Cardiology Flashcards
Ostium secundum
Formed as tissue degenerates in superior septum primum
Septum secundum
Contains F ovale
Truncus arteriosus
Becomes ascending aorta and pulmonary trunk
Bulbus cordis
Becomes smooth parts ventricles
Left horn of sinus venosus
Becomes coronary sinus
Right horn of sinus venosus
Becomes smooth part RA
Right common and Right anterior cardinal veins
Becomes SVC
ASD
Most common type=ostium secundum type. Usu asymptomatic until adulthood.
Signs: wide fixed splitting S2, ESM in aortic area.
VSD
Most comm congenital heart malformation. Most commonly from incomplete fusion AV cushions. Most small and resolve spontaneously.
Sxs: easy fatiguability, harsh holosystolic murmur best heard at tricuspid area
Aorticopulmonary septum
Separates truncus arteriosus into aorta and pulmonary trunks.
Left to right shunts
VSD, ASD, PDA.
Late cyanosis.
If do not close and continued high flow in pulm circulation, can cause hypertrophy of pulm arterial system and even fibrosis.
Right to left shunts
TOF TGA TAPVR Tricuspid atresia Truncus arteriosus
Early cyanosis and squatting
Eisenmenger syndrome
Initial L to R shunt but then continued high flow in pulm vasculature causes hypertrophy, RVH until shunt reverses. Late cyanosis.
Squatting-mechanism to alleviate sxs
Occurs in R-L shunts. Squatting increases systemic vascular resistance (L sided P) by compressing femorals. Decreases pressure gradient between R and L sides of heart so may alleviate sxs.
1st aortic arch
Becomes part of maxillary artery
2nd aortic arch
Becomes stapedial artery and hyoid artery
3rd aortic arch
Becomes common carotid and proximal internal carotid artery
4th aortic arch
Becomes aortic arch and proximal R subclavian artery
5th aortic arch
Regresses in humans
6th aortic arch
Becomes proximal pulmonary arteries and ductus arteriosus
Pre-ductal coarctation of aorta
Proximal to DA. DA typically remains patent
Post-ductal coarctation of aorta
Distal to DA. Increased BP in arms, decreased BP in legs, weak/absent femoral pulses, collateral circulation.
*Rib notching due to increased flow through intercostal arteries.
PDA
L-R shunt. Most common in premies. Does not result in early cyanosis. Give prostaglandin inhibitors-indomethacin, NSAIDs.
22q11 deletion
Assoc with truncus arteriosus, TOF
Down’s syndrome
Associated with ASD (especially), VSD, AV septal defect
Child of diabetic mother
Association with TGA
Congential rubella-cardiac defects
Septal defects, PDA, pulmonary artery stenosis
Marfans
Aortic insufficiency=late complication
Signs of tamponade
Decreased MAP, distended neck veins (inability SVC to drain), pulsus paradoxus, electrical alternans on ECG
Subendocardial infarct
Repeated episodes of temporary occlusion of coronary artery (unstable angina) or severe anemia/hypotension. ST depression.
*If flow through coronary artery compromised, subendocardial tissue most vulnerable to ischemic injury sicne farthest from either blood supply.
Causes pericarditis
SLE, RA, MI, TB, malignancy
Fastest conduction velocity in heart’s electrical system
His-Purkinje
Slowest conduction velocity in heart’s electrical system
AV node
Decreased contractility
Beta blockers, CCBs, HF, parasymp stimulation, acidosis, hypoxia, hypercapnia
Venous O2
Can be measured at pulmonary artery
Ficks CO equation
CO=O2 consumption/(arterial O2-venous O2)
S2 splitting
Inspiration increases.
Wide-RV emptying delayed, e.g. RBBB, pulmonic stenosis
Fixed-ASD.
Paradoxical-delayed LV emptying (AS, LBBB). P2A2…when inspire, split eliminated since P2 delayed.
Carotid baroreceptors
Tonically active
Increased activity indicates increase in BP.
Trasmitted by CN IX
Aortic arch baroreceptors
Transmitted by CN X
Arterioles
Largest resistance in CV system
Serum
plasma-clotting factors
Fastest to Slowest conduction velovity
His-Purkinje, Atrial, Ventricular, AVN
Absolute refractory period
Phases 0-2
Effective refractory period
Conducted AP cannot be generated.
