Steve Colbert's Cardiac Comedy Clues Flashcards
What does this embryonic structure grow into: Truncus arteriosus
Ascending aorta and pulmonary trunk
What does this embryonic structure grow into: Bulbus cordis
Smooth parts (outflow tract) of left and right ventricles
What does this embryonic structure grow into: Primitive atria
Trabeculated part of left and right atria
What does this embryonic structure grow into: Primitive ventricle
Trabeculated part of left and right ventricles
What does this embryonic structure grow into: Primitive pulmonary vein
smooth part of left atrium
What does this embryonic structure grow into: Left horn of sinus venosus (SV)
Coronary sinus
What does this embryonic structure grow into: right horn of SV
smooth part of right atrium
What does this embryonic structure grow into: Right common cardinal vein and right anterior cardinal vein
SVC
Heart embryo morphogenesis
first functional organ to develop in vertebrate embryos; beats spontaneously by 4th week
Cardiac looping in embryo
primary heart tube loops to establish left-right polarity; begins in week 4 of gestation; defect in left right dynein (involved in R/L asymmetry) can lead to dextrocardia, as seen in Kartagener syndrome (primary ciliary dyskinesia)
Walk through the steps of the separation of the heart chambers in embryo
1) Septum primum grows toward endocardial cushions, narrowing foramen primum; 2) Foramen secundum forms in septim primum (foramen primum disappears); 3) Septim secundum maintains R to L shunt; 4) Septum secundum expands and covers most of the foramen secundum. THe residual Foramen is the foramen ovale; 5) Remaining portion of septum primum forms valve of foramen ovale; 6) Septum secundum and septum primum fuse to form the atrial septum; 7) formane ovale usually closes soon after birth because of increase LA pressure.
Patent foramen ovale
caused by failure of septum primum and septum secundum to fuse after birth; most are left untreated; can lead to paradoxical emboli (venous thromboemboli that enter systemic arterial circulation), similar to those resulting from an ASD
Walk through the steps of ventricle formation in ventricles
1) muscular ventricles septum forms. Opening is called interventricular foramen. 2) Aorticopulmonary septim rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular setpum. 3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of the interventricular septum.
Ventricular septal defect (VSD)
most commonly occurs in the membranous septum; acyanotic at birth due to L to R shunt
Outflow tract formation in embryo
Truncus arteriosus rotates; neural crest and endocardial cell migrations leading to truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum leading to the ascending aorta and pulmonary trunk
Conotruncal abnormalities
Transposition of great vessels; Tetralogy of fallot; Persistent truncus arteriosus
Valve development: Aortic/pulmonary
derived from endocardial cushions of outflow tract
Valve development: Mitral/tricuspid
Derived from fused endocardial cushions of the AV canal
Ebstein anomlay
Displaced valves from abnormal development
Fetal erythropoiesis
Yolk sac (3 to 8 weeks); Liver (6 weeks to brith); Spleen (10-28 weeks); Bone marrow (18 weeks to adult); “Young Liver Synthesizes Blood”
Hemoglobin development
Fetal hemoglobin=HbF (alpha2Gamma2);
Adult hemoglobin=HbA (alpha2beta2);
HbF has higher O2 affinity for oxygen due to less avid binding of 2,3 BPG;
Fetal circulation;
Blood entering fetus through the umbilical vein is conducted via the ductus venous into the IVC to bypass the hepatic circulation; Oxygenated Blood from IVC goes through heart and is shunted through foramen ovale; Deoxygenated blood entering the RA from the SVC goes into the RA into the RV into the main PA into the patent ductus arteriousus into the descending aorta
At birth the infant takes its first breath then:
the resistance in pulmonary vasculature decreases leading to an increase in left atrial pressure vs right atrial pressure; foramen ovale closes (now called fossa ovalis; increase in O2 (from respiration) and decrease in PGE (from placental separation) leads to closure of ductus arteriosus
fetal-postnatal derivatives: umbilical vein turns into
ligamentum teres hepatis; contained in falciform ligament
fetal-postnatal derivatives: umbilical arteries turns into
Medial umbilical ligaments
fetal-postnatal derivatives: Ductus arteriosus turns into
Ligamentum arteriosum
fetal-postnatal derivatives: Dustus venosus turns into
Ligamentum venosum
fetal-postnatal derivatives: Foramen ovale turns into
fossa
fetal-postnatal derivatives: Allantois turns into
Urachus-median umbilical ligament; the urachus is the part of the allantoic duct between the bladder and the umbilicus. Urachal cyst or sinus is a remnant
fetal-postnatal derivatives: Notochord turns into
Nucleus pulposus of intervertebral disc
SA and AV nodes are usually supplied by what artery
Right Carotid Artery; Infract may cause nodal dysfunction (bradycardia or heart block)
Right dominant heart circulation
85% of people are this way; PDA arises from RCA
Left dominant heart circulation
8% of people are this way; PDA arises form LCX (left circumflex coronary artery)
