Cardiology Flashcards
Jugular venous pulse
Usu. only R-side. C = S1. a wave = Right atrial contraction in LATE diastole. c wave = tricuspid billowing into the RA during systole. x descent = negative pressure b/c of blood going through pulmonary artery. v wave = filling up of RA right at the beginning of diastole. y wave = blood going down from RA to RV.
Tricuspid stenosis
GIANT A wave.
Tricuspid regurgitation.
GIANT Cv wave.
Turbidity of plasma?
Due to TG’s NOT cholesterol.
What carries the TG’s?
Chylomicrons (from gut). You don’t have to fast for cholesterol levels! But you do for accurate triglyceride levels. VLDL - what we make in liver from G3P from glucose. VLDL > chylomicron in density.
Xanthelasma
Cholesterol is high.
Familial hypercholesterolemia
AD. Absent LDL receptor. Tendon xanthoma. Type II hyperproteinlipoproteinemia.
Atherosclerosis
Injury to the endothelial cell lining elastic and muscular arteries. Cigarette (ammonium, CO). LDL esp. if oxidized. Infections (Chlamydia pneumoniae?). Homocysteine. Damaged endothelial cells = plt sticking. PDGF -> smooth muscle of media to proliferate (hyperplasia). Migrate to the subintimal level. Fatty streak 2/2 SMC + macrophages w/ LDL in them. Injury. Fibroblasts -> fibro-fatty plaque. Dystrophic calcification, fissuring, thrombosis.
Hyaline arteriosclerosis
Small vessel disease. DM and HTN. DM - non-enzymatic glycosylation (glucose attached to protein). E.g. HbA1C ~ 6-8 week of blood glucose levels + osmotic damage (lens, pericytes of the retina, schwann cells, have aldose reductase -> sorbitol = damage). Glycosylation of BM -> BM permeable to protein -> hyalinization of the vessels. In glomerulus –> proteinuria. HTN mechanism is protein driven by hydrostatic pressure through BM.
Hyperplastic arteriosclerosis
Seen in malignant hypertension.
Aneurysm
Area of out pouching of vessel 2/2 WEAKENING of vessel wall
Etio of vessel wall weakening?
Atherosclerosis
LaPlace law
Wall tension = pressure x radius / 2 x wall thickness
All aneurysms will rupture
B/c once you increase radius -> increase wall tension.
Why is aorta below renal arteries most common location for aneurysm?
No vaso vasorum. Peripheral areas are more susceptible to ischemia. Atherosclerosis -> weakening -> aneurysm
Ruptured AAA presentation?
LEFT flank pain, hypotension, pulsatile mass on physical exam = ruptured AAA
Aortic arch aneurysm?
Most common cause is tertiary syphilis. Pathology of syphilis is vasculitis of arterioles (plasma cell). Ischemic necrosis -> dead neurons -> painless chancre. Treponema infects the vaso vasorum (of the arch b/c it is very rich) = endarteritis obliterans. AR b/c of stretched ring or damaged valve. Will have increased SV b/c of increased volume in the LV (but dec. EF). Stretched recurrent laryngeal nerve = hoarseness.
Aortic dissection
HTN is the key factor. Weakening of the wall 2/2 elastic tissue fragmentation + cystic medial necrosis (glycosaminoglycans -> cystic pockets. Most of the tears are in the arch of the aorta. Loss of pulse. CP a tearing pain to the back. CXR is screening test - widening of aortic knob. Dx = angiography/TEE.
Predisposing to dissection
Marfan - chromosome 15, defect in fibrillin -> weakened elastic tissue (dislocated lens, MVP, dissection). Ehlers-Danlos syndrome. Pregnancy b/c of increased plasma volume.
SVC syndrome
Retinal vein engorgement. Usu. 2/2 to lung cancer.
Sturge Weber syndrome
In trigeminal nerve distribution - port-wine. AV malformation on the SAME side in the brain, which pre-disposes to bleeding.
Spider angioma
Normal in pregnant women. 2/2 hyperestrogenism. WILL blanch b/c it’s an AV fistula. Cirrhosis -> can’t metabolize estrogen. Petechiae will NOT blanch.
