Cardiology Flashcards
Romano-Ward syndrome
Q from the bond is a giant standing in the back/form of congenital long QT syndrome. Femdom chick whipping him/autosomal dominant. /pure cardiac phenotype (no deafness). Arthur spinning/can predispose to torsades de pointes, causing syncopal episodes + sudden cardiac death. /thought to result from mutations in a K= channel protein that contributes to the delayed rectifier current (Ik) of the cardiac action potential.
Jervell and Lange-Nielsen syndrome
Q from the bond is a giant /form of congenital long QT syndrome. Tyrion running down the hall/autosomal recessive. Nelson has big headphones on/sensorineural deafness. /common presentation = syncope in an otherwise healthy person. Arthur spinning/can predispose to torsades de pointes + sudden cardiac death. /thought to result from mutations in a K+ channel protein that contributes to the delayed rectifier current (Ik) of the cardiac action potential.
Brugada syndrome
Tuong: he’s being whipped by a FEMDOM/autosomal dominant disorder most common in Asian males. Huge bundle of sticks in the right corner + mountains on backwall with hat bone on left and hambone on right/ECG pattern of pseudo-right bundle branch block + ST elevations in V1-V3. Jonny kenser dead on the floor + /increased risk of ventricular tachyarrhythmias + SCD (sudden cardiac death). He has an implanted cardioverter-defibrillator/prevent SCD with implantable cardioverter-defibrillator (ICD).
Wolff-Parkinson-White syndrome
o Parker from woodlands. Electric shock to the chest and lightning bolt that has down wall and across floor and up to Parker/very common ventricular pre-excitation syndrome. Abnormally fast accessory conduction pathway from atria to ventricle bypasses the rate-slowing AV node ventricles begin to partially depolarize earlier. May result in reentry circuit SVT. Camouflaged delta commanders coming out of the ground that have suffered strokes and are slurring their words + a morbidly obese Q from James bond (QRS complex code) + a midget media crew shooting photos on left/ECG = characteristic delta wave, described as “slurred upstroke of the QRS complex” + widened QRS complex + shortened PR interval on ECF. Amy young riding her hippo is there + vera wing in the back + Aidan Melville juggling in front of door/treatment = amiodarone + adenosine + verapamil. Tigger firing rocket launcher at parker/digoxin is contraindicated (can enhance transmission of impulses through accessory pathways by reentry or possible triggered membrane activity) extremely fast ventricular rate OR Vfib.
Potassium channel problem in romano-ward
DELAYED rectifier potassium channel.
truncus arteriosus gives rise to…
ascending aorta + pulmonary trunk
bulbus cordis gives rise to
smooth parts (outflow tract) of left and right ventricles
endocardial cushions give rise to
1) atrial septum
2) membranous inter ventricular septum
3) AV and semilunar valves
AV valves
mitral and tricuspid
semilunar valves
aortic + pulmonary valves
Primitive atrium gives rise to…
Trabeculated part of left and right atria
Primitive ventricle gives rise to
trabeculated part of left and right ventricles
Primitive pulmonary vein gives rise to…
smooth part of left atrium
Left horn of sinus venosus gives rise to…
coronary sinus
Right horn of sinus venosus gives rise to…
Smooth part of right atrium (sinus venarum)
What is SVC derived from
right common cardinal vein + right anterior cardinal vein
When does cardiac looping begin?
Week 4
Dextrocardia etiology
Defect in left-right dynein (dynes are involved in L/R asymmetry)
PFO etiology
Failure of septum premum and septum secundum to fuse.
underlying etiology of paradoxical emboli
1) ASD
2) VSD
3) PFO
Separation of cardiac chambers
1) septum primum grows toward endocardial cushions, narrowing foramen primum.
2) Foramen secundum forms in septum premum (foramen premium disappears)
3) Septum secundum develops as foramen secundum maintains right-to-left shunt.
4) septum secundum expands and covers most of the foramen secundum. Residual foramen is foramen ovale.
5) Remaining portion of septum premum forms valve of foramen ovale.
Most common location of VSD
membranous septum
Ventricle formation/morphogenesis
1) Muscular inter ventricular septum forms. Opening is inter ventricular foramen
2) Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous inter ventricular septum, closing inter ventricular foramen.
3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of interventricular septum.
Outflow tract formation
Neural crest and endocardial cell migrations lead to truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum. Lead to ascending aorta and pulmonary trunk.
Persistent truncus arteriosus etiology
Failed neural crest migration
Tetralogy of fallot etiology
failed neural crest migration
transposition of great vessels etiology
failed neural crest migration
aortic/pulmonary valve origin
derived from endocardial cushions of outflow tract.
Mitral/tricuspid origin
Derived from fused endocardial cushions of the AV canal.
PO2 of umbilical vein blood
30 mm HG
umbilical vein blood saturation
80%
Path of most highly oxygenated blood reaching heart…
Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the aorta to supply the body.
path of deoxygenated blood from the SVC
SVC –> RA –> RV –> main pulmonary artery –> PDA –> descending aorta.
closing of foramen ovale mechanism
Decreased resistance in pulmonary vasculature leads to increased left atrial pressure vs. right atrial pressure –> closes.
Closure of ductus mechanism
Increase in O2 + decrees in prostaglandins (from placental separation)
Remnant of ductus arteriosus
Ligamentum arteriosum
What can you use to maintain the PDA?
PGE1 + PGE2
Median umbilical ligament derived from…
urachus
Remnant of ductus venosus…
ligamentum venosum
Remnant of foramen ovale
Fossa ovalis
Remnant of notochord
nucleus pulposus
Medial umbilical ligaments derived from
umbilical arteries
remnant of umbilical vein
ligamentum teres hepatis (contained in falciform ligament)
What supplies the SA and AV nodes usually?
RCA
Which circulation type is more common
Right-dominant
When does coronary blood flow peak?
Early diastole
Most posterior part of the heart
Left atrium
Layers of pericardium (from outer to inner)
1) Fibrous pericardium
2) Parietal layer of serous pericardium
3) Visceral layer of serous pericardium
Where is the pericardial cavity?
Lies between parietal and visceral layers
How is CO maintained in early and late stages of exercise?
Early –> increased HR + SV
Late –> increased HR only (SV plateaus)
Examples of increased pulse pressure
1) hyperthyroidism
2) aortic regurgitation
3) aortic stiffening (isolated systolic hypertension in elderly)
4) OSA (due to increased sympathetic tone)
5) Exercise (transient)
Examples of decreased pulse pressure
1) aortic stenosis
2) cardiogenic shock
3) cardiac tamponade
4) advanced heart failure (HF)
Catecholamines and increased contractility mechanism
Inhibition of phospholamban leads to increased calcium entry into sarcoplasmic reticulum –> increased calcium induced calcium release.
What increases contractility?
1) catecholamines
2) increased intracellular calcium
3) decreased extracellular sodium (decreased activity of Na/Ca exchanger)
4) digitalis
digitalis mechanism
Blocks Na/K+ pump, leading to increased intracellular sodium, decreased Na/Ca exchanger activity, and increased intracellular calcium.
Causes of decreased contractility
1) Beta-blockade
2) HF with systolic dysfunction
3) acidosis
4) hypoxia/hypercapnia
5) non-dihydropyridine Ca2+ channel blockers
Wall tension (Laplace’s law)
Wall tension = (pressure x radius)/(2 x wall thickness)
What approximates afterload?