Co-dominant heart circulation
7% of people are this way; PDA arises from both the LCX and RCA
Coronary artery occlusion normally occurs in the
LAD (Left Anterior Descending artery)
When is is coronary blood flow at its highest point (systole or diastole)
Highest at early diastole
The most posterior part of the heart is the Left atrium; enlargement of this can cause
Dysphagia (compression of esophagus); or hoarseness (compression of left recurrent laryngeal nerve, a branch of the vagus)
Left circumflex artery (LCX) supplies
lateral and posterior walls of left ventricle
Left anterior descending artery (LAD) supplies
anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of left ventricle
Posterior Descending/Interventricular artery (PDA) supples the
posterior 1/3 of interventricular septum and posterior walls of ventricles
Acute marginal artery supplies the
Right ventricle
Formula for Cardiac output
CO=stroke volume x HR
Fick principle equation
CO=(rate of O2 consumption)/arterial O2 content-Venous O2 content)
Mean arterial pressure equation
MAP= CO x TPR; or MAP= 2/3 diastolic + 1/3 systolic
Pulse pressure equation
pulse pressure= systolic- diastolic pressure; Pulse pressure is proportional to SV, inversely proportional to arterial compliance
Stroke volume equation
SV= EDV-ESV
When you exercise how is Cardiac output maintained
Early stages of exercise: CO is maintained by increase HR and SV; during late exercise CO is maintained by increase HR only (SV plateaus)
When you increase HR your diastolic goes down which leads to
decreased CO
When do you see increased Pulse Pressure
in hyperthyroidism; aortic regurgitation; arteriosclerosis; obstructive sleep apnea (increase sympathetic tone), exercise (transient)
when do you see decreased pulse pressure
in aortic stenosis; cardiogenic shock; cardiac tamponade; and advanced heart failure
Stroke Volume: what affects it
SV affected by contractility, afterload, and preload (SV CAP); increased SV when increased contactility, increased preload, or decreased afterload
Way to calculate total peripheral resistance
TPR=(MAP-right Atrial pressure)/CO
Contractility of the heart (and SV) is increased by
Catecholamines (increased activity of Ca2+ pump in SR); increased intracellular Calcium; decreased extracellular Na (decreased activity of the Na/Ca exchanger; Digitalis (blocks Na/K pump which decreases Na/Ca exchanger which increases intracellular Calcium
Contractility of the heart (and SV) is decreased by
beta1 blockade (decreased cAMP); Heart failure with systolic dysfunction; acidosis; hypoxia/hypercapnea; non-dihydropyridine calcium channel blockers
Myocardial O2 demand is increased by
increased afterload; increased contractility; increased HR; increased ventricular diameter
Preload
preload approximated by ventricular EDV; depends on venous tone and circulating blood volume; Venodilators decrease preload (nitro)
Afterload
approximated by MAP; relation of LV size and afterload called Laplace’s law: Wall tension= (pressure X radius)/ 2X wall thickness); LV compensates for increased afterload by thickening (hypertrophy) to decrease wall tension; Vasodilators decrease afterload (hydralazine); ACE inhibitors and ARBs decreases afterload and preload; chronic HTN increases MAP causing LV hypertrophy
Ejection fraction
EF=SV/EDV= (EDV-ESV)/EDV; left ventricular EF is an index of ventricular contractility; normal EF is 55% or greater; decreased EF in systolic heart failure; EF is normal in diastolic heart failure
Artery Venous fistula causes
increased HR, increased SV, increased CO, increased mixed venous O2 content; decreased systemic resistance; decreased diastolic BP
Starling curve is a theory that says what
force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload); increased contractility with catecholamines, digoxin; decreased contractility with loss of myocardium (e.g. MI), beta blockers, Calcium channel blockers, dilated cardiomyopathy
When is viscosity of blood changes
increased viscosity in: polycythemia, hyperproteinemic states (e.g. MS), and hereditary spherocytosis;
decreased viscosity in: anemia
Inotropy
is the measure of the force of contraction; positive inotrope would be catecholamines and digoxin; negative inotrope would be uncompensated heart failure, narcotic overdose
Venous return on cardiac and vascular function curves
Changes in circulating volume or venous tone leads to altered RA pressure for a give CO. Mean systemic pressure (x-intercept) changes with volume/venous tone; Fluid infusion and sympathetic activity increase venous return; acute hemorrhage, spinal anesthesia decreases venous return
Total peripheral resistance
Changes in TPR lead to altered CO at a given RA pressure, however, mean systemic pressure is unchanged; Vasopressor increase TPR; Exercise, AV shunt decrease TPR
S1 heart sounds
mitral and tricuspid valve closure. Loudest at mitral area
S2 heart sounds
aortic and pulmonary valve closure; loudest at left sternal border.
S3 heart sounds
in early diastole during rapid ventricular filling phase. Associated with increase filling pressure (e.g. mitral regurgitation, CHF) and more common in dilated ventricles (but normal in children and pregnant women).
