Cardiology Flashcards
Jugular Venous Pulse graph
a- right atrial contraction
c- Bulging of tricuspid valve during right ventricular contraction
x- right atrial relaxation
v- continued inflow of venous blood
y- passive emptying of right atrium after tricuspid opening
Myxoma
Histologically, these tumors are composed of scattered cells within a mucopolysaccharide stroma, abnormal blood vessels, and hemorrhagic. Myxomas produce large amounts of vascular endothelial growth factor, which contribute to angiogenesis hemorrhaging ( seen as hemosiderin deposition [brown]), and friability seen in these tumors. Myxomas also produce large amounts of interlukin 6, thus patients frequently present with constitutional symptoms (e.g. weight loss, fever).
Heart Normal pressures
Right atrium (0,8), right ventricle (4,25), pulmonary artery (9,25), Left atrium (2,12), Left ventricle (9,130), Aorta (70,130)
Familial dysbetalipoproteinemia (type II hyperlipoproteinemia)
characterized clinically by xanthomas and premature coronary and peripheral vascular disease. The primary defects in familial dysbetalipoproteinemia are in Apo E3 and ApoE4, apolipoproteins found on chylomicrons and VLDL that are responsible for binding hepatic apoliportein receptors. Without E3 and #4, the liver cannot effeciently remove chylomicrons and VLDL remnants from the circulation, causing their accumulation in the serum and resultant elevations in cholesterol and triglyceride levels.
Apolipoproteins
ApoA-I: LCAT activation (cholesterol esterification)
ApoB-48: CHylomicron assembly and secreation by the intestine
ApoB-100: LDL particle uptake by extrahepatic cells.
ApoC-II: Lipoprotein lipase activation
ApoE-3&4: VLDL and chylomicron remnant uptake by liver cells
Pulses paradoxus
Decreased systemic blood pressure during inspiration (acute cardiac tamponade, constrictive percarditis, sever obstructive lung disease, and restrictive cardiomyopathy.)
Class 1 antiarrhythmic
Class 1 A (Disopyranide, Quinidine, Procainamide (Double Quarter Pounder) Intermediate ihib phase 0, prolonged effect on length of action potential; Class 1B (Lidocaine, Tocainide, Mexiletive (Lettuce, Tomato, May)) weak, shortened; Class 1 C (Marcizine, Flecainide, Propafenone (More Fries Please)) Strong, no change.
Heart embryology
Truncus arteriosus (TA) - Ascending aorta and pulmonary trunk
Bulbus cordis - Smooth parts (outflow tract) of left and right ventricles
Primitive atria - Trabeculated part of left and right atria
Primitive ventricle - Trabeculated part of left and right ventricles
Primitive pulmonary vein - smooth part of left atium
Left horn of sinus venosus (SV) - Coronary sinus
Right horn of SV - Smooth part of right atrium
Right common cardinal vein and right anterior cardinal vein - SVC
Coronary artery anatomy
FA 266
Cardiac output
CO = stroke volum (SV) x heart rate (HR)
Fick principle: CO = rate of O2 consumption/ (arterial O2 content - venouse O2 conent)
Mean arterial pressure (MAP) = CO x TPR
MAP = 2/3 diastolic pressure + 1/3 systolic pressure
Pulse pressure = systolic pressure - diastolic pressure (increased in hyperthyroidism, aortic regurgitation, arteriosclerosis, obstructive sleep apnea, exercise (transient)). Pulse pressure is proportional to SV, inversely proportional to arterial compliance. (decrease pulse pressure in aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced heart failure.)