MAP
Drugs that decrease both preload and after load…
ACE inhibitors and ARBs
Normal EF
greater than 55%
EF in systolic vs diastolic HF
Decreased in systolic HF, normal in diastolic HF
Other things that decrease contractility
1) Beta-blockers (acutely)
2) non-dihydropyridine Calcium channel blockers
3) narcotic overdose
4) uncompensated HF
Volumetric flow rate (Q)
Q = flow velocity (v) x cross-sectional area (A)
Total resistance of vessels in series
Rt = R1 + R2 + R3
What does viscosity depend on?
Primarily hematocrit
When is viscosity increased?
1) polycythemia
2) hyperproteinemic states (eg multiple myeloma)
Where is flow velocity lowest?
Capillaries
What is the effect of removing organs in parallel (eg nephrectomy)?
1) decreased TPR
2) increased CO
Factors that would cause a left shift in venous return graph
1) acute hemorrhage
2) spinal anesthesia
Exercise on cardiac function curve
1) increased inotropy
2) decreased TPR
* think about how this would affect graph
Compensated heart failure
Isotropy drops in order to maintain fluid retention and increase preload to maintain CO.
What will decrease TPR
1) exercise
2) AV shunt
vasopressor?
Antihypotensive meds. Anything that raises reduced blood pressure.
JVP: a wave
atrial contraction
JVP: c wave
RV contraction
JVP: x descent
atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction?
Absent x was on JVP?
tricuspid regurgitation
Prominent x wave on JVP indicates…
1) Tricuspid insufficiency
2) right HF
V wave on JVP
Increased right atrial pressure due to filling against closed tricuspid valve.
Y descent on JVP?
RA emptying into RV
When is y descent prominent?
Constrictive pericarditis
When is y descent absent?
Cardiac tamponade
What is S1?
Mitral and tricuspid valve closure.
What is S2?
Aortic and pulmonary valve closure.
atrial kick?
S4
Isovolumetric contraction?
Period between mitral valve closing and aortic valve opening.
When is O2 consumption highest in cardiac cycle?
Isovolumetric contraction.
Systolic ejection on PV loop?
Period between aortic valve opening and closing.
Isovolumetric relaxation on PV loop?
Period between aortic valve closing and mitral opening.
Rapid filling on PV loop?
Period just after mitral valve opening.
Reduced filling on PV loop?
Period just before mitral valve closing
How will increased contractility affect PV loop?
FA 270
How will increased afterload affect PV loop?
FA 270
How will increased preload affect PV loop?
FA 270
What causes normal splitting?
Inspiration –> drop in intrathoracic pressure –> increased venous return –> increased RV filling –> increased RV stroke volume –> increased RV ejection time –> delayed closure of pulmonic valve.
pulmonary impedance?
capacity of the pulmonary circulation
When is wide splitting seen?
Conditions that delay RV emptying.
What does wide splitting indicate?
Delayed pulmonic, as seen in…
1) pulmonic stenosis
2) right bundle branch block
Why does fixed splitting occur in ASDs?
Delay in pulmonic closure due to increased flow through pulmonic valve due to left-to-right shunt.
When does paradoxical splitting occur?
Conditions that delay aortic valve closure.
Conditions in which paradoxical splitting is seen…
1) aortic stenosis
2) left bundle branch block
What is paradoxical splitting?
Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore in inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split.
VSD – systolic or diastolic?
systolic (holosystolic)
ASD – systolic or diastolic?
diastolic
Where are ASD’s best auscultated?
tricuspid area
Where are VSD’s best auscultated?
tricuspid area
holosystolic murmurs…
1) Tricuspid regurgitation
2) VSDs
3) mitral regurgitation
Affect of hand grip?
Increase afterload
What will hand grip increase intensity of?
1) MR + AR + VSD murmurs
diastolic heart sounds
1) aortic/pulmonic regurgitation
2) mitral/tricuspid stenosis
Affect of increased after load on MVP?
Later onset of click/murmur
What will hand grip decrease intensity of?
hypertrophic cardiomyopathy
Affect of Phase II valsalva?
Decreased preload
What will valsava decrease intensity of?
Most murmurs (including AS)
Affect of valsalva on MVP?
Earlier onset of click/murmur.
What will valsava increase intensity of?
hypertrophic cardiomyopathy
Affect of rapid squatting?
1) increased venous return
2) increased preload
3) increased afterload
Affect of squatting on HOCM?
decrease intensity
Affect of squatting on AS?
increase intensity
Affect of squatting on MVP?
Later onset of click/murmur
AS radiation
Loudest at base; radiates to carotids.
“Pulses parvus et tardus”
Pulses are weak with a delayed peak.
AS presentation
syncope + angina + dyspnea on exertion
Murmur radiating to right sternal border
tricuspid regurg
Rheumatic fever caveat
Can cause either MR or TR
MVP murmur
Late systolic crescendo murmur with mid systolic click
What is mid systolic click due to
Sudden tensing of chordae tendinae.
Most frequent valvular lesion?
MVP
MVP best location for auscultation?
Apex
When is MVP loudest?
Just before S2.
Some causes of MVP
1) Marfan’s
2) Ehlers-Dalos
3) rheumatic fever
4) chordae rupture
When are PDAs loudest?
S2
Most common causes of PDAs
1) congenital rubella
2) prematurity
Where are PDAs best heard?
Left infraclavicular area
aortic regurg murmur description
High-pitched blowing early diastolic decrescendo murmur.
aortic regurg characteristics
1) long diastolic murmur
2) hyperdynamic pulse
3) head bobbing when severe or chronic
4) wide pulse pressure
Aortic regurg causes
1) aortic root dilation
2) bicuspid aortic valve
3) endocarditis
4) RF
What causes opening snap in mitral stenosis?
Abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips.
What correlates with severity in mitral stenosis?
Decreased interval between S2 and OS.
Sequela of chronic mitral stenosis
LA dilatation
What underlies phase 1 in myocardial action potential?
1) inactivation of voltage-gated Na channels
2) voltage-gated K+ channels begin to open.
What underlies phase 2 in myocardial action potential?
Plateau..
1) Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux.
2) Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.
What underlies phase 3 in myocardial action potential?
Rapid repolarization–massive K+ efflux due to opening of voltage-gated slow potassium channels and closure of voltage-gated Ca2+ channels.
What underlies phase 4 in myocardial action potential?
Resting potential–high K+ permeability through K+ channels.
What are the differences between myocardial action potential and skeletal muscle action potential?
1) Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux.
2) Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from sarcoplasmic reticulum (Ca2+ induced Ca2+ release).
3) electrical coupling with gap junctions.
Phases of pacemaker action potential…
Phase 0, phase 3, phase 4.
*NO phase 1 or 2.
What underlies phase 0 in pacemaker action potential?
Upstroke–opening of voltage-gated Ca2+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission.
What underlies phase 3 in pacemaker action potential?
Inactivation of Ca2+ channels + increased activation of K+ channels leading to potassium efflux.
What underlies phase 4 in pacemaker action potential?
Slow spontaneous diastolic depolarization due to If (funny current).
If channels (funny current)
Slow, mixed Na/K inward current
What accounts for automacity of SA and AV nodes?
If channels (funny current)
What determines heart rate?
Slope of phase 4 in SA node.
Affect of adenosine on pacemaker action potential?
Decreases the rate of diastolic depolarization and decreases HR.
How does sympathetic stimulation increase HR?
Increases the chance that If channels are open and thus increases HR.
Conduction pathway in heart
SA node –> atria –> AV node –> bundle of His –> right and left bundle branches –> Purkinje fibers –> ventricles.
Why is the SA node the dominant pacemaker?
slow phase of upstroke
AV node location
Posteroinferior part of intertribal septum.
