Cardiology Flashcards
Bulbus cordis becomes
Smooth parts (out ow tract) of left and right ventricles
Endocardial cushion becomes
Atrial septum, membranous interventricular septum; AV and semilunar valves
Primitive atrium becomes
Trabeculated part of left and right atria
Primitive ventricle becomes
Trabeculated part of left and right ventricles
Primitive pulmonary vein becomes
Smooth part of left atrium
Left horn of sinus venosus becomes
Coronary sinus
Right horn of sinus venosus becomes
Smooth part of right atrium (sinus venarum)
Right common cardinal vein and right anterior cardinal vein becomes
Superior vena cava (SVC)
When does fetal heart begin to beat spontaneously
week 4 of development
Blood supply to SA and AV node
branches of the RCA
3 layers of the pericardium:
from outer to inner:
Fibrous pericardium
Parietal layer of serous pericardium
Visceral layer of serous pericardium
Innervation to the pericardium
Phrenic nerve
Cardiac output
Stroke volume x HR or
rate of O2 use)/(art O2 - venous O2
Mean arterial pressure
CO x TPR or
2/3 diastolic pressure + 1/3 systolic pressure
Variables that effect SV
affected by Contractility, Afterload, and Preload (SV CAP)
↑ SV with:
↑ contractility and preload
↓ afterload
Variables effecting contractility
Contractility ↑ with:
Catecholamine stimulation B1 (↑ IC Ca)
↓r EC Na
Digitalis
↓ with: B1 blockade HF w/sytolic dysfunction Acidosis Hypocia/hypercapnia ND CCB
Variables with ↑ myocardial O2 demand
↑ contractility, afterload, HR, diameter of ventricle
Preload
approximated by ventricular EDV
↓ w/venous dilation
Afterload
Approximated by MAP
↓ w/arterial dilation
↑ afterload leads to LVH
When would fixed splitting of S2 occur?
In ASD (L to R shunt ↑ right sided volume)
Causes of paradoxical splitting
Anything that delays aortic valve closure: aortic stenosis, LBBB
Inspiration during auscultation
↑ intensity of right heart sounds
Hand grip during auscultation
↑ after-load
↑ intensity of MR, AR, VSD
↓ AS and MVP
Valsalva during auscultation
↓ preload
↓ most murmurs
↑ intensity of hypertrophic cardiomyopathy MVP
Rapid squatting during auscultation
↑ venous return, preload and afterload
↓ hypertrophic sounds
↑ AS, MR, VSD
Diastolic heart sounds
murmurs of aortic/pulmonic regurgitation, mitral/tricuspid stenosis
Murmur of aortic stenosis
Crescendo-decrescendo systolic ejection murmur (ejection click may be present)
Loudest at base; radiates to carotids
Murmur of mitral or tricuspid regurg
Holosystolic, high-pitched “blowing murmur.”
Murmur of MVP
Late systolic crescendo murmur with midsystolic click; loudest just before S2
Murmur of VSD
Holosystolic, harsh-sounding murmur. Loudest at tricuspid area.
Murmur of aortic regurg
High-pitched “blowing” early diastolic decrescendo murmur.
Murmur of mitral stenosis
Opening snap with delayed rumbling mid-to-late diastolic murmur
Murmur of PDA
Holosystolic machine-like murmur
Loudest at S2.
Congenital long QT syndrome
Inherited disorder of myocardial repolarization, typically due to ion channel defects
Defects associated with in utero alcohol exposure
VSD, PDA, ASD, tetralogy of Fallot
Defects associated with Congenital rubella
PDA, pulmonary artery stenosis, septal defects
Defects associated with Down syndrome
AV septal defect (endocardial cushion defect), VSD, ASD
Defects associated with Infant of diabetic mother
Transposition of great vessels
Defects associated with Marfan syndrome
MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
Defects associated with Prenatal lithium exposure
Ebstein anomaly: displacement of tricuspid valve leaflets downward into RV, artificially “atrializing” the ventricle
tricuspid regurgitation and right HF
Defects associated with Turner syndrome
Bicuspid aortic valve, coarctation of aorta
Defects associated with Williams syndrome
Supravalvular aortic stenosis
Defects associated with 22q11 syndromes
Truncus arteriosus, tetralogy of Fallot
Progression of atherosclerosis
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 (d/t platelet release of cytokines) -> fibrous plaque -> complex atheromas
Most common type of ventricular pre- excitation syndrome
Wolf -Parkinson-White syndrome
Wol -Parkinson-White syndrome
Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node
Delta wave with wide QRS, short PR
B-type (brain) natriuretic peptide
Released from ventricular myocytes in response to ↑ tension
Acts like ANP with longer 1/2 life
Good to diagnose HF
Aortic arch receptors
Transmit via vagus to solitary nucleus of medulla in response to↑ and ↓ BP
Carotid sinus receptors
Via glossopharyngeal n (IX) to solitary nucleus of medulla in response to ↑ and ↓ BP
Cardiac baroreceptors
Respond to hypotension: ↓ arterial pressure decreases stretch and afferent baroreceptor firing: ↑ efferent SNS firing/↓ PSNS: vasoconstriction, ↑ HR and BP
MOA of carotid massage
↑ pressure on carotid sinus -> ↑ stretch -> ↑ afferent firing -> ↑ AV node refractory period -> ↓ HR
Peripheral vs central chemoreceptors
Peripheral stimulated by O2, CO2 and pH
Central only stimulated by pH and CO2
Total anomalous pulmonary venous return
Pulmonary veins drain into right heart circulation
Corneal arcus
Lipid deposit in cornea
Arteriolosclerosis
Small arteries and arterioles
Hyaline (HTN or DM) and hyper plastic (onion skinning)
Mönckeberg sclerosis (medial calcifc sclerosis)
Affects medium-sized arteries
Calcification of internal elastic lamina and media of arteries causes stiffening
Location of atherosclerosis frequency
Abdominal aorta > coronary artery > popliteal artery > carotid artery
Thoracic aortic aneurysm
Associated with cystic medial degeneration
Traumatic aortic rupture
Due to trauma and/or deceleration injury, most commonly at aortic isthmus
Postinfarction brinous pericarditis
Occurs 1–3 days after MI. Friction rub.