SV = EDV - ESV
Cardiac and vascular function curves
FA 269
Pressure-volume loops and cardiac cycle
FA 270
Aortic area
Systolic murmur - Aortic stenosis, flow murmur, aortic valve sclerosis
Left sternal border
Diastolic murmur - Aortic regurgitation, pulmonic regurgitation
Systolic murmur - Hypertrophic cardiomyopathy
Pulmonic area
Systolic ejection murmur - Pulmonic stenosis, flow murmur
Tricuspid area
Pansystolic murmur - Tricuspid regurgitation, ventricular septal defect
Diastolic murmur - Tricuspid stenosis, Atrial septal defect
Mitral area
Systolic murmur - Mitral regurgitation
Diastolic murmur - Mitral stenosis
Heart murmurs
FA 273
Speed of conduction
Purkinje > atria > ventricles > AV node
Some Risky Meds Can Prolong QT
Sotalol, Risperidone (antipsychotics), Macrolides, Chloroquine, Protease inhibitors (-navir), Quinidine (class Ia; also class III), Thiazides
Congential long QT syndrome
Inherited disorder of myocardial repolarization, typically due to ion channel defects; inc risk of sudden cardiac death due to torsades de points. Includes:
Romano-Ward syndrom - autosomal dominant, pure cardiac phenotype (no deafness).
Jervell and Lange-Nielsen syndrome - autosomal recessive, sensorineural deafness
Wolf-Parkinson-White syndrome
Most common type of ventricular pre-excitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG. May result in reentry circuit -> supraventricular tachycardia.
Atrial fibrillation
Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly space QRS complexes. Can result in atrial stasis and lead to thromboembolic stroke. Treatment includes rate control, anticoagulation, and possible pharmacological or electrical cardioversion.
Atrial flutter
A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves. Pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmics. Rate control: b-blocker or CCB. Definitive treatment is catheter ablation
Ventricular fibrillation
A completely erratic rhythm with no identifiable waves. Fatal arrhytmia without immediate CPR and defibrillation.
1st degree av block
The PR interval is prolonged (>200 msec). Benign and asymptomatic. No treatment required
2nd degree AV block
Mobitz type I - Progressive lenghtening of the PR interval until a beat is “dropped” ( a P wave not followed by a QRS complex). Usually asymptomatic
Mobitz type II - Dropped beats that are not preceded by a change in the length of the PR interval. It is often found as 2:1 block, where there are 2 or more P waves to 1 QRS response. May progress to 3rd-degree block. Often treated with a pacemaker.
3rd degree AV block
The atria and ventricles beat independtly of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treated with pacemaker. Lyme disease can result in 3rd-degree heart block.
Atrial natriuretic peptide
Released from atrial myocytes in response to inc blood volume and atrial pressure. Causes vasodilation and dec Na reabsorption at the renal collecting tubule. Constricts efferent renal arterioles and dilates afferent arterioles via cGMP, promoting diuresis and contributing to “aldosterone escape” mechanism
B-type (brain) natriuretic peptide
Released from ventricular myocytes in response to inc tension. Similar physiologic action to ANP, with longer half-life. BNP blood test used for diagnosisng heart failure (very good negative predictive value). Available in recombinant form (nesiritide) for treatment of heart failure.
Receptors:
Aortic arch transmits via vagus nerve to solitary nucleus of medulla (responds only to Inc BP)
Carotid sinus (dilated region at cartoid bifurcation) transmits via glossopharyngeal nerve to solitary nuclus of medulla (responds to dec and inc in BP)
Right-to-left shunts
Early cyanosis - “blue babies”. Often diagnosed prenatally or become evident immediately after birth. usually require urgent surgical correction and/or maintenance of a PDA.
The 5 T’s: 1. Truncus arteriosus 2. Transposition 3. Tricuspid atresia 4. Tetralogy of Fallot 5. TAPVR
Persistent truncus arteriosus
Failure of truncus arteriosus to divide into pulmonary trunk and aorta; most patients have accompanying VSD.
D-transposition of great vessels
Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) -> separation of systemic and pulmonary circulations. Not compatible with life unless a shunt is present to allow mixing of blood (e.g., VSD, PDA, or patent forament ovale). Due to failure of the aorticopulmonary septum to spiral.Without surgical intervention, most infacnts die within the first few months of life.