Pacemaker rates
SA, AV, bundle of His/Purkinje/ventricles
Speed of conduction
Purkinje, atria, ventricles, AV node
PR interval
Time from start of atrial depolarization to start of ventricular depolarization
Normal PR interval
Less than 200 msec
Normal QRS
less than 120 msec
What does QT interval represent?
ventricular depolarization + mechanical contraction of the ventricles + ventricular depolarization.
What does T wave represent?
Ventricular repolarization
What does a T-wave inversion indicate?
Recent MI.
What is the J point?
Junction between end of QRS complex and start of ST segment.
What does the ST segment represent?
Isoelectric period in which ventricles are depolarized.
When is a U wave prominent?
1) hypokalemia
2) bradycardia
treatment for torsades de pointes?
magnesium sulfate
What causes torsades de pointes?
1) long QT syndromes
2) drugs
3) hypokalemia
4) hypomagnesemia
Drugs causing torsades de pointes?
1) antiarrhythmics (class IA, III)
2) macrolides
3) haloperidol
4) TCAs
5) ondansetron
Wolff-Parkinson-White syndrome etiology
Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses rate-slowing AV node. This causes ventricles to depolarize early.
What is a delta wave?
shortened PR interval (due to early depolarization)
Wolff-Parkinson-White sequela
Reentry circuit leading to SVT.
Most common RF’s for afib
1) HTN
2) CAD
definitive treatment for atrial flutter
catheter ablation
1st degree AV block
Prolonged PR interval. Benign and asymptomatic condition that doesn’t require treatment.
Mobitz type I (wenckebach)
Type of 2nd degree heart block. Progressive lengthening of PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Variable RR interval with a pattern (regularly irregular)
Mobitz type I prognosis
usually asymptomatic
Mobitz type II
Form of second degree that block. Dropped beats that aren’t preceded by a change in length of PR interval.
Mobitz type II sequela
Can progress to 3rd degree block.
Mobitz type II management
Often treated with a pacemaker.
3rd degree heart block pathophys
atria and ventricles beat independently of each other.
3rd degree heart block on ECG
P waves and QRS complexes not rhythmically associated.
3rd degree heart block management
pacemaker
ANP effects
1) vasodilation
2) decreased Na+ reabsorption at *collecting tubule
3) dilates afferent arterioles + constricts efferent arterioles, promoting diuresis and contributing to aldosterone escape.
Difference between ANP and BNP?
BNP has a longer half-life.
nesiritide
recombinant BNP
Diagnostic relevance of BNP?
Blood test used for diagnosing HF (very good negative predictive value)
aortic chemoreceptor pathway
Transmits via vagus nerve to solitary nucleus of medulla.
Carotid sinus pathway
Transmits via glossopharyngeal nerve to solitary nucleus of medulla.
Carotid massage mechanism
Increased pressure on carotid sinus leads to increased stretch –> increased afferent baroreceptor firing –> increased AV node refractory period –> decreased HR.
Cushing reaction setting
Triad of HTN + bradycardia + respiratory depression
Cushing reaction pathophys
Increased ICP constricts arterioles leading to cerebral ischemia leading to increased PCO2 and decreased pH –> central reflex sympathetic increase in perfusion pressure (HTN) –> increased stretch –> increased peripheral reflex baroreceptor-induced bradycardia.
Better explanation:
With increased ICP, cushing reflex increases MAP in an attempt to restore cerebral perfusion pressure. Bradycardia occurs because baroreceptors in the carotid and aortic arch don’t know what’s going on in brain and just ease hypertension.
What triggers peripheral chemoreceptors?
1) decreased Po2
2) increased PCO2
3) decreased pH
What triggers central chemoreceptors?
Changes in pH and pCO2 of brain interstitial fluid (which are influenced by arterial CO2).
How do you determine mitral stenosis from cardiac pressures?
PCWP greater than LV EDV.
Normal cardiac pressures
FA 280
cardiac pressures from codebook
o Code: covered in ivy/right atrium = 0,8. Covered in hair + nails pounded in everywhere/right ventricle = 4,25. Nails + big hoops/pulmonary artery = 9,25. Hens + walls made out of tin cans/left atrium = 2,12. Hoops on walls + mice drinking mimosas/left ventricle = 9,130. Mice drinking mimosas + carrying briefcases/aorta = 70,130. Wedge of tissue sitting in middle of road covered in tin cans/wedge pressure = 12 (remember that wedge pressure is an indication of left atrial pressure).
o Location: Intersection of montview and colorado
what determines auto regulation in the heart?
Local vasodilatory metabolites: adenosine, NO, CO2, decreased O2.
What determines auto regulation in the brain?
CO2 (pH)
What determines auto regulation in the kidney?
Myogenic + tubuloglomerular feedback
Tubuloglomerular feedback
just macula dense and RAAS mechanism
myogenic mechanism
reflex vasoconstriction that occurs when perfusion pressure increases
what determines skeletal muscle regulation with exercise?
local metabolites: lactate, adenosine, K+, H+, CO2
what determines skeletal muscle regulation at rest?
sympathetic tone
what determines auto regulation in the skin?
sympathetic stimulation most impt
Thing to remember about about capillary oncotic pressure
Pushes fluid into capillary.
Why does lymphatic blockage cause edema?
Increased interstitial fluid colloid osmotic pressure because proteins aren’t drained into lymphatics
Managing early cyanosis
urgent surgery + maintain PDA
congenital heart diseases presenting with early cyanosis
5 Ts: Truncus arteriosus Transposition Tricuspid atresia Tetralogy of ballot TAPVR
Persistent truncus arteriosus etiology
Truncus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation; most patients have accompanying VSD.
Etiology of transposition of great vessels
Failure of aorticopulmonary septum to spiral.
hypoplastic RV in cyanotic newborn suggests…
tricuspid atresia
TOF etiology
anterosuperior displacement of the infundibular septum.
shunt in TOF
Pulmonary stenosis forces right-to-left flow across VSD leading to RVH
What are “tet spells”
characteristic of TOF. exacerbation of RV outflow obstruction.
Why does squatting help TOF patients?
Increased SVR, decreased right to left shunt, improves cyanosis.
TAPVR mechanism
Pulmonary veins drain into right heart circulation.
Epstein anomaly associations
Tricuspid regurgitation + right HF.
Relative frequency of ASD, PDA, VSD
VSD, ASD, PDA
difference in presentation between right-to-left and left-to-right shunts?
Right-to-Left shunts: eaRLy cyanosis.
Left-to-Right shunts: “LateR” cyanosis.
Most common congenital cardiac defect
VSD
How does VSD present in terms of O2 saturation?
Increased in RV and pulmonary artery.
More common defect in ASD
Ostium secundum defects most common.
Difference between ASD and PFO
In ASDs, septa are missing tissue rather than unfused.
Increased O2 sat in RA, RV, and pulmonary artery?
ASD
What happens to PDA in neonatal period?
With decreased pulmonary vascular resistance, shunt becomes left to right, leading to progressive RVH and/or LVH and HF.
Eisenmenger mechanism
Uncorrected left-to-right shunt (VSD, ASD, PDA) leads to increased pulmonary blood flow –> pathologic remodeling of vasculature –> increased pulmonary arterial HTN and compensatory RVH –> shunt switches to become right to left.
