and may radiate to the trapezius muscle • Patients may reveal the pathognomonic finding for pericarditis: the pericardial friction rub • ECHO is a more accurate test Cardiac Tamponade • Results from accumulation of fluid in the pericardial sac; the heart has an inability to contract due to space restriction • Chest pain, dyspnea, cough, tachycardia, tachypnea, pulsus paradoxus (fall in BP > 10 mmHg with inspiration), edema and ascites may be seen