Tricuspid atresia
Absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability
Tetralogy of Fallot
Caused by anterosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis. 1. Pulmonary infundibular stenosis (most important determinant for prognosis) 2. RVH - boot-shaped heart on CXR. 3. Overriding aorta. 4. VSD
Pulmonary stenosis forces right-to-left flow across VSD -> early cyanotic “tet spells”, RVH
Total anomalous pulmonary venous return (TAPVR)
Pulmonary veins drain into right hear circulation (SVC, cornoary sinus, etc); assocated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.
Ventricular septal defect
Most common congenital cardiac defect. Asymptomatic at birth, may manifest weeks later or remain asymptomatic throught life. Most self resovle; larger lesions may lead to LV overload and heart failure.
Atrial septal defect
Defect in interatrial septum; loud S1; wide, fixed split S2. Usually occurs in septum secundum; septum primum defects usually occur with other anomalies. Symptoms range from none to heart failure. Distinct from patent forament ovale in that septa are missing tissue rather than unfused
Patent ductus arteriosus
In fetal period, shunt is right to left (normal). In neonatal period, dec lung resistance -> shunt becomes left to right -> progressive RVH and/or LVH and heart failure. Associated with a continous, “machine-like” murmur. Patency is maintained by PGE synthesis and low O2 tension. Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis)
Eisenmenger syndrome
Uncorrected left-to-right shunt (VSD, ASD, PDA) -> inc pulmonary blood flow -> pathologic remodeling of vasculature -> pulmonary arteriolar hypertension. RVH occurs to compensate -> shunt becomes right to left. Causes late cyanosis, clubbing, and polycythemia. Age of onset varies.
Hypertensive emergency
Sever hypertension (>180/120) with evidence of acute, ongoing target organ damage (e.g. papilledema, mental status changes)
Atherosclerotic progression
Inflammation important in pathogenesis.
Endothelial cell dysfunction -> macrophage and LDL accumulation -> foam cell formation -> fatty streaks -> smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition -> fibrous plaque -> complex atheromas
Abdominal aorta>coronary arter>popliteal arter>carotid arter
Aortic dissection
Longitudinal intraluminal tear forming a false lumen. Associated with hypertension, bicuspid aortic valve, and inherited conective tissue disorders (e.g., Marfan syndrome). Can present with tearting chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in arms. CXR shows mediastinal widening. The false lumen can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta. Can result in pericardial tamponade, aortic rupture, and death.
ECG diagnosis of MI
Anterior wall (LAD) - V1-V4
Anteroseptal (LAD) - V1-V2
Anterolateral (LAD or LCX) - V4-V6
Lateral wall (LCX) - I, aVL
Inferior wall (RCA) - II, III, aVF
Dilated cardiomyopathy
Most common cardiomyopathy (90% of cases). Often diopathic or congenital. Other etiologies include chronic alcohol abuse, wet beriberi, coxsackie B virus myocarditis, chronic cocaine use, Chagas disease, Docorubicin toxicity, hemocrhomatosis, and peripartum cardiomopathy.
Findings: heart failure, S3, dilated heart on echocardiogram, balloon appearance of heart on CXR.
Treatment: Na restriction, ACE inhibitors, B-blockers, diuretics, digoxin, implantable cardioverter defibrillator (ICD), heart transplant.
Hypertrophic cardiomyopathy
60-70% of cases are familial, autosomal dominant (commonly a B-myosin heavy-chain mutation). Rarely can be associated with Friedreich ataxia. Cause of sudden death in young athletes, due to ventricular arrhythmia. Findings: S4, systolic murmur.
Treatment: Cessation of high-intensity athletics, use of B-blocker or non-dihydropyridine calcium channel blockers (e.g., verapamil). ICD if patient is high risk.
Restrictive/infiltrative cardiomyopathy
Major causes include sarcoidosis, amyloidosis, postradation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis (dilated cardiomyopathy can also occur).
CHF
FA 291
Aschoff bodies
Associated with rheumatic fever (granuloma with giant cells).
Kussmaul sign
Increase in JVP on inspiration instead of a normal decrease.