Eisenmenger presentation
Late cyanosis + clubbing + polycythemia.
aortic coarctation associations
1) bicuspid aortic valve
2) congenital heart defects
3) Turner syndrome
Complications of aortic coarctation…
1) HF
2) Increased risk of cerebral hemorrhage (berry aneurysm)
3) aortic rupture
4) endocarditis.
fetal alcohol syndrome congenital cardiac defect associations
ASDs, VSDs, PDA, TOF
congenital rubella congenital cardiac defect associations
1) PDA
2) pulmonary artery stenosis
3) septal defects
Infant of diabetic mother: congenital cardiac defect associations
transposition of great vessels
Marfan syndrome: congenital cardiac defect associations
1) MVP
2) aortic regurgitation
3) thoracic aortic aneurysm and dissection
Williams syndrome: congenital cardiac defect associations
supravalvular aortic stenosis
22q11 syndromes: congenital cardiac defect associations
1) truncus arteriosus
2) TOF
HTN ethnic incidence
AA, caucasian, asian
HTN definition
persistent systolic greater than 140 and/or diastolic greater than 90
most hypertension is primary (essential) and due to..
Increased CO or increased TPR
Classic radiologic finding in FMD
“string of beads” appearance of arteries
hypertensive urgency
severe (greater than 180 or greater than 120) HTN without acute end-organ damage.
Hypertensive emergency
Severe HTN with evidence of acute end-organ damage (eg encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia).
Post-MI murmur?
Probably mitral regurg due to papillary muscle rupture.
Note – don’t assume VSD with holosystolic murmur.
OK
Flow rate expressed in…
L/min
calculation note: DO NOT forgot to convert units
OK.
Cubic centimeter in liter
1000 cubic cm = 1 liter
Pericarditis presentation
Sharp pain aggravated by inspiration + relieved by sitting up and leaning forward.
Characteristic physical exam finding in pericarditis
Friction rub (described as harsh as scratchy sound present in both systole and diastole)
Pericarditis associations
1) Idiopathic (presumed viral)
2) coxsackievirus
3) neoplasia
4) SLE
5) arthritis
6) uremia
7) cardiovascular (acute STEMI or Dressler syndrome)
8) radiation therapy
Hagemann factor Function
part of intrinsic pathway, activates kallikrein.
Important complication of horseshoe kidney
Variant arterial supply. Anomalous origins of multiple renal arteries to each kidney.
What do xanthomas consist of ?
lipid-laden histiocytes
xanthelaasma?
xanthomas in the eyelids
corneal arcus
Lipid deposits in cornea. Looks like ring around eye. Don’t confuse with Kaiser-Fleischer rings.
Arteriosclerosis finding in essential HTN
Hyaline arteriolosclerosis
Diabetes mellitus arteriosclerosis finding
hyaline arteriolosclerosis
Severe HTN arteriosclerosis finding and etiology
Hyperplastic arteriosclerosis (onion skinning with proliferation of smooth muscle cells).
Monckeberg description
medial calcific sclerosis
Classic radiologic finding of Monckeberg’s
pipestem appearance.
Monckeberg etiology
Calcification of internal elastic lamina and media. ***no intimal involvement.
atherosclerosis epidemiology location
abdominal aorta, coronary artery, popliteal, carotid
nonmodifiable RF’s for atherosclerosis
1) Age
2) Sex
3) Family history
Sex at increased risk for atherosclerosis?
Increased in men + postmenopausal women
claudication is a sign of…
atherosclerosis.
atherosclerosis pathogenesis.
Inflammation impt. endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle cell migration, proliferation, and ECM deposition –> fibrous plaque –> complex atheroma.
What causes smooth muscle cell migration in atheroma formation?
PDGF and FGF
If someone has abdominal and/or back pain and a bulge/aneurysm what does this indicate?
Aneurysm is leaking, dissected, or rupture is imminent.
AAA RF’s
1) tobacco use
2) increased age
3) male sex
4) family history
RF’s for thoracic aortic aneurysms
1) HTN
2) bicuspid aortic valve
3) connective tissue disease (Marfan’s)
abdominal vs thoracic aneurysms?
Abdominal associated with atherosclerosis, thoracic associated with HTN and cystic medial degeneration.
Aneurysm type in tertiary syphilis?
thoracic aortic aneurysm
cystic medial degeneration?
Degenerative breakdown of collagen, elastin, and smooth muscle.
Where does traumatic aortic rupture most commonly occur?
Aortic isthmus
What is the aortic isthmus?
Proximal descending aorta just distal to origin of left subclavian
Aortic dissection associations
1) HTN
2) **bicuspid aortic valve
3) inherited connective tissue disorders
Markedly unequal BP in arms suggests….
Aortic dissection
CXR finding of aortic dissection
Mediastinal widening.
Aortic dissection:
Stanford type A
Proximal aortic dissection; involves Ascending aorta. May extend to aortic arch or descending aorta.
Stanford type A treatment
surgery
Stanford type A complications
Acute aortic regurgitation or cardiac tamponade
Stanford type B aortic dissection
Distal. Involves descending aorta and/or aortic arch.
Stanford type B aortic dissection management.
B-blockers then vasodilators.
Angina caveat
No myocyte necrosis.
Stable angina on ECG
ST depression
Variant (prinzmetal) angina triggers
1) tobacco
2) cocaine
3) triptans
variant angina treatment
1) Ca2+ channel blockers
2) nitrates
3) smoking cessation
unstable angina pathophys
Thrombosis with incomplete coronary artery occlusion.
Unstable angina on ECG + markers
+/- ST depression and/or T wave inversion buT NO cardiac biomarker elevation.
How do you distinguish NSTEMI from unstable angina?
biomarker elevation with NSTEMI, none with unstable.
difference in presentation from stable and unstable angina
Stable usually exertion chest pain; unstable is either increase in frequency or intensity of pain or pain at rest.
coronary steal syndrome pathophy
Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators dilates normal vessels and shunts blood toward well-perfused areas leading to decreased flow and ischemia in poststenotic region.
regadenoson
vasodilator
dipyridamole use and MOA
1) vasodilator, inhibits clot formation
2) phosphodiesterase inhibitor
SCD definition
death from cardiac causes within 1 hour of onset
large majority of cases of SCD are caused by…
CAD
What is chronic ischemic heart disease?
Progressive onset of HF over many years due to chronic ischemic myocardial damage.
STEMI pathophys
Transmural infarct. Full thickness of myocardial wall involved.
STEMI on ECG
ST elevation + Q waves
NSTEMI pathophys
subendocardial infarcts
commonly occluded coronary arteries
LAD, RCA, circumflex
finding I don’t often think of with MI’s
Pain in left arm and/or jaw
0-24 MI timeframe light microscopy
1) Early coagulative necrosis
2) release of necrotic cell contents into blood
3) edema, hemorrhage, wavy fibers.
4) neutrophils appear
0-24 MI etiology
Repercussion injury, associated with generation of free radicals, leads to hyper contraction of myofibrils through increased free calcium influx.
0-24 hr timeframe complications
1) ventricular arrhythmias
2) HF
3) cardiogenic shock
1-3 day timeframe complication
Postinfarction fibrinous pericarditis.
macroscopic appearance of heart in 1-3 day timeframe
hyperemia
hyperemia
increased blood flow to different tissues in body
1-3 day microscope chagnes
1) coagulative necrosis
2) *tissue surrounding infarct shows acute inflammation + neutrophils.
3-14 day macroscopic appearance
- hyperemic border; central yellow-born softening.
- maximally yellow and soft by 10 days.
Papillary muscle rupture leads to…
mitral regurgitation
morphologic appearance 2 weeks to several months
- Reanalyzed artery.
- Gray-white appearance
True vs false ventricular aneurysms
True occur later (after 2 weeks), false in 3-14 day timeframe.
complication of true ventricular aneurysm
Mural thrombus.