Bacillary angiomatosis
Bartonella hensalae. Silver stain. Seen in AIDS. Tx with sulfa drug. Also causes cat-scratch disease
Angiosarcoma of the liver
VAT - vinyl chloride (plastics), Arsenic (pesticides), Thoratract?
Small vessel vasculitis
99% it will be type III HS = IC deposition. Activates complement, neutrophils = fibrinoid necrosis. PALPABLE PURPURA.
Medium vessel vasculitis (muscular)
INFARCTIONS.
Elastic artery vasculitis
Pulseless disease (Takayasu’s), strokes (carotids)
Temporal arteritis
Unilateral HA. Multinucleated giant cell = granuloma. Can cause blindness b/c of opthalmic. Screen for temporal arteritis with ESR! Tx = corticosteroids immediately x 1 year. Associated with polymyalgia rheumatica = NO CK elevation. But polymyositis will have increased CK.
Buerger disease (thromboangiitis obliterans)
Smokers. Digital vessel thrombosis = auto infarction of fingers and toes.
HSP
Most common vasculitis in children. Buttocks, legs. IC. Anti-IgA IC. RBC cast 2/2 glomerulonephritis (IgA nephropathy). Palpable purpura.
Wegener’s
Saddle nose (NOT congenital syphilis). Sinus, upper respi, glomerular. Granulomatosis + vasculitis. c-ANCA = Dx (highly specific). Tx = Cyclophosphamide. C and C. (Cyclo can cause hemorrhagic cystits - use mesna - and bladder cancer)
Polyarteritis nodosa
Male. Muscular arteries (infarctions). p-ANCA. Hepatitis B surface antigenemia.
RMSF
Spots are petechiae. Ricketssiae attack vasculature. Extremities to TRUNK. Vector = tick.
DKA with cerebral abscess. Fungus
Mucormycosis. Cribiform, frontal lobe, infarct.
Raynaud’s phenomenon
Different causes. Cold-reacting antibodies (IgM cold agglutinin, cryoglobulinemia = Hepatitis C). Vasculitis causes = scleroderma + CREST syndrome. Eventually will autoamputate fingers. Vasoconstriction causes - ergot derivatives
CREST
Calcinosis (dystrophic calcification) + Centromere antibody, Raynaud, Esophageal dysmotility, sclerodactyly, telangiectasia
Hypertension
MI, Stroke, Renal failure are most common causes of death.
Mechanism of salt-retaining HTN
Salt is retained in ECF. Plasma volume will be increased -> increased SV (systolic HTN). Salt likes to go into SMC (peripheral resistance arterioles) -> opens up Ca2+ channels -> increased vasoconstriction -> inc. diastolic pressure. Tx = HCTZ; But with HLD, then use ACEi. This is a low renin type of HTN.
Complications of HTN
MI, stroke - hypertensive stroke (basal ganglia 2/2 lenticulostriate off of MCA form aneurysm called Charcot-Bouchard aneurysms that rupture 2/2 HTN). Renal failure - hyaline arteriosclerosis -> ischemia, atrophy of tubules, glomeruli destruction. LVH 2/2 afterload.
Concentric hypertrophy vs. dilated hypertrophy
Afterload vs. preload problem
S3
Usually pathologic if > 35. Volume overloaded chamber in early diastole -> turbulence.
S4
Late-diastole = atrial kick. Compliance problem = stiff heart wall vibrating during atrial kick.
Use breathing to determine which side the S3/S4 is coming from
Decreased thoracic pressure = sucked into RV.
Aortic stenosis
Systole. Crescendo decrescendo. Ejection murmur. Radiate into carotid. Intensity increases on expiration. Probably hear a S4.
Mitral stenosis
Diastolic. Atrial dilation - aFib, thrombus. Opening snap. Mid-diastolic rumble. Underfilling the LV. No hypertrophy of LV. Apex.
Mitral regurgitation
Decreased SV, LA gets excess blood. Volume overload. Pan-Systolic murmur. S3 and S4.