Inspiration -> negative intrathoracic pressure not transmitted to heart -> impaired filling of right ventricle -> blood back up into venae cavae -> JVD. May be seen with constrictive pericardiits, restrictive cardiomyopathies, right atrial or ventricular tumors.
Strawberry hemangioma
Genign capillary hemangioma of infancy. Appears in first few weeks of life (1/200 births); grows rapidly and regresses spontaneously at 5-8 years old.
Cherry hemangioma
Benign capillary hemangioma of the elderly. Does not regress. Frequency inc with age
Pyogenic granuloma
Polpyoid capillary hemangioma that can ulcerate and bleed. Assocated with trauma and pregnancy
Cystic hygroma
Cavernous lymphangioma of the neck. Associated with Turner syndrome.
Glomus tumor
Benign, painful, red-blue tumor under fingernails. Arises from modified smooth muscle cells of glomus body.
Bacillary angiomatosis
Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaked for Kaposi sarcoma.
Angiosarcoma
Rare blood vessel malignancy typically occuring in the head, neck, and breast areas. Usually in the elderly, on sun-exposed areas. Associated with radiation therapy and arsenic exposure. Very aggressive and difficult to resect due to delay in diagnosis.
Lymphangiosarcoma
Lymphatic malignancy associated with persistent lympedema (e.g., post-radical mastectomy).
Kaposi sarcoma
Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis.
Temporal (giant cell) arteritis
Generally elderly females. Unilateral headache (temporal artery), jaw claudication. May lead to irreversible blindness due to ophthalmic artery occlusion. Associated with polymyalgia rheumatica.
Most commonly affects branches of carotid artery. Focal granulomatous inflammation. inc ESR. Treat with high-dose corticosteoids prior to temporal artery biopsy to prvent vision loss.
Takayasu arteritis
Asian females <40 years old. “pulseless disease” (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances.
Granulomatous thickening and narrowing of aortic arch and proximal great vessels. inc ESR. Treat with corticosteroids.
Polyarteritis nodosa
Young adults. Hepatitis B seropositivity in 30% of patients. Fever, weight loss, malaise, headache. GI: abdominal pain, melena. Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage.
Typically involves renal and visceral vessels, not pulmonary arteries. Immune complex mediated. Transmural inflammation of the arterial wall with fibrinoid necrosis. Innumerable microaneurysms and spasm on arteriogram. Treat with corticosteroids, cyclophosphamide.
Kawasaki disease
Asian children <4 y.o. Fever, cervical lympadenitis, conjunctival injection, changes in lips/oral mucosa (“strawberry tongue”), had-foot erythema, desquamating rash.
May develop coronary artery aneurysms, thrombosis -> MI rupture. Treat with IV immunoglobulin and aspirin.
Buerger disease
Heavy smokers, males <40 years old. Intermitten claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis. Raynaud phenomenon is often present.
Segmental thrombosing vasculitis. Treat with smoking cessation.
Granulomatosis with polyangiitis (Wegener)
Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis. Lower respiratory tract: hemoptysis, cough, dyspnea. Renal: hematuria, red cell casts.
Triad: focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, necrotizing glomerulonephritis. PR3-ANCA/c-ANCA (anti-proteinase 3). CXR: large nodular densities. Treat with cyclophosphamide, corticosteroids.
Microscopic Polyangitis
Necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura. Presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement.
No granulomas. MPO-ANCA/p-ANCA (anti-myeloperoxidase). Treat with cyclophosphamide and corticosteroids.
Churg-Strauss syndrome
Asthma, sinusitis, palpable purpura, peripheral neuropathy (e.g., wrist/foot drop). Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis).
Granulomatous, necrotizing vasulitis with eosinophilia. MPO-ANCA/p-ANCA, inc IgE level.
Henoch-Schonlein purpura
Most common childhood systemic vasculitis. Often follow URI. Classic triad: Skin: palpable purpura on buttock/legs; arthralgias; GI: abdominal pain, melena, multiple lesions of same age.
Vasculitis secondary to IgA complex deposition. Associated with IgA nephropathy.