MI diagnosis and timeframe
- In the first 6 hours, ECG is the gold standard.
- Biomarkers afterward.
Troponin timeframe
1) Rises after 4 hours
2) Peaks at 24 hours
3) elevated for 7–10 days
CK-MB timeframe
1) Rises after 6-12 hours
2) Peaks at 16-24 hours
3) Returns to baseline at 48 hours
CK-MB downfall and use
It’s also found in skeletal muscle so not as specific, but good at diagnosing reinfarction since levels fall earlier.
hyperacute T waves
peak T-waves
Other ECG findings related to MI’s
1) hyper acute T waves
2) T-wave inversion
3) new left bundle branch block
4) pathologic Q waves
5) poor R wave progression
What does poor R wave progression on ECG indicate?
evolving or old transmural infarct. R wave should become progressively taller, but remains low.
Anteroseptal leads
V1-V2
Anteroapical leads
V3-V4
Anterolateral leads
V5-V6
Lateral leads
I, aVL
What leads will be elated with an anteroseptal (LAD) infarct?
V1-V2
What leads will be elated with an anteroseptal (distal LAD) infarct?
V3-V4
What leads will be elated with an anterolateral (LAD or LCX) infarct?
V5-V6
What leads will be elevated with a lateral (LCX) infarct?
I, aVL
What leads will be elated with an inferior (RCA) infarct?
II, III, aVF
What leads will be elated with a posterior (PDA) infarct?
V7-V9, ST depression in V1-V3 with tall R waves
tall R waves suggests..
posterior infarct
most impt complication within first 24 hours post-MI?
arrhythmia
What does a friction rub post MI indicate?
post infarction fibrinous pericarditis
Where is papillary muscle rupture most likely to occur and why?
Posteromedially, due to single blood supply from PDA.
When do inter ventricular septal ruptures occur?
3-5 days post MI
What mediates interventricualr septal ruptures?
Macrophages
Complications of ventricular pseudoaneurysms…
1) decreased CO
2) increased risk of arrhythmia
3) embolus from mural thrombus
sequela of free wall rupture
cardiac tamponade
How do true ventricular aneurysms present?
Outward bulge with contraction (“dyskinesia”) associated with fibrosis.
Sign of LV infarction?
pulmonary edema
Sign of papillary muscle rupture?
mitral regurg leading to pulmonary edema
Unstable angina/NSTEMI management
1) heparin for anticoagulation
2) anti platelet therapy (aspirin + clopidogrel)
3) beta-blocker
4) ACE inhibitor
5) statins
clopidogrel mechanism
ADP receptor inhibitor
How do you control symptoms with unstable angina/NSTEMI?
Nitroglycerin + morphine.
STEMI management?
Same as NSTEMI but you need repercussion therapy with PCI (preferred over fibrinolysis).
Most common cardiomyopathy?
Dilated cardiomyopathy
Common dilated cardiomyopathy etiologies
1) chronic alcohol abuse
2) wet beriberi
3) coxsackie B
4) chronic cocaine use
5) Chagas disease
6) doxorubicin
7) hemochromatosis
8) sarcoidosis
9) peripartum cardiomyopathy
Murmur with dilated cardiomyopathy?
Systolic regurgitant murmur.
hypertrophy associated with dilated cardiomyopathy?
Eccentric hypertrophy.
Dilated cardiomyopathy treatment?
1) Na restriction
2) ACE inhibitors
3) beta-blockers
4) diuretics
5) digoxin
6) ICD
7) heart transplant
Eccentric hypertrophy etiology
sarcomeres added in series.
Concentric hypertrophy?
There’s no overall enlargement of ventricle. The walls are thickened.
concentric hypertrophy associations
Volume overload, such as which HTN or aortic stenosis.
Auscultation findings in HOCM
1) S4
2) systolic murmur
3) Mitral regurg possible due to impaired mitral valve closure.
HOCM management
1) no high intensity sports
2) b-blocker or non-dihydropyridine Ca-blocker (verapamil)
3) ICD if high risk
HOCM macroscopic findings
myofibrillar disarray + fibrosis
Obstructive HOCM
subtype of HOCM characterized by asymmetric septal hypertrophy + systolic anterior motion of mitral valve, leading to outflow obstruction, dyspnea and possible syncope
infiltrative cardiomyopathy?
restrictive cardiomyopathy
What are some major causes of restrictive cardiomyopathy?
1) sarcoidosis
2) amyloidosis
3) postradiation fibrosis
4) endocardial fibroelastosis
5) Loffler syndrome
6) hemochromatosis
endocardial fibroelastosis?
thick fibroelastic tissue in endocardium of young children.
Loftier syndrome
Endomyocardial fibrosis with a prominent eosinophilic infiltrate.
ECG and restrictive cardiomyopathy
Low-voltage ECG
rales?
another name for crackles
systolic dysfunction characteristics
Reduced EF + increased EDV + decreased contractility
Diastolic dysfunction characteristics
Preserved EF + *normal EDV + decreased compliance (secondary to myocardial hypertrophy)
Most common cause of right HF
Left HF
cor pumonale
Isolated right HF due to pulmonary cause
Drug contraindicated in acute decompensated HF?
beta-blockers
What decreases mortality with heart failure?
1) ACEIs
2) ARBs
3) beta-blockers (except in acute decompensated)
What drugs improve both symptoms in mortality in HF patients?
Hydralazine with nitrate therapy.
Orthopnea etiology?
Increased venous return from redistribution of blood (gravity effect)
paroxysmal nocturnal dyspnea etiology
same as orthopnea, increased venous return from redistribution of blood
Rare complication of hepatomegaly?
cardiac cirrhosis
Causes of hypovolemic shock?
1) hemorrhage
2) dehydration
3) *burns
Obstructive shock
reduced CO due to cardiac tamponade or PE
Distributive shock and causes
Inadequate organ perfusion due to…
1) sepsis
2) anaphylaxis
3) CNS injury
Skin findings that distinguish distributive vs. other types of shock
Distributive shock presents with warm or dry skin. Other forms of shock present with cold, clammy skin.
Hypovolemic shock treatment
IV fluids
Cariogenic shock treatment
Inotropes + diuresis
Obstructive shock treatment?
Relieve obstruction
Sepsis, anaphylaxis, CNS injury shock treatment?
IV fluids + pressors
hypovolemic shock
1) PCWP
2) CO
3) SVR
1) very reduced. Remember - this is preload
2) reduced.
3) Increased. this is afterload
PCWP importance
= preload
obstructive shock
1) PCWP
2) CO
3) SVR
1) increased
2) decreased a lot
3) increased
SVR significance
afterload
cardiogenic shock
1) PCWP
2) CO
3) SVR
1) increased
2) decreased a lot
3) increased
Sepsis, anaphylaxis..
1) PCWP
2) CO
3) SVR
1) decreased
2) increased
3) severely decreased
Shock related to CNS injury..
1) PCWP
2) CO
3) SVR
1) decreased
2) **decreased
3) severely decreased
Skin findings with shock related to CNS injury
dry
Skin findings with shock related to sepsis, anaphylaxis…
warm
Roth spots description
Round white spots on retina surrounded by hemorrhage
osler nodes description
tender raised lesson on finger or toe pads
Janeway lesions description
Small, painless, erythematous lesions on palm or sole
caveat about bacterial endocarditis
You need multiple blood cultures for diagnosis.
vegetations in acute vs subacute endocarditis
With acute you get large vegetation on previously normal valves, with subacute you get smaller vegetations on congenitally abnormal or diseased valves.