AR
Austin-Flint murmur = significant leaflet.
L heart failure
Etio - high afterload, volume overload, infarctions -> dec. contractility. EDV increased. Pulmonary congestion. “HF cells” = alveolar macrophages that have phagocytosed RBC. Main symptom = dyspnea. Pillow orthopnea, paroxysmal nocturnal dyspnea. You decrease Right heard return.
R heart failure
Dx of signs. Back-up into systemic venous circulation. Neck vein distention. Hepatomegaly = “Nutmeg” liver.
Treatment for HF
Restrict water and salt. ACEi = decreases preload (dec. aldo) AND afterload (dec. vasoconstrictive)
High output failure etios
(Viscosity / r^4.) Septic shock, thiamine deficiency (ATP depletion -> SMC’s can’t vasoconstrict), Graves disease (thyroid hormone increases synthesis of Beta receptors in the heart), AV fistula (faster return).
Fetal circulation
Oxygen comes from chorionic villi extracting blood from placenta. Req. high affinity Hb = HbF to get oxygen (left-shifted). Newborns have “polycythemia” to get around how HbF has such as high affinity for O2 (and doesn’t want to let it go). Syncytotrophoblast, cytotrophoblast -> myxomatous stroma of chorionic villus -> blood vessel. Coalesce to umbilical VEIN (highest oxygen) -> liver [hepatic sinusoids OR ductus venosus -> IVC] -> R heart -> mostly Foramen ovale -> LV -> aorta. Superior venal caval blood? SVC blood tends to go straight down into Tricuspid valve into the RV -> pulmonary circulation (high resistance) -> needs the patent ductus arteriosus (PGE2 made by placenta) -> R-L shunt -> aorta —> —> TWO umbilical arteries (LEAST oxygen)
Birth = change in fetal circulation
When baby breathes, all the pulmonary vessels open. Sudden decrease of resistance.
VSD
L to right shunt. Increased O2 in RV and Pulmonary artery. Volume overloaded R heart = pulmonary htn over time = Eisenmengers = cyanosis -> RVH -> reverse the shunt if R stronger than L.
ASD
Left to right shunt. RA will have increased O2. RV increased O2. THEREFORE, an ASD has an increased O2 in RA! Volume overloaded Right side = risk for eisenmengers.
Most common teratogen for ASD?
Fetal alcohol syndrome
Patent ductus arteriosus
L to right shunt. Pulmonary a. higher O2. Machine-like murmur in supraclavicular region. Ductus empties DISTAL to the subclavian artery = pink and top and cyanotic and bond. Associated with congenital rubella. Tx = indomethacin
Tetralogy of Fallot
Most common cyanotic congenital heart disease. Overriding aorta (straddles the septum), VSD, pulmonic stenosis BELOW the valve, RVH. The level of pulmonic stenosis = cyanosis b/c the greater the stenosis the more R to L shunt you have. What are the cardioprotective shunts in TOF? ASD and patent ductus arteriousus. ASD will L-R shunt. Patent ductus will also L-R shunt to oxygenate more blood via the pulmonary artery. Polycythemia, infective endocarditis risk.
Transposition of great vessels
Not associated with Kartagener (normal heart on right side of chest). Transposed aorta and pulmonary artery. Spiral septum didn’t spiral. Always need shunts - patent ductus, foramen, atrial septal defect to get oxygenated blood into the right atrium to get to the RV and aorta.
Aortic coarctation
Pre-ductal and post-ductal. Pre-ductal occurs in Turner’s syndrome. Post-ductal’s are found after birth. Systolic murmur between the shoulder blades. Increased risk for Berry aneurysm, SAH. Aortic regurgitation 2/2 stretching aortic ring. Dissecting aortic aneurysm. Distal to coarct = claudication, inc. RAS system -> HTN 2/2 renal a. stenosis. Rib notching 2/2 to intercostal artery collaterals.
Most common cause of TRUE ventricular aneurysm?
HF. NOT free wall rupture.
Mitral valve prolapse
Closer to S1 or S2? Increased volume –> click and murmur closer to S2. Decreased preload —> click and murmur closer to S1 b/c less time to do everything.