How cardiac muscle differs from skeletal
Has: plateau, spontaneous depolarization, gap junctions, more mitochindria, increased contractile force through changes in fiber contractility (vs #fibers recruited in skel muscle)
Measure of contractility
EF
Bowditch effect
Myocardial contractility increases with higher heart rates. Possibly due to inability of Na+/K+-ATPase to keep up with influx od Na so increased Ca within myocyte.
Aka Treppe phenomenon or staircase effect
Frank Starling law
Force of systolic contraction proportional to initial length of cardiac muscle in diastole. (i.e. increased stretch or preload will increase FOC).
S2-effect of inspiration
Increases splitting
Wide splitting S2
Where RV emptying delayed, e.g. pulmonic stenosis, RBBB
Carotid stretch receptors
Tonically active. Transmitted by CNIX
Aortic arch stretch receptors
Transmitted by CNX
Mediation of arteriolar dilation and venous constriction
Histamine and bradykinin
TXA2
Vasoconstrictor
Prostacyclin
vasodilator
Capacitance
=V/P. Ability to store charge, i.e. how distensible a BV is. Inversely related to elastance
Hypertension
> 140 and/or >90 on 3+ readings or single reading >170/110
Prehypertension
120-139/80-89
Stage 1 HTN
140-159/90-99
Stage 2 HTN
> 160/>100
Initial medication for primary HTN
Thiazides
Secondary HTN-causes
Renal artery stenosis, renal parenchymal disease, OCP, glucocorticoids, phenylephrine, NSAIDS, pheo, Conns, hyperthyroidism, Cushings, coarctation, fibromuscular dysplasia
Hypertensive retinopathy
AV nicking, pappiledema, loss venous pulsation, flame hemorrhages
Malignant hypertension
Severe, rapid increase in BO, usu >240/120. Assoc with end organ damage (“flea bitten kidneys). Young African-Americans, LVH, papilledema, retinal hemorrhage
Munckeberg arteriosclerosis
Benign medical calcification of medium sized muscular arteries. Elderly, those with DM, metabolic syndrome, HTN.
Arteriolosclerosis
Affects INTIMA of small arterioles and arteries. most often in those with DM, metabolic syndrome, HTN
Hyaline arteriolosclerosis
Protein deposits in essential HTN-pink arterial wall thickening with luminal narrowing. DM-due to advanced glycosylation end products being deposited in BM. HTN-increased pressure forces proteins into wall causing hardening of arteries.
Hyperplastic arteriolosclerosis
In malignant HTN. Increase in smooth muscle cell proliferation and BM duplication-“onion skinning”. Esp prevalent in renal arterioles.
Myocarditis-causes
Most common cause in developed world is viral–coxsackie B, rubella, CMV. Worldwide-Chagas disease. Bacterial in immunocompromised (S aureus, C diphtheriae, H influenzae). Others: toxoplasmosis, Kaposis, Lyme, ARF, RhF, lupus, doxorubicin
Subacute Bacterial Endocarditis
Usually affects previously damaged valves. VIRIDANS. May see ring enhancing lesions in brain due to septic emboli. Staph epidermidis on prosthetic valves.
Duke criteria for endocarditis
Positive serial cultures, prior endocardial involvement, IV drug use, fever, vasc/immune phenomenon, valvular lesions on echo
Marantic Endocarditis
Non-Bacterial Thrombotic Endocarditis. Small sterile fibrin vegetations on heart valves of those with devastating disease. Paraneoplastic syndrome-mucin secreting tumors (usu colon or pancreatic)
Libman-Sacks Endocarditis
Ab damage to valves from SLE/ Sterile vegetations on BOTH SIDES of heart valves. Oft asymptomatic but may have a heart murmur.
DCM-causes
Idiopathic (most common), EtOH abuse, thiamine deficinecy, coxsackie B, Chagas, HIV, cocaine doxorubicin, Lyme, sarcoidois, hypothyroidism, Wegener granulomatosis, acromegaly, peripartum CM
DCM-presentation
4 chamber enlargement. R or L HF. Decreased EF, JVD, edema, orthopnea, hepatomegaly, cardiomegaly.
HCM-presentation
Syncope, dyspnea, S4, cardiomegaly, MR, pain releived by squatting and exacerbated by strenuous exercise
Diastolic HF-causes
Impaired filling: MS, tamponade, pericardial contstriction.
Impaired relaxation: hypertrophy, CM, ischemia
Impaired compliance
“Heart failure cells”
Intra-alveolar hemosiderin-laden macrophages