Papillary muscle rupture
Occurs 2–7 days after MI. Posteromedial papillary muscle rupture; single blood supply for posterior descending artery
Interventricular septal rupture
Occurs 3–5 days after MI. Macrophage-mediated degradation
Ventricular free wall rupture
Occurs 5–14 days after MI. Free wall rupture leads to tamponade
LV hypertrophy and previous MI protect against free wall rupture
Causes of dilated cardiomyopathy
hronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy
Findings in dilated cardiomyopathy
HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on CXR
Treatment of dilated cardiomyopathy
Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant.
Causes of Hypertrophic cardiomyopathy
Most are familial
Sudden death in young athletes
Treatment of hypertrophic cardiomyopathy
cessation of high-intensity athletics, use of β-blocker or non-dihydropyridine Ca2+ channel blockers (eg, verapamil). ICD if patient is high risk.
Findings in hypertrophic cardiomyopathy
S4, systolic murmur. May see mitral regurgitation due to impaired mitral valve closure.
Causes of restrictive cardiomyopathy
Postradiation brosis, Lofffler syndrome, Endocardial broelastosis (thick broelastic tissue in endocardium of young children), Amyloidosis, Sarcoidosis
Acute pericarditis presentation and causes
presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward; friction rub
Causes include idiopathic (most common; presumed viral), confirmed infection (Coxsackievirus), neoplasia, autoimmune (eg, SLE, RA), uremia, cardiovascular (acute STEMI or Dressler syndrome), radiation therapy
Cardiac tamponade
Beck triad (hypotension, distended neck veins, distant heart sounds), ↑ HR, pulsus paradoxus
Myxomas
Most common 1° cardiac tumor in adults
90% occur in the atria (mostly left atrium)
“ball valve” obstruction in the left atrium leading to syncope
Rhabdomyomas
Most frequent 1° cardiac tumor in children (associated with tuberous sclerosis). Histology: hamartomatous growths
Kussmaul sign
↑ in JVP instead of ↓ during inspiration
Giant cell (temporal) arteritis
Large cell vasculitis
Focal granulomatous inflammation, ↑ ESR
Takayasu arteritis
Large cell vasculitis
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
Polyarteritis nodosa
Medium-vessel vasculitis
Hepatitis B in 30% of patients
Fever, weight loss, malaise, HA; GI: abdominal pain, melena, HTN, neurologic dysfunction, cutaneous eruptions, renal damage
Typically involves renal and visceral vessels, not pulmonary arteries
Inflammation of arterial wall with fibrinoid necrosis
Treat with corticosteroids, cyclophosphamide.
Kawasaki disease (mucocutaneous lymph node syndrome)
Medium-vessel vasculitis
Asian children < 4 years old
Conjunctival injection, Rash (desquamating), Adenopathy (cervical), Strawberry tongue (oral mucositis), Hand- foot changes (edema, erythema), fever
Treat with IV immunoglobulin and aspirin
Granulomatosis with polyangiitis (Wegener)
Small-vessel vasculitis
PR3-ANCA/c-ANCA
CXR: large nodular densities.
Treat with cyclophosphamide, corticosteroids
Microscopic polyangiitis
Small-vessel vasculitis
Necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura
No granulomas; MPO-ANCA/p-ANCA
Treat with cyclophosphamide, corticosteroids
Eosinophilic granulomatosis with polyangiitis (Churg- Strauss)
Small-vessel vasculitis
Asthma, sinusitis, skin nodules or purpura, peripheral neuropathy
Granulomatous, necrotizing vasculitis with eosinophilia
MPO-ANCA/p-ANCA, IgE level
Henoch-Schönlein purpura
Small-vessel vasculitis
Most common childhood systemic vasculitis
Classic triad:
Skin: palpable purpura on buttocks/legs, Arthralgias, GI: abdominal pain
2° to IgA immune complex
deposition
Hereditary hemorrhagic telangiectasia aka Osler-Weber-Rendu syndrome
Blanching skin lesions (telangiectasias), recurrent epistaxis, skin discolorations, arteriovenous malformations (AVMs), GI bleeding, hematuria
Tetralogy of Fallot
VSD, pulmonary stenosis, RV hypertrophy, overriding aorta
Findings in diastolic HF?
↑ LV end-diastolic pressure
Normal LV end-diastolic volume and EF