Causes of nonbacterial endocarditis?
1) malignancy
2) hyper coagulable state
3) lupus
bugs causing tricuspid valve endocarditis
1) S aureus
2) pseudomonas
3) candida
bugs causing culture negative endocarditis
1) Coxiella brunette
2) bartonella
3) HACEK bugs
HACEK bugs
Haemophilus Aggregatibacter (formerly actinobacillus) Cardiobacterium Eikenella Kingella
Valves affected in RF in order
mitral then aortic then tricuspid (high-pressure valves affected most)
Anitschkow cells
Rheumatic fever
Anitschkow cell description
enlarged macrophages with ovoid, wavy, rod-like nucleus
rheumatic fever pathophys
Type II hypersensitivity. Antibodies to M protein cross-react with self antigens (molecular mimicry)
Rheumatic fever treatment
penicillin
joint presentation of rheumatic fever
migratory polyarthritis
common complication of acute pericarditis
Pericardial effusion
physical exam finding for pericarditis
friction rub
ECG for pericarditis
Widespread ST-segment elevation and/or PR depression
Causes of acute pericarditis
1) idiopathic (presumed viral)
2) coxsackie
3) neoplasia
4) SLE
5) RA
6) uremia
7) acute STEMI
8) dressler
9) radiation therapy
what happens to pressure in cardiac chambers with tamponade?
Equilibration of pressure in all 4 chambers.
ECG in tamponade
low-voltage QRS + electrical alternans
what is pulsus paradoxus?
Decrease in amplitude of systolic BP by greater than 10 mm Hg during inspiration.
Pulsus paradoxes seen in..
1) cardiac tamponade
2) asthma
3) OSA
4) pericarditis
5) croup
Most common heart tumor…
metastasis
What is kussmaul sign?
Increase in JVP on inspiration instead of a normal decrease.
JVD pathophys
inspiration –> negative intrathoracic pressure not transmitted to heart –> impaired filling of right ventricle –> blood backs up into venae cavae
Kussmaul sign + elevated JVP associations
1) constrictive pericarditis
2) restrictive cardiomyopathies
3) right atrial or ventricular tumors
Pathophys of eye injury with GCA
Ophthalmic artery can become occluded
What arteries are most commonly affected by GCA?
Branches of carotid
Takayasu affects..
Large-vessels: aortic arch and proximal great vessels
Takayasu presentatoin
1) “pulseless disease” (weak upper extremity pulses)
2) fever + night sweats + arthritis + myalgias + skin nodules + ocular disturbances
Takayasu treatment
corticosteroids
polyarteritis nodosa classic demographic
young adults
PAN presentation
Fever + weight loss + malaise + headache + abdominal pain + melon.
HTN + neurologic dysfunction + cutaneous eruptions + renal damage.
what arteries are usually involved in PAN?
Renal and visceral vessels, NOT pulmonary arteries.
Hypersensitivity type in PAN?
immune complex mediated
PAN treatment
1) corticosteroids
2) cyclophosphamide
Impt findings in PAN
1) transmural inflammation with fibrinoid necrosis
2) different stages of inflammation coexisting in different vessels
3) innumerable renal micro aneurysms and spasms on arteriogram.
Other name for Kawasaki
mucocutaneous lymph node syndrome
kawasaki presentation
conjunctival injection + rash (desquamating) + cervical adenopathy + strawberry tongue + hand foot changes + fever
strawberry tongue medical term
oral mucositis
Kawasaki treatment
IVIG + aspirin
Other name for Buerger’s…
Thromboangiitis obliterans
other impt finding in Buerger’s…
superficial nodular phlebitis
Wegener’s upper respiratory presentation
1) perforated nasal septum
2) chronic sinusitis
3) otitis media
4) mastoiditis
mastoiditis
mastoid sits behind the ear (battle sign)
renal presentation of Wegener’s
hematuria + red cell casts
wegener’s triad
focal necrotizing vasculitis + necrotizing granulomas in lung and upper airway + necrotizing glomerulonephritis.
other term for c-ANCA
anti-proteinase 3
CXR in wegener’s
large nodular densities
Wegener’s treatment
Cyclophosphamide + corticosteroids
microscopic polyangiitis presentation
Necrotizing vasculitis commonly involved lung + kidneys + skin with pauci-immune glomerulonephritis and palpable purpura.
How do you differentiate microscopic polyangiitis from wagerer’s?
in microscopic polyangiitsis, there’s no nasopharyngeal involvement + no granulomas.
other name for p-ANCA
anti-myeloperoxidase
microscopic polyangiits treatment
cyclophosphamide + corticosteroids
Churn-Strauss presentation
asthma + sinusitis + skin nodules or purpura + peripheral neuropathy. Can involve heart, GI, kidneys.
churg-strauss path
Granulomatous, necrotizing vasculitis with eosinophilia.
Labs in churg-strauss
1) *increased IgE
2) MPO-ANCA/p-ANCA
HSP pathophys
IgA immune complex deposition
Essential HTN management
1) thiazides
2) ACEIs/ARBs
3) *dihydropyridine Ca2+ channel blockers
HTN with heart failure management
1) diuretics
2) ACEI’s/ARBs
3) b-blockers (compensated) (to prevent cardiac remodeling)
4) aldosterone antagonists (to prevent from being fluid overloaded)
HTN with DM management
1) ACE/ARBs (both are protective against diabetic nephropathy)
2) Ca2+ channel blockers
3) thiazides
4) beta-blockers
Drugs for HTN in pregnancy?
1) hydrazine
2) labetalol
3) methyldopa
4) nifedipine
dihydropyridines vs nondihydropyridines
dihyropyridines act on vascular smooth muscle, non-dihydropyridines act on heart
dihydropyridines
all the -pines
non-dihydropyridines
dilimiazem + verapamil
Ca-channel blocker mechanism
Block voltage-dependent *L-type calcium channels of cardiac and smooth muscle leading to decreased contractility.
order of action of calcium channel blockers on vascular smooth muscle
Amlodipine + nifedipine, then diltiazem, then verapamil
order of efficacy of calcium channel blockers on heart
verapamil, diltiazem, amlodipine = nifedipine (verapamil for ventricle)
dihydropyridine you can’t use for HTN, angina, or Raynaud’s
nimodipine
clevidipine clinal use?
hypertensive urgency or emergency.
other use for non-dihydropyridines
afib/ a flutter
AE’s of non-dihydropyridines
cardiac depression + AV block + hyperprolactinemia + constipation
AE’s of dihydropyridines
peripheral edema + flushing + dizziness + gingival hyperplasia
hydrazine mechanism
increases cGMP leading to smooth muscle relaxation. Vasodilates arterioles more so than veins, leading to after load reduction.
when is hydralazine contraindicated?
angina/CAD (due to compensatory tachycardia)
hydralazine AE’s
fluid retention + headache + angina + lupus-like syndrome
hypertensive emergency drugs
1) clevidipine
2) fenoldopam
3) labetalol
4) nicardipine
5) nitroprusside
Nitroprusside MOA
short acting, increases cGMP via direct release of NO.
Nitroprusside AE
can cause cyanide toxicity (releases cyanide)
Fenoldopam MOA
Dopamine D1 receptor agonist– coronary, peripheral, renal, and splanchnic vasodilation. Decreases BP, increases natriuresis
What drug is commonly used postop for anti hypertension?
fenoldopam
Fenoldopam SE’s
hypotension + tachycardia
nitrates effect on veins or arteries?