S4 heart sounds
“atrial kick” in late diastole. high atrial pressure. Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall
Jugular venous pulse: has 5 distinct waves
A wave-atrial contraction;
C wave-RV contraction (closed tricuspid valve bulging into atrium);
X descent-atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction. Absent in tricuspid regurgitation.absent in tricuspid regurgitation;
V wave- increased right atrial pressure due to filling against closed tricuspid valve;
Y descent-blood flow from RA to RV
Normal splitting of S2: caused by what
Inspiration leads to drop in intrathoracic pressure which increases venous return to the RV leading to increased RV stroke volume leading to increased RV ejection time causing delayed closure of pulmonic valve. Decreased pulmonary impedance (increased capacity or the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve
Wide splitting of S2: what causes it
Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block). delay in RV emptying causes delayed pulmonic sound (regardless of breath). an exaggeration of normal splitting
Fixed splitting of S2: caused by
Seen in ASD. ADS leads to left to Right shunt causing increased RA and RV volumes causing increased flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
Paradoxical splitting of S2: caused by
Seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block). normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2, thereby paradoxically eliminating the split
When listening to the heart what does the following due to change the heart’s function: inspiration
increases intensity of right heart sounds
When listening to the heart what does the following due to change the heart’s function: Valsalva (phase II), standing (decrease venous return)
Decreases intensity of most murmur (including AS);
Increase intensity of hypertrophic cardiomyopathy murmur;
MVPL decrease murmur intensity, earlier onset of click/murmur
When listening to the heart what does the following due to change the heart’s function: Hand grip
Increases intensity of MR, AR, VSD murmurs;
Decrease intensity of AS, hypertrophic cardiomyopathy murmurs;
MVP: increase murmur intensity, later onset of click/murmur
When listening to the heart what does the following due to change the heart’s function: Rapid squatting (increased venous return, preload, and afterload with prolonged squatting)
Decrease intensity of hypertrophic cardiomyopathy murmur;
Increase intensity of AS murmur;
MCP: increase murmur, later onset of click/murmur
Describe the sound of a mitral/tricuspid regurg murmur
Holosystolic, high pitched blowing murmur;
Mitral: is loudest at apex, radiates to axilla, enhanced by maneuvers that increase TPR (squats and hand grips). MR is often due to ischemic heart disease, MVP, or LV dilation;
Tricuspid: loudest at tricuspid area and radiates to right sternal border. Enhanced by maneuvers that increase RA return (e.g. inspiration). TR commonly caused by RV dilation. Rheumatic fever and infective endocarditis can cause either MR or TR
Describe the sound of an Aortic stenosis
Crescendo-decrescendo systolic ejection murmur. LV»_space; aortic pressure during systole. Loudest at heart base; radiates to carotids. “Pulsus parvus et tardus” (pulses are weak with a delayed peak). Can lead to syncope, angina, and dyspnea on exertion. Often due to age-related calcific aortic stenosis or bicuspid aortic valve.
Ventral septal defect makes what sounds
Holosystolic, harsh murmur. Loudest at the tricuspid area, accentuated by hand grip due to increased afterload
Mitral valve prolapse sounds like what
Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae). Most frequent valvular lesion. Best heard over the apex. Loudest just before S2. Usually benign. Can predispose to infective endocarditis. Can be caused my myxomatous degeneration, rheumatic fever, or chordae rupture. Occurs earlier with maneuvers that decrease venous return (e.g. standing or Valsalva).
Aortic regurgitation sounds like
High-pitched blowing early diastolic decrescendo murmur. Wide pulse pressure when chronic, can present with bounding pulses and head bobbing. often due to aortic root dilation, bicuspid aortic valve, endocarditis, or rheumatic fever. Increased murmur with hand grip. Vasodilators decrease intensity of murmur. Large stroke volume, heard lower left sternal border
Mitral stenosis sounds like
Floowins opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fused leaflet tips). Delayed rumbling late diastolic murmur; Decreased interval between S2 and OS correlates with increased severity. LA»_space; LV pressure during diastole. Often occurs secondary to rheumatic fever. Chronic MS can result in LA dilation. Enhanced by maneuvers that increase LA return (e.g. expiration)
PDA sounds like
Continuous machine like murmur. Loudest at S2. Often due to congenital rubella or prematurity. Best heard at left infraclavicular area
Ventricular action potentials: phases
Phase 0= rapid upstroke and depolarization- voltage gated Na channels open;
Phase 1= initial repolarization, inactivation of voltage gated Na channels, Voltage gated K start to open;
Phase 2= plateau- Calcium influx through voltage gated Ca channels balances K efflux. Ca influx triggers Ca release from SR and myocyte contraction.
Phase 3= rapid repolarization- Massive K efflux due to opening of voltage gated slow K channels and closure of voltage gated Ca channels
Phase 4= resting potential-High K permeability through K channels
Pacemaker action potential: differences between ventricular action potential and pacemaker
Occurs in the SA and AV nodes. Key differences from the ventricular action potential include;
Phase 0=upstroke-opening of voltage gated Ca channels. fast voltage gated Na channels are permanently inactivated because of the less negative resting voltage of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission form the atria to ventricles;
Phase 3: inactivation of Ca channels and increased activation of K channels leading to K influx;
Phase 4: Slow diastolic repolarization; Na conductance from funny channels increases. accounts for the automaticity of AV and SA nodes.
