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111 Cards in this Set
- Front
- Back
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Most common location of coronary occlusion
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LCA, AKA the widowmaker
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4 cardiac veins
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Great, middle, small, and posterior
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Why are the pectinate muscles of the R auricle important
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sulci between are sites of connection between endo and epicardium (no muscle), they are easily pierced by a catheter.
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Order of the valves
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tricuspid-pulmonary-bicuspid-aorta
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Cusps of tricuspid valve
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Anterior, posterior, and septal
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Significance of conus/infundibulum
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Only exists on right, area of muscle
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Size difference between atrial appendages
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The right is much larger
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Most common site of throbus formation (at least in the heart)
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Left atrial appendage
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Pacemaker of the heart
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SA node
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Location of SA node
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between SVC and RA appendage
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Anatomical landmarks for SA node
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Internal- crista terminalis
External- sulcus terminalis |
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Location of AV node
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next to membranous septum
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Short axis-
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cross section
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Pressure of RV and LV
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20-25 mmHg and 120mmHg
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How do you orient yourself when looking at a bread loaf slice of the heart?
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The posterior wall is flat from sitting on te diaphragm, the anterior is convex
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Difference in trabeculations between RV and LV
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much coarser on R
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Color of heart chambers
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brown, except for LA because of thickened endocardium.
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Significance of left papillary muscles and chordae tendinae
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all of chordae on left attach to papillary muscles. This is to prevent regurgitation, whereas on the right, it is more common.
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Anatomical association of mitral and aortic valves
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Anterior leaflet of mitral valve makes wall of outflow tract
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alias of anterior leaflet of mitral valve
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mitro-aortic fibrous continuity
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Three cusps of aortic valve
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left coronary ostium, non-coronary (posterior) cusp, and right coronary ostium
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Location of membranous septum in relation to aortic cusps
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between right and non-coronary
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Number of pulmonary veins entering LA
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4
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Proportion of myocytes- size and number
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75% size, 33% number
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I band
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actin only
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A band
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duration of myosin
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Z line
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in middle of I band
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Purpose of desmosome
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Connect cytoskeletal proteins of adjacent myocytes.
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Purpose of the nexus
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ionic continuity
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stenosis of heart valves to what physiological change(s)
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hypertrophy due to increased intracardiac pressure
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Types of collagens in extracellular matrix of heart
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1,3,4,5,6,fibronicetin, elastin, and proteoglycans
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Volume overload change causes
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decreased ECM
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Pressure overload
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increased ECM
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Controls fractional distribution of blood and has highest resistance
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arterioles
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Cellular composition of capillaries
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Only endothelial cells
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arteriosclerosis
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general term for degenerative changes in arteries, making them less elastic
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atherosclerosis
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deposition of plaque on walls
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Amount of capillaries with blood in them normally
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5-10%
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Hydrostatic and osmotic pressure in capillaries
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Higher hydrostatic pressure, lower osmotic
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Hydrostatic and osmotic pressure in venules
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lower hydrostatic pressure
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What percentage of total blood supply is held in the venous system
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2/3
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What happens to venous pressure when you inhale?
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Intrathoracic pressure decreases, leading to an increase in pressure delivered to right atrium, also the diaphragm compresses blood out of the abdominal cavity.
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What are the differences between the pulmonary and systemic circuits?
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Larger diameter capillaries, but fewer number. Less pressure. The output of the left and right side of the heart must be equal.
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Pressures of right chambers of the heart and pulmonary circuit
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RA 0, RV 25/0, Pulmonary artery 25/8, only about 6 in capillaries and veins
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The largest drop in pressure takes place where?
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Arterioles, from 85-35
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compliance=
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distensibility*volume
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mean arterial pressure (pressure distance)=
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change in flow*resistance
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Mean arterial pressure =
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diastolic+ 1/3 pulse pressure
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Name of BP sounds
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Karotkoff sounds
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Poiseuille's law
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Q(flow)=change in p*r^4*pie/8n(viscosity)L
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How is turbulent flow affected by fluid viscosity?
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More turbulent flow occurs with less viscous fluid
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Most common site of vascular stenosis
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Large arteries
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Components of intercalated discs and purpose of these structures
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desmosomes- anchor cells, gap junctions- fast communication with little resistance
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Where does most of the calcium involved in muscle contraction come from?
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Not trigger, but sarcoplasma
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Mechanism of action of digitalis
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blocks na k pump, leading to increased intracellular na, which means less ca is excreted, increasing contractility.
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Which receptor does NE work on
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alpha 1, IP3 and phospholipase Cpathway, stimulates Gq proteins which stimulate PLC influences release of ca
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Which receptor does angiotensin work on
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AT1
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Which receptor does endothelin work on
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endothelin receptor
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Process of G protein mediated by NE or E
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Activate B1 or B2 receptors, linked to Gs proteins, stimulates adenylyl cyclase to form camp from ATP, camp makes protein kinase a make more release of Ca
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Process of parasympathetic action in heart
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adenosine or acetylcholine simulate Gi protein receptors, decrease production of Camp, decreases activity of L type Ca channels which means less Ca from extracellular area.
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Through what process does most of the blood enter the ventricle
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3/4 passive movement
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Pacemaker of the heart
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SA node
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Purpose of AV node
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slows signal down from SA node in order to allow mechanical pumping difference between atria and ventricle
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CO=
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SV*HR
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Ionic current which sets resting membrane potential
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Ik, current is created through inwardly rectifying potassium channel
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Na gates of cardiac myocytes
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M- fast opening, creates almost vertical graphy
H- fast closing, occurs as a time dependent process only reopens after hyperpolarization |
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Phase 1
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slight repolarization due to Ito1 and 2 which are voltage gated K channels independent of Ca. Voltage change leads to their opening, causes transient outward movement of K. Ito2 is Ca activated chloride currents causing outward current.