Dilate veins more than arteries, thus DECREASING preload
other use for nitrates
pulmonary edema
nitrates AE’s
reflex tachycardia + hypotension + flushing + headache.
Describe Monday disease
exposure to nitrates leads to development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend. So they show up to work and become tachy, dizzy, and have a headache upon exposure.
MVO2
myocardial oxygen consumption
What beta-agonists are contraindicated in angina?
pindolol and acebutolol
pindolol MOA
partial B-antagonist (Only partial among nonselective)
B-blocker effect on EDV?
no effect or increased
Nitrate effect on ejection time?
decrease
Beta-blocker effect on ejection time?
Increase
Combined effect of nitrates + beta-blockers on
1) EDV
2) BP
3) contractility
4) HR
5) ejection time
6) MVO2
1) no effect or decreased
2) decreased
3) little/no effect
4) no effect or decreased
5) little/no effect
6) decreased significantly
**Ranolazine MOA
Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. *No affect on HR or contractility.
What is ranolazine used for?
angina refractory to other medical therapies
Ranolazine AE’s
constipation + dizziness + headache + nausea + QT prolongation
Statin mechanism
HMG-CoA reductase inhibitors: inhibit conversion of HMG-CoA to mevalonate
Mevalonate
precursor to cholesterol
when is myopathy a concern with statins?
When used with fibrates or niacin.
Name bile acid resin drugs
1) cholestyramine
2) colestipol
3) colesevelam
Bile acid resins affect on…
1) LDL
2) HDL
3) triglycerides
1) decrease (2 arrows)
2) slight increase
3) slight increase
Bile acid AE’s
1) GI upset
2) decrease absorption of other drugs and fat-soluble vitamins
Ezetimibe MOA
Prevents cholesterol absorption at small intestine brush border.
1) LDL
2) HDL
3) triglycerides
1) decrease (2 arrows)
2) null
3) null
Ezetimibe AE’s
rare hepatoxicity + diarrhea
Fibrate affect on…
1) LDL
2) HDL
3) triglycerides
1) decrease
2) increase
3) major decrease
fibrate mechanism
1) up regulate LPL leading to increased TG clearance
2) activates PPAR-alpha to induce HDL synthesis
Vibrate AE
myopathy + cholesterol gallstones
Niacin affects on…
1) LDL
2) HDL
3) triglycerides
1) significant decrease (2 arrows)
2) significant increase
3) decrease
Niacin mechanism as a lipid lowering agent
1) Inhibits lipolysis (HSL) in adipose tissue. Thus this prevents FFA from getting into the bloodstream and uptake into liver where cholesterol synthesis occurs.
2) reduces hepatic VLDL synthesis
Other niacin AE’s
hyperglycemia + hyperuricemia
Cholesterol synthesis pathway
Acetyl CoA –> HMG-CoA –> mevalonate –> cholesterol
digoxin affect on vagus nerve
Stimulates vagus nerve leading to decreased HR.
Factors predisposing to digoxin toxicity
1) renal failure
2) hypokalemia (this leads to increase binding at K+ binding site on ATPase because there’s less potassium).
3) decreased clearance with verapamil, amiodarone, and quinidine
Management of digoxin toxicity
1) Slowly normalize K+
2) cardiac pacer
3) anti-dig FAB
4) Mg2+
Class IA antiarrhytmics
Quinine + procainamide + disopyramide
Class IA affects
1) Increased AP duration
2) increase effective refractory period
3) increase QT interval
When are class IA’s used?
atrial and ventricular arrhythmias
Treatment for re-entrant and ectopic SVT and VT?
Class IA’s
cinchonism
headache + tinnitus with quinidine
disopyramide AE
HF
Other 1A SE’s
thrombocytopenia + torsades de pointes
1B drugs
Lidocaine + mexiletine + (phenytoin)
1B affects on action potential
Decrease AP duration.
1B MOA
Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.
Best anti-arrhythmic post-MI?
IB’s (IB is Best post MI)
Arrhythmias for digitalis induced?
1B’s (lidocaine or mexiletine)
1B AE’s
CNS stimulation/depression + cardiovascular depression
IC drugs
fleicanide + propafenone
IC mechanism
Significantly prolong ERP in AV node and accessory bypass tracts. No effect on ERP in purkinje and ventricular tissue.
- No affect on AP duration.
antiarrhythmics contraindicated post-MI?
IC (IC Contraindicated post MI)
antiarrhythmics contraindicated in structural and ischemic heart disease?
IC (IC contraindicated)
beta-blocker mechanism
Decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents.
How do beta-blockers suppress abnormal pacemakers?
Decreasing slope of phase 4.
esmolol caveat
very short acting
Why is PR interval increased with beta-blockers?
AV node particularly sensitive
metoprolol other AE
dyslipidemia
propranolol other AE
Can exacerbate vasospasm in prinzmetal angina
carvedilol and labetalol MOA
nonselective alpha and b-antagonists
Problem with giving b-blockers for cocaine toxicity or pheochromocytoma?
Cause unopposed alpha1 agonism if given alone.
Beta-Blocker overdose management
saline + atropine + glucagon
Class III antiarrhytmics mechanism
Increase AP duration + increase ERP + increase QT interval
Class IIIs used for V tach
amiodarone + sotalol
antiarrhythmics for afib
Anything except 1B or 1C
Sotalol AE’s
torsades de pointes + excessive betablockade
Ibutilide AE’s
torsades de pointes
amiodarone AE’s
1) PF
2) hepatotoxic
3) hypothyroidism
4) *hyperthyroidism (amiodarone is 40% iodine by weight)
5) corneal deposits + blue/gray skin deposits resulting in photo dermatitis
6) neurologic effects
7) constipation
8) bradycardia + heart block + HF
What will class III look like on action potential graph?
markedly prolonged repolraization
Why does amiodarone cause corneal deposits and skin deposits?
Acts as a happen.
Caveat about amiodarone
Lipophilic and has class I, II, III, and IV effects.
Class IV mechanism
Decreased conduction velocity + increased ERP + increased PR interval
What do you use for rate control in fib?
Class IV channel blockers
Which anti arrhythmic can depress the sinus node?
class IV - verapamil, diltiazem.
adenosine
Moves K+ out of cells leading to hyper polarization of cell and decreased caclium
Drug of choice in diagnosing/terminating certain forms of SVT?
adenosine (very short acting)
Adenosine contraindications
theophylline + caffeine will blunt effects because both are adenosine receptor antagonists
Adenosine AE’s
flushing + hypotension + chest pain + sense of impending doom + bronchospasm
What do you use to treat torsades de points?
Mg2+
Displaced PMI indicates…
cardiomegaly
Mixed osteolytic and blastic lesions
1) gastric
2) breast
acute decompensated heart failure
Decompensation of chronic stable heart failure. Eg from illness, MI, abnormal rhythm, uncontrolled HTN, or increased fluids.
Where do internal thoracics come off of?
subclavian
Pathophys of rib notching
with increased flow through the internal thoracic-anterior intercostal arterial system, retrograde flow through the posterior intercostal arteries develops, providing oxygenated blood to the descending aorta distal to the coarctation. /this is what causes rib notching (increased flow through the intercostals enlarges the arteries resulting in resorption of bone along the lower borders of the ribs.
murmur in aortic coarctation
harsh systolic ejection murmur.
carotid occlusion
procedure in which occlusion of the carotid results in less stretch of the carotid baroreceptors and less afferent nerve activity. Basically tricks body into thinking it has a lower blood pressure than it actually has. /thus, a baroreceptor reflex is elicited, leading to an increase in sympathetic tone increasing mean blood pressure + HR.