ECG: P wave
atrial depolarization; atrial repolarization blocked by QRS complex
ECG: PR interval
conduction delay through the AV node (about 200 msec)
ECG: QRS complex
ventricular depolarization: normally
ECG: QT interval
mechanical contraction of the ventricles
ECG: T wave
ventricular repolarization: T wave inversion may indicate previous MI
ECG: ST segment
isoelectric, ventricular depolarization
ECG: U wave
caused by hypokalemia, bradycardia
Heart conduction pathway
SA node to the atria to the AV node to the common bundle to the bundle branches to the purkinje fibers to the ventricles
Speed of different conduction fibers through the heart
Purkinje; atria; ventricles; AV node
Pacemaker speed in the heart:
SA node is fastest pacemaker> AV> Bundle of his/purkinje/ventricles
AV node delay
AV node delay is about 100 msec and atrioventricular delay; allows time for ventricular filling
Torsades de pointes
Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to ventricular fibrillation; long QT interval predisposes to torsades de pointes. Caused by drugs, decreased K, decreased Mg, other abnormalities. Treatment includes magnesium sulfate
Torsades de pointes is caused by what meds
Some Risky Meds Can Prolong QT; Sotalol, Risperidone, Macrolides, Chloroquine, Protease inhibitors, Quinidine; Thiazides
Congenital long QT syndrome
Inherited disorder of myocardial repolarization, typically due to ion channel defects; increased risk of sudden cardiac death due to torsades de pointes, Includes: Romano Ward syndrome and Jervell and Lange-Nielson Syndrome
Romano-Ward syndrome
congenital long QT syndrome: autosomal dominant, pure cardiac phenotypes (no deafness)
Jervell and Lange-Nielsen syndrome
Congenital long QT syndrome: autosomal recessive recessive, sensorineural deafness
Wolff Parkinson White syndrome
Most common type of ventricular pre-excitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node. As a result, ventricles begin to depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG. May result in reentry circuit leading to supraventricular tachycardia; if you give WPW syndrome patient digoxin they get V fib
Atrial fibrillation
Chaotic and erratic baseline (irregularly irregular) with no discrete waves in between irregularly spaced QRS complexes. Can result in atrial stasis and lead to thromboembolitic stroke. Treatment includes rate control, anticoagulation, and possible pharmacological or electrical cardioversion
Atrial flutter
a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the sawtooth appearance of the flutter waves. Pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmics. Rate control: Beta blocker or calcium channel blocker. Definitive treatment is catheter ablation
Ventricular fibrillation
A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.
AV block: 1st degree
The PR interval is prolonged (> 200 msec). Benign and asymptomatic. No treatment required
AV block: 2nd degree, Mobitz type I (wenckebach)
Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Usually asymptomatic.
AV block: 2nd degree, Motitz type 2
Dropped beats that are not preceded by a change in the length of the PR interval (as in type I) it is often found as 2:1 block, where there are 2 or more P waves to 1 QRS response. May progress to 3rd degree heart block. Treated with pacemaker
AV block: 3rd degree
The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves beat no relation to the QRS complexes. the atrial rate is faster than the ventricular rate. Usually treated with pacemaker. Lyme disease can result in 3rd degree heart block.
Atrial natriuretic peptide
Released from atrial myocytes in response to increase blood volume and atrial pressure. Causes vasodilation and decreased Na reabsorption at the renal collecting tubule. Constricts efferent renal arterioles and dilates afferent arterioles via cGMP, promoting diuresis and contributing to “aldosterone escape” mechanism
B-type (brain) natriuretic peptide
released form ventricular myocytes in response to increase tension. Similar physiologic action to ANP, with longer half life. BNP blood test used for diagnosing heart failure (Very good negative predictive value). Available in recombinant form (nesiritide) for treatment of heart failure.
During V-FIB the heart stops pumping out blood and the systemic blood pressures do what
all blood pressures equalize in the body: RA=venous=arterial and so on
Preventricular contraction (PVC)
Less end diastolic volume, no pave, no atrial contraction
The aortic arch receptors transmit signal using the
vagus nerve to the solitary nucleus of medulla (responds only to increased BP)
The Carotid sinus receptors transmit signal using the
glossopharyngeal nerve to the solitary nucleus of the medulla (responds to decreased and increased BP)
Baroreceptor mechanism when you have hypotension
hypotension leads to decreased arterial pressure causing decreased stretch leading to decreased afferent baroreceptor firing causing increased efferent sympathetic firing and decreased efferent parasympathetic stimulation leading to vasoconstriction, increased HR, increased contractility, increased BP;
important in the response to severe hemorrhage
Mechanism of carotid massage
increased pressure on carotid sinus leads to increased stretch and therefore increased afferent baroreceptor firing causing increased AV node refractory period leading to decreased HR
Baroreceptors and Cushing syndrome: mechanism of that
Increased intracranial pressure constricts arterioles which leads to cerebral ischemia and reflex sympathetic output in perfusion pressure (HTN) causing increased stretch and reflex baroreceptor induced bradycardia
Chemoreceptors: Peripheral
Carotid and aortic bodies are stimulated by decrease Po2 (
Chemoreceptors: Central
Are stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Does not directly respond to O2.