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Phase 2
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Both conductance pathways are equal, so no change. During depolarization, voltage gated Ca channels open. Ltype open at -10, and inactivate slowly, prolongs the plateau phase. T type are more rare, transient because they inactivate quickly. Movement into cell.
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Role of K channels in AP
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voltage gated channels open , leading to outward movement of K and positive charge.
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Phase 3
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Ca channels begin to close, leaving K as predominant. During positive potentials, Ik is closed structurally.
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Why is the resting potential of automatic cells less negative?
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fewer Ik1 channels, lower permeability to K.
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Pacemaker current
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If, brings resting membrane potential to threshold in pacemaker cells. Activates nonselective NAK channels.
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What does the phase 0 of pacemaker AP look like
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much shallower slope, because it is due to activation of voltage dependent Ca channels, not Na.
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how does automaticity with If start
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when cell begins to become more negative, If channels bring it back to threshold. T type opens at -75, causing L type to open, t type clo. This opens voltage K channels for the Ik current. When Ca channels close intrinsically, K conductance incrfeasesmoving back to RMP.
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What type of channel is Ik1?
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inwardly rectifying K channel involved in maintenance of RMP
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Effect of Ach on cardiac cells
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Act on M2 receptor, decreasing activity of If. Less binding of cAMP to cells, not activation of the ion channels through PKA. This also reduces Ca current, so less upstroke of AP. Also causes RMP to be more negative
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Effect of Catecholamines
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act through beta 1 adrenergic receptors, increasing cAMP, increases If currents, increases steepness of phase 4.
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VEGF
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vascular endothelial growth factor- naturally occurring and promotes angiogenesis in endothelial cells
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FGF
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responds to injury from catheterization, lays down collagen which can recauses stenosis
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active hyperemia
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triggered by a need for increased blood flow, increased metabolic activity of the muscle uses O2 and increases metabolites which leads to arterial dilation, responds to need for more bloodflow from activity
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reactive hyperemia
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pinking after transient ischemia
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Term for intermittent contraction and relaxation of metarteriole sphincters every 5-10 min
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Vasomotion
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Location of fenestrations
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Kidneys, SI, choroid plexuses, endocrine glands
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Location of sinusoids
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basment membranes of liver, bone marrow, and spleen
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Heart defect associated with downs
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Atrioventricular septal defect
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Heart defect associated with Williams
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Suprvalvular aortic stenosis
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Heart defect associated with Turner
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Coarctation of the aorta
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Most characteristic finding for CVS
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conotruncal heart defects
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Velocardial Facial syndrome
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bifid uvula, OCD, social immaturity, altered facial appearance, long tapering fingers, and interesting speech manerisms
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Williams Syndrome
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Supravalvular aortic stenosis, low receptive verbal IQ, cocktail personality, abnormality in elastin gene
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Dilated Cardiomyopathy
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Enlarged heart muscle but thinned cardiac wall and increase in volume, thought to be infectious at first, but then found to be common within families in 1/3 of cases, causes death by arrythmia
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Hypertrophic Cardiomyopathy
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increases in mass and wall, but decrease in volume, can be benign, problem with betamyosin heavy chain, very common 1/500
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noncompaction ventricular myocardium
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Incomplete formation of myocardium, leaving islands of non muscle cells incapable of functioning, can be severe or not, used to be associated with Barth's
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Use of genetic testing
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Not used in cardiomyopathy, but definitely used in long QT
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Long QT syndrome
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Cause of swimming accidents, MVA, SIDS, and unexplained death, actual phenotype is ventricular arrhythmia, episodes provoked by stress or sudden change in temperature, GENETIC TESTING to determine treatment
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Tx for LQT syndrome
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Beta blocker is standard, but LQTS3 is not responsive, put in a defibrillator for this because it is dangerous
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Brugada syndrome
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RBBB leading to vfib, AD, ST elevation, like LQT3
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Anderson-Tawil
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Syndactyly, K sensitive periodic paralysis
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Gene for CAD
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MEF2A
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Mechanism of LDL leading to plaque formation
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Oxidization of LDL causes leukocyte migration which forms foam cell, sends out chemotactic factors
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Treatment for Sinus Bradycardia (sinus node dysfunction)
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Stop meds, pacemaker if still experienceing symptoms. Most common indication for pacemaking in US.
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Tachy Brady syndrome
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Tachycardia, often A fib or flutter, followed by long run of brady for SA node to pick up. Usually requires pacemaker.
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SAN block
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exactly halve rate because you skip one beat, caused by drugs, age, or heart disease, rheumatic disease
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1 av block tx
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rarely pacemaker
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RBBB
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lead V1 rSR' triphasic pattern
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LBBB
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QS all downward, RBBB is up
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2nd AV block
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ALWAYS PACEMAKER
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Mech of Class 1a
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blocks fast na channel, used on atrial and vent arrhythmias
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Class 2
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phase 4 and beta blockers for atrial and excessive catecholamine arrhythmias
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class 3
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Phase 3 and k channel blockers, prolong refractory period, used for primary reentry arrhythmias
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class 4
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phase 4 and ca channel blockers, used for atrial and AMI arrhythmias, decrease automaticity of ectopic foci
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