What happens to preload when CO decreases?
Increases because blood is redistributed to the veins. Blood flow ceases, and then flows from high pressure arterial system to low pressure venous system.
MCFP
mean circulatory filling pressure. Equilibrated pressure when pressure is equal throughout CV system.
Mean systemic filling pressure (MSFP)
Measure of volume of blood and compliance of vessels.
Relation of venous compliance to preload
Decreased compliance = increased preload.
Bainbridge reflex
Increase in HR due to increase in CVP.
Increased blood volume –> increased volume sensed by baroreceptors –> B-fibers reflex with heart affecting sympathetic and parasympathetic pathways –> increased HR.
Auto regulation of blood flow in heart?
ATP consumption increases with increased work –> increased adenosine –> vasodilation –> increased oxygen delivery.
What happens to arterial PO2 and arterial O2 sat at high elevation?
Low. Even with acclimatization since these are independent of hematocrit. Just depend on O2 availability.
Changes with acclimatization…
1) arterial PO2 and O2 sat stay low
2) systemic arterial O2 content increases to normal
3) pH normal (increased ventilation)
acute changes to altitude
decreased PAO2 and PaO2 + decreased PACO2 and PaCO2 + increased systemic arterial pH + decreased Hb% sat + decreased systemic arterial O2.
What happens to compliance and CVP with exercise?
Increased sympathetic activity causes venous smooth muscle constriction –> decreased compliance –> increased CVP –> increases CO
adenosine half-life
minutes
TPR and CO changes with dynamic, endurance exercise?
Increased CO + decreased TPR due to metabolic vasodilation.
static exercise changes in…
1) blood flow
2) MAP
3) ATP/ADP ratio
Contraction of skeletal muscles compress blood vessels and decreases blood flow. This increases vascular resistance + profound increase of MAP.
3) decreased.
What happens to blood flow with dynamic exercise?
Increased blood flow due to metabolic vasodilation of arterioles due to local vasodilator actions.
PV loop changes with LV dilation
Only slightly increased EDP (compliance increases but not a significant change in pressure).
Hypertonic contraction
Loss of hypotonic fluid
Hypertonic expansion
Excessive intake of sodium chloride.
Approach to Darrow Yannett diagrams
Just draw cell and think about osmolar effect.
Causes of isotonic fluid loss
1) hemorrhaging
2) diarrhea
3) vomiting
Affect of isotonic fluid loss on:
1) osmolarity
2) ICF volume
3) ECF volume
1) no change
2) no change (no force pushing fluid out of cell)
3) decreased
Causes of hypotonic fluid loss:
1) dehydration
2) DI
3) alcoholism
Affect of hypotonic fluid loss on:
1) osmolarity
2) ICF volume
3) ECF volume
1) Increased
2) decreased
3) decreased
Affect of isotonic fluid gain on:
1) osmolarity
2) ICF volume
3) ECF volume
1) no change
2) no change
3) increased
Causes of hypotonic fluid gain
1) hypotonic saline
2) water intoxication
Affect of hypotonic fluid gain on:
1) osmolarity
2) ICF volume
3) ECF volume
1) decreased
2) increased
3) increased
Premature contraction of the ventricle (PVC) on ECG
no P wave
Premature contraction of the ventricle (PVC)
presentation = either asymptomatic or palpitations or syncopale episodes. /can present after MIs in which tissue damage in ventricular tissue produces ectopic (non-SA node) sites of electrical activation. When these sites depolarize the ventricles contract independently and generate premature and abnormal QRS patterns seen on ECG.
afib on ECG
absent P waves + irregularly irregular QRS
premortem thrombi (lines of zahn) suggests…
afib prior to death
treatment of choice for V tach?
amiodarone
AV fistula
1) presentation
2) scenario
3) findings
1) coldness of extremity (due to lack of arterial flow)
2) post surgery
3) palpable thrill over area of wound. Continuous murmur. Diminished pulse. Doppler showing turbulence.
Nutmeg appearance of heart may also indicate…
right heart failure
Adult pressures in the cardiac chambers (minimum, maximum)
Code: covered in ivy/right atrium = 0,8. Covered in hair + nails pounded in everywhere/right ventricle = 4,25. Nails + big hoops/pulmonary artery = 9,25. Hens + walls made out of tin cans/left atrium = 2,12. Hoops on walls + mice drinking mimosas/left ventricle = 9,130. Mice drinking mimosas + carrying briefcases/aorta = 70,130. Wedge of tissue sitting in middle of road covered in tin cans/wedge pressure = 12
Common treatment for bradycardia?
atropine (decreases vagal influence on the SA and AV nodes).
valsalva maneuver pathophys
pathophys: pressure increase in chest forces blood out of pulmonary circulation into left atrium. ALSO return of systemic blood to the heart is impeded by increased pressure in chest. /effect = decreases preload + decreases afterload
What signifies the development of a complicated atheromatous plaque?
Calcification
“foci of calcification”
atherosclerotic plaque
ruptured free wall presentation
profound hypotension + dyspnea + muffled hear sounds and elevated JVP.
What does coronary sinus dilation often suggest
pulmonary hypertension.
bronchiolitis obliterans
lymphocytic inflammation and necrosis of bronchiolar walls, leading to scarring and progressive obliteration of small airway lumens.
SERCA proteins
Sarcoplasmic reticulum Ca ATPase. Pump Ca, and thus a net positive charge out of the cytosol into the sarcoplasmic reticulum (thus sequester Calcium)
sarcoplasmic reticulum
stores calcium
Ryanodine receptor functions
Mediates calcium-induced calcium release
When does ischemic injury become irreversible?
half hour
When does loss of cardiomyocyte contractility occur with ischemia?
after 60 seconds.
If radius of an artery decreases by 50%, what is change in blood flow?
Decreases by 1/16 (flow is proportional to radius ^ 4th power) so (1/2)^4 = 1/16
Systolic pressure in downstream arteries is actually slightly higher than in aorta.
So renal artery pressure is actually higher than aorta.
What happens with extra systolic beats?
There’s more calcium in the myocyte so contractility increases. Thus, pulse pressure increases.
What does 2 P waves breeding each QRS complex indicate?
Only every other P wave is conducted through AV node to ventricle. Thus, conduction velocity through AV node must be decreased.
What determines pulse pressure?
Stroke volume
When is the aortic pressure highest in the cardiac cycle?
- Reduced ventricular filling (diastasis).
- Aortic pressure reaches its highest level immediately after rapid ejection of blood during systole.
Affect of histamine on vasculature
1) vasodilation of arterioles, thus increasing filtration.
2) constriction of veins
Hodgkin’s lytic or blastic mets?
blastic
What happens to TPR during exercise?
Decreases. Although there is increased sympathetic flow to blood vessels, there is an overriding vasodilation of skeletal muscle arterioles.
During which phase of the cardiac cycle is ventricular volume lowest?
Isovolumetric ventricular relaxation (ventricle is relaxed just before filling occurs).
Why does standing cause an increase in HR?
Blood pools and due to decreased venous return, baroreceptors sense this and stimulate increased HR.
During which phase of ventricular action potential is membrane potential closest o K+?
Phase 4
What receptors mediate slowing of the heart?
Muscarinic (via ACh in the SA node)
Other cause of decreased inotropy…
- Acetylcholine (on atria)
How do sympathetic stimulation and NE increase contractility?
Increasing calcium entry during the plateau phase and increasing storage of Ca by the sarcoplasmic reticulum.96
pulses finding in AS
“pulses parvus et tardus”– pulses are weak with a delayed peak.