Which organ gets 100% of the bodies cardiac output (not the heart you smarty pants)
The lungs!
Which organ has the largest share of systemic cardiac output
liver
Which organ has the highest blood flow per gram of tissue
kidney
what is pulmonary capillary wedge pressure used for?
is a good approximation of left atrial pressure. In mitral stenosis PCWP is greater than LV diastolic pressure; measured by Swan Ganz catheter
Normal pressure in RA
Normal RV pressure
25/5 mmHg
normal pulmonary blood pressure
25/10 mmHg
normal LA pressure
Normal LV pressure
130/10 mmHg
Normal Aorta blood pressure
130/90 mmHg
Factors that influence autoregulation in the heart
Local metabolites (vasodilatory): CO2, adenosine, NO
What is autoregulation referring to
how blood flow to an organ is maintained constant over a wide range of perfusion pressures
Factors that influence autoregulation in the brain
Local metabolites (vasodilatory): CO2 (pH)
Factors that influence autoregulation in the Kidneys
myogenic and tubuloglomerular feedback
Factors that influence autoregulation in the Lungs
hypoxia causes vasoconstriction (ONLY ORGAN TO DO THIS, normally a blood vessel with dilate when hypoxic)
Factors that influence autoregulation in the skeletal muscles
local metabolites: lactate, adenosine, K, H, CO2
Factors that influence autoregulation in the Skin
sympathetic stimulation most important mechanism-temperature control
Edema is excess fluid outflow into the interstitium: this is caused by different factors including
Increased capillary pressure (heart failure);
Decreased plasma proteins (nephrotic syndrome, liver failure);
Increased capillary pressure (toxins, infections, burns)
Increased interstitial colloid osmotic pressure (lymphatic blockage)
Right to Left shunts: when are they present, what are the types
Present at birth or shortly after, usually require emergency surgery or maintenance of PDA;
5 T’s: 1) Truncus arteriosus (1 vessel), 2) Transposition (2 vessels) 3) TRIcuspid atresia (3=tri) 4) TETRAlogy of Fallot (4=tetra) 5) TAPVR (5 letters)
Persistent truncus arteriosus
Failure of truncus arteriosus to divide into pulmonary trunk and aorta; most patients have accompanying VSD which increases pulmonary pressure; associated with 22q11 (Digeorge); conotruncal ridges fail to develop; R to L shunt
D-transposition of great vessels
Aorta leaves RV (anterior) and the pulmonary trunk leaves LV (posterior) leading to separation of pulmonic and systemic circulation. Will die unless shunt is present (like PDA, VSD or patent foramen ovale); due to aoritcopulmonary septum to spiral; without surgery you die; associated with maternal diabetes; 1/3 of x rays will show eggs on a string appearance; R to L shunt
Tricuspid atresia
absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability; R to L shunt
Tetralogy of Fallot
Caused by antereosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis.
1) pulmonary infundibular stenosis (most important determinant for prognosis)
2) RV hypertrophy (boot shaped heart on x ray)
3) Overriding Aorta
4) VSD; Pulmonary stenosis forces R to L shunt across VSD;
Squatting increases SVR, decreases R to L shunt and improves cyanosis
Total anomalous pulmonary venous return
Pulmonary veins drain into the right heart circulation (SVC, coronary sinus, etc); associated with ASD and sometimes PDA to allow for R to L shunting to maintain CO
Bicuspid aortic valve
Asymptomatic until adult; hear systolic click and there is a systolic ejection murmur @ right upper sternal border which radiates to carotids
Ventral septal defect
Most common congenital cardiac defect;
Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life;
Most self resolve; larger lesions may lead to LV overload and heart failure; L to R shunt
Atrial septal defect
defect in the interarterial septum; loud S1; side, fixed split S2; Usually occurs in septum secundum; septum primum defects usually occur with no other abnormalities;
Symptoms range from none to heart failure; distinct from patent foramen ovale in that septa are missing tissue rather than unfused; usually presents as exercise intolerance; L to R shunt
Patent ductus arteriosus
If fetal period shunt is R to L; in neonatal where you have decreased lung resistance shunt becomes L to R and you get progressive RVH and/or LVH and heart failure;
Get a persistent machine like murmur; Patency maintained by PGE synthesis and low O2 tension (give indomethacin to close, PGE (alprostadil to keep open); Uncorrected PDA can lead to cyanosis in lower extremities
Eisenmenger syndrome
Uncorrect L to R shunt (VSD, ASD, PDA) leads to increased pulmonary blood flow causing pathogenic remodeling of vasculature leading to pulmonary arteriolar HTN. RVH occurs and then shunt becomes R to L. Causes late cyanosis, clubbing, and polycythemia
Coarctation of the aorta is associated with
Bicuspid aortic valve
Coarctation of the aorta: infantile type
Associated with PDA; aorta narrowing is proximal to insertion of ductus arteriosus (preductal). Associated with Turner syndrome. Can present with closure of the ductus arteriosus (reverse it with PGE2)
Coarctation of the aorta: Adult type
Aorta narrowing is distal to ligamentum arteriosum (postductal). Associated with notching of the ribs AKA scalloping (collateral circulation), HTN in upper extremities, and weak, delayed pulses in lower extremities; Patient will c/o leg pain while exercising