Aortic stenosis
Radiates into neck. Increased intensity with INC preload. This is what distinguishing this murmur from HOCM. Diminished pulse. Low SV. Syncope with exercise. Angina with exercise possible.
Mitral stenosis
Diastole. OS + rumble. Most common etio = rheumatic fever
Rheumatic fever
ARF 2/2 GAS (strep pyogenes). Usu. post-pharyngitis. Post-strep glomerulonephritis can be either pharyngitis or skin infection. Blood cx negative in rheumatic fever. M-protein? pathogenic of GAS. Molecular mimicry. Vegetations around the opening of the valve. Polyarthritis is the most common symptom. ACUTE valvular problem = MR NOT MS. MS takes time to develop. Erythema marginatum. SQ nodules. ASO.
LA enlargement signs
Ortner’s syndrome (hoarseness b/c of recurrent). AF. Dysphagia b/c onto esophagus.
Two genetic syndromes with MVP
Marfan’s and Ehler-Danlos syndrome
Sudden death in Marfans?
Not dissection b/c not quick enough. Serious MVP with conduction defects.
Tricuspid regurgitation
IV drug abuse with infective endocarditis
Carcinoid syndrome
REQUIRES METASTASES to the liver. 5-Ht -> venous blood -> bathes right heart and produces fibrosis of the valves. Tricuspid insufficiency and Pulmonic stenosis. TIPS.
Infective endocarditis
Most common organisms = Viridians strep. 2nd = staph aureus, which can infect both normal and damaged valves. Most common valve involved = Mitral. 2nd = aortic. IV drug abuser -> tricuspid valve (TR), aortic valve (AR). Colon cancer or ulcerative colitis -> strep bovis (group D strep). Associated VSD -> aortic regurg
Osler node vs. Janeway’s lesions
Painful vs. not
Koplik spot of the eye
Red with white center = Roth spots
ARF
IC-vasculitis.
Libman-Sack’s endocarditis
SLE. Pericarditis is most common heart manifestations. VEGETATIONS EVERYWHERE>
Merantic vegetations
Paraneoplastic syndrome. Vegetations around the margins of the valve.
Coxsackie B
Myocarditis and pericarditis. Viral meningitis. Hand-foot-mouth disease. Herpangina.
Coxsackie B Myocarditis
Path - lymphocytic infiltrates. Endomyocardial bx.
Dilated cardiomyopathy
Disease of the cardiac muscle. Etios - postpartum (~6 wk), Coxsackie myocarditis, doxorubicin, TCA’s, EtOH -> thiamine deficiency,
HOCM
VERY thick septum. Asymmetric hypertrophy. Anterior leaflet of the mitral valve against septum obstructs blood flow. Obstruction in the LVOT 2/2 Venturi phenomenon (neg pressure). Increased preload will pull away the leaflet and lead to LESS obstruction/murmur. NO DIGITALIS. Beta-blocker or CCB can slow down -> increased preload.
HOCM histology
Septum has muscle all over the place. BAD CONDUCTION defects -> risk of V-tach.
Endocardial fibroelastosis
Most common restrictive cardiomyopathy in children.
Restrictive Cardiomyopathies
Pompe, Fe overload, amyloid
Cardiac myxoma
85% in LA. 15% in right. Benign tumors. Attached by stalk and can move -> blockage of valve -> syncope or embolization.
Tumor in the heart of the kid?
Rhabdomyoma 2/2 tuberous sclerosis.
Water bottle configuration
Muffled heart sounds, Kussmaul’s sign (neck veins distend on inspiration), >10 mmHg drop in Bp on inspiration (Pulsus paradoxus). Beck’s triad. Pericardial effusion. Most common etio is pericarditis.
Young woman with unexplained pleural effusion or pericardial effusion?
SLE.
Constrictive pericarditis
TB in 3rd world. Previous cardiac surgery. Can’t fill up. Once it hits the pericardium = Pericardial RUB! Dystrophic calcifications would see on X-ray. RESP is next.