What cardiac abnormality is associated with: 22q11
Truncus arteriosus, tetralogy of fallot
What cardiac abnormality is associated with: Down syndrome
ASD, VSD, AV septal defect (endocardial cushion defect)
What cardiac abnormality is associated with: Congenital rubella
PDA, Septal defects, pulmonary stenosis
What cardiac abnormality is associated with: Turner syndrome
Bicuspid aortic valve coarctation of the aorta (preductal or infantile form)
What cardiac abnormality is associated with: Marfan Syndrome
Mitral Valve prolapse; Thoracic aortic aneurysm and dissection, Aortic regurgitation
What cardiac abnormality is associated with: Infant of diabetic mother
Transposition of the great vessels
HTN: Risk factors
increased age, obesity, diabetes, smoking, genetics, blacks > white > asian
HTN: features of it
90% of HTN is primary (essential) and is related to increased CO and TPR; remaining 10% is secondary to renal disease including fibromuscular dysplasia in young people/
Hypertensive emergency
Severe HTN (180/120 or greater) with evidence of acute, ongoing target organ damage (e.g. papilledema, mental status changes)
HTN predisposes you to
Atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, and aortic dissection; if long standing HTN then you get decreased blood flow in end organ damage and decreased number of arterioles
Fibromuscular dysplasia
narrowing of the lumen (thickening of the wall) in medium and large vessels. Unknown cause.
Targets renal arteries and cerebral vessels; leads to stroke, TIA, headache; hear bilateral bruits on abdominal exam leading to decrease kidney function
Sudden cardiac death
has to be no abnormalities and no drug use;
Long QT; Brugada syndrome; Catecholaminergic polymorphic ventricular tachycardia
Hyperlipidemia signs: what can you see on physical exam (massive hyperlipidemia)
Xanthomas: plaques or nodules composed of lipid laden histiocytes in the skin, especially the eyelids (xanthelasma);
Tendinous Xanthomas are lipid deposits in tendons, especially Achilles (usually sign of familial hyperlipidemia);
Corneal arcus: lipid deposits in cornea, appears early in life with hypercholesterolemia. common in elderly (arcus senilis)
Mockenburg arteriosclerosis
Mock it, nobody cares;
uncommon, calcification in the media of the arteries, especially radial or ulnar, usually benign; pipestem arteries on x ray; does not obstruct blood flow; intima not involved
Arteriolosclerosis
common, two types. 1) hyaline (thickening of small arteries in essential HTN or diabetes) and 2) hyperplastic (onion skin as seen in severe HTN)
Atherosclerosis is a disease of what
Disease of elastic arteries and large and medium size muscular arteries
what are the risk factors for atherosclerosis
Modifiable: smoking, hyperlipidemia, HTN, diabetes
Nonmodifiable: age, sex (Males and postmenopausal women have increased chance), and family history
Disease progression of atherosclerosis
inflammation is important in the disease process;
Endothelial cell dysfunction gives macrophages and LDL a place to enter leading to foam cell formation which eventually turns into fatty streaks. Smooth muscle cell migration (PDGF and FGF), proliferation, and extracellular matrix deposition leads to fibrous plaques and complex atheromas
Complications of atherosclerosis
Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
Location of atherosclerosis
Abdominal Aorta > coronary artery > popliteal artery > carotid artery
Aortic aneurysm
localized pathologic dilation of the aorta. May cause pain, which is a sign of leaking, dissection, or imminent rupture
Abdominal aortic aneurysm
associated with atherosclerosis. Occurs more frequently in HTN male smokers > 50 years old
Thoracic aortic aneurysm
Associated with cystic medial degeneration due to HTN (old patients) or Marfan (younger patients). Also tertiary syphilis (obliterative endarteritis of the vasa vasorum)
Aortic dissection
Longitudinal intraluminal tear forming a false lumen. Associated with HTN, bicuspid aortic valve, and inherited connective tissue disorders (Marfan). Can present as tearing chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in different arms. CXR shows mediastinal widening.
False lumen can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta.
Can result in cardiac tamponade, aortic rupture, and death
Angina: what is it
Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm; no myocyte necoris.
Angina: what are the types
Stable: usually secondary to atherosclerosis; exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest. Variant Type (Prinzmetal): occurs at rest secondary to coronary artery spasm; transient ST elevation on ECG; triggers include tobacco, cocaine, triptans. Treat with Ca channel blocker, nitrates, and stop smoking Unstable/Crescendo: Thrombosis with incomplete coronary artery occlusion; ST depression on ECG (increased frequency or intensity of chest pain; any chest pain at rest)
Coronary steel syndrome
Distal to coronary stenosis, vessels are maximally dilated at rest. Administration of vasodilators (dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well perfused areas leading to decreased flow and ischemia in the post-stenotic region. Principle behind stress tests.
Myocardial infarction
most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis. If transmural ECG will show ST elevation, if subendocardial ECG may show ST depression. Cardio biomarkers (Troponin I, CK-MB) are diagnostic.
Sudden cardiac death
Death from cardiac causes within 1 hour of symptoms, most commonly due to a lethal arrhythmia (like V fib). Associated with CAD, cardiomyopathy, and hereditary ion channelopathies
Chronic ischemic heart disease
progressive onset of CHF over years due to chronic ischemic myocardial damage.
What are the most common carotid arteries to occlude
LAD > RCA > Circumflex
Morphologic changes in heart after a heart attack: 0-4 hours
no gross or microscopic changes; complications to look for would be arrhythmias, HF cardiogenic shock, death
Morphologic changes in heart after a heart attack: 4-12 hours
Grossly you will start to see infarcted area, dark mottling, looks pale with tetrazolium stain;
Microscopically: Early coagulative necrosis, release of necrotic cell contents into blood stream, edema, hemorrhage, wavy;
complications to look for would be arrhythmias, HF, cardiogenic shock, death
Morphologic changes in heart after a heart attack: 12-24 hours
Grossly you will start to see infarcted area, dark mottling, looks pale with tetrazolium stain;
Microscope you see: neutrophil migration starts. Reperfusion injury may cause contraction bands (due to free radical damage);
Complications to look out for: Arrhythmias, HF, cardiogenic shock, death
Morphologic changes in heart after a heart attack: 1-3 days
Grossly you see hyperemia;
Microscope shows: extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation w/ neutrophils
Complications: Fibrinous pericarditis (presents as friction rub and chest pain)
Morphologic changes in heart after a heart attack: 3 to 14 days
grossly: hyperemic borders, central yellow-brown softening, maximally soft and yellow at day 10;
Microscopic findings: Macrophages, then granulation tissue at margins
Complications: free wall rupture leading to a tamponade; papillary muscle rupture leading to mitral regurgitation; inter-ventricular septal rupture due to macrophage mediated structural degradation. LV pseudoaneurysm (mural thrombosis plugs hole in myocardium which leads to “time bomb”
Morphologic changes in heart after a heart attack: 2 weeks to several months
grossly you see gray white scar, recanalized artery;
microscope you see: contracted scar complete;
Complications: dressler syndrome, HF, arrhythmias, true ventricular aneurysm (outward bulge during contraction, “dyskinesia or akinesia”)
How do you diagnose a MI
in first 6 hours ECG is gold standard which shows ST elevation in STEMI and acute transmural infarct, ST depression in subendocardial infarcts, and pathologic Q waves (evolving or old transmural infarct)
Cardiac troponin I is elevated after 4 hours and stays up for 7 to 10 days (most specific marker);
CK-MB is predominantly found in mycardium but is also found in skeletal muscle. Useful in diagnosing reinfarction following MI because levels drop to normal after 48 hours
Types of infarcts
Transural infarcts: increase infarcts, affects entire wall, ST elevation on ECG, Q waves
Subendocardial infarcts: Due to ischemic necrosis
ECG Diagnosis of MI, what leads will show this type of infarct: Anterior Wall (LAD)
V1-V4
ECG Diagnosis of MI, what leads will show this type of infarct: Anteroseptal (LAD)
V1-V2
ECG Diagnosis of MI, what leads will show this type of infarct: Anterolateral (LAD and LCX)
V4-V6
ECG Diagnosis of MI, what leads will show this type of infarct: Lateral wall (LCX)
I, aVL
ECG Diagnosis of MI, what leads will show this type of infarct: Inferior wall (RCA)
II, III, aVF
Dressler syndrome
autoimmune reaction after an MI. Attacks the fibrinous pericarditis (4-6 weeks post MI);
Fever, positional substernal chest pain, loud friction rub, Diffuse ST elevations
Dilated Cardiomyopathies: Causes
Most common type of cardiomyopathy; often idiopathic or congenital; known causes include Alcohol abuse, wet Beriberi, Coxsackie B virus, Cocaine, Chagas, Doxorubicin toxicity, hemocrhomatosis and peripartum cardiomyopathy
Dilated cardiomyopathies: Findings and treatments
Findings: Heart failure, S3, dilated heart on echo, balloon appearance of heart on CXR, systolic dysfunction (decreased ejection fraction and contractility)
Treatment: Na restriction, ACE inhibitors, Beta blockers, diuretics, digozin, implantable cardioverter defibrillator, heart transplant (goal is to decrease BP, HR, and heart workload)
Hypertrophic cardiomyopathies
60 to 70% are familial, autosomal dominant (commonly a beta myosin heavy chain mutation). Rarely can be associated with Friedreich ataxia. Causes sudden death in athletes, due to ventricular arrhythmia.
Findings: S4, systolic murmur, diastolic dysfunction (preserved EF or increased EF)
Treatment: stop strenuous activity, use beta blockers or non dihydropyridine Ca channel blockers (verapamil). ICD if patient is high risk.
What is the mechanism of obstructive cardiomyopathies
a subset of hypertrophic; hypertrophied septum too close to anterior mitral leaflet causing outflow obstruction leading to dyspnea, possible syncope
Restrictive/infiltrative cardiomyopathies
Major causes are sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis (dilated cardiomyopathy can also occur);
Get diastolic dysfunction. Can have low voltage ECG even though you have thick myocardium (especially amyloid)
CHF
Clinical syndrome of cardiac pump dysfunction. Symptoms include dyspnea, orthopnea, and fatigue, signs include rales, JVD, and pitting edema.
CHF: systolic dysfunction
Low EF, poor contractility, often secondary to ischemic heart disease or DCM.
CHF: diastolic dysfunction
preserved or increased EF, normal contractility, impaired relaxation, decreased compliance (S4 sound),
CHF: right heart failure
usually secondary to left heart failure; isolated right heart failure usually due to cor pulmonale
CHF: Treatments
ACE inhibitors, beta blockers (except in acute decompensated HF), angiotensin II receptor blockers, and spironolactone decrease mortality. Thiazide and loop diuretics are for symptomatic relief. Hydralazine with nitro therapy improves both symptoms and mortality in some patients.
CHF: hemosiderin laden macrophages
AKA heart failure cells. Blood backs up in lungs increases pressure, RBCs lead out, macrophages eat them, macrophages fill with iron from RBCs.
Hepatomegaly from heart failure
due to Right heart failure; increased central venous pressure causing increased resistance to portal flow. see nutmeg liver and can progress to “cardiac cirrhosis”
Jugular venous distension measures
measures central venous pressure (which is a reflection of RA pressure and not volume). Great than 4 cm and you have a problem.
Bacterial Endocarditis: symptoms, valves involved, complications
Fever (most common symptom), new murmur, Roth spots (round white spots on retina surrounded by hemorrhage), Osler nodes (tender raised lesions on finger or toe pads), Janeway lesions (small, painless, erythematous lesions on palm and sole), anemia, splinter hemorrhages on nail bed. Multiple blood cultures necessary for diagnosis;
Mitral valve is most frequently involved, Tricuspid think IV drug abuse;
Chordae rupture, glomerulonephritis, suppurative pericarditis, emboli
Acute Bacterial Endocarditis: what bug
S. aureus (high virulence), Large vegetations on previously on previously normal valves. Rapid onset.
Subacute bacterial endocarditis: what bug
Viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.
Culture negative endocarditis: what bugs
Most likely Coxiella burnetti and Bartonella spp.
What are roth spots
Type III Hypersensitivity causes emboli, retinal hemorrhage
What are Osler nodes
Type III hypersensitivity causes emboli; painful red raised lesions found on hands and feet
What are Janeway Lesions
Emboli, not immune mediated; non tender red lesions on hands and feet
What are Nail-bed hemorrhage
Emboli, not immune mediated; blood clots that happen under the nails due to small vessels
Rheumatic fever
consequence of Beta hemolysis strep. Early deaths due to myocarditis, Late sequelae includes rheumatic heart disease, which affects heart valves Mitral > Aortic >> tricuspid (high pressure valves), Early lesion is mitral valve regurgitation. Late lesion is mitral stenosis. Associated with Aschoff bodies (granuloma with giant cells), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod like nucleus), Increase ASO titer; Immune mediated (Type II) not a direct effect of bacteria, Antibodies to M protein react with heart valve cells
Rheumatic FEVERSS stands for
Fever, Erythema marginatum, Valvular damage (vegetation and fibrosis), increased Esr, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, St. Vitus’ dance (Sydenham chorea)
Acute pericaridits
Commonly presents with sharp pain, aggravated by inspiration, relieved by sitting up and leaning forward, friction rub, ECG shows widespread ST elevation and/or PR depression; 3 types Fibrinous, Serous, Suppurative/Purulent
Acute pericarditis: Fibrinous type
Caused by Dressler syndrome, uremia, radiation. Presents with loud friction rub.
Acute pericarditis: Serous type
Viral pericarditis (often resolves spontaneously); noninfectious inflammatory diseases (e.g. rheumatoid arthritis, SLE)
Acute pericarditis: Suppurative/Purulent type
Usually caused by bacterial infections (e.g. pneumococcus, Streptococcus). Rare now with antibiotics.
Cardiac Tamponade
Compression of heart by fluid in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers. Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), increased HR, pulsus paradoxus, Kussmaul sign, ECG shows low voltage QRS and electric alternans (due to “swinging” movement of heart in large effusions
What is pulsus paradoxus
Decrease in amplitude of systolic blood pressure by >10 mmHg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup
Syphilitic heart disease
Tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilation of the aorta and valve ring;
May see calcification of the aortic root and ascending aortic arch. leads to tree bark appearance of the aorta.
Cardiac tumors are mostly
most common heart tumor is a metastasis (e.g. melanoma, lymphoma), but it is still rare.
Cardiac tumors: Myxoma
Most common primary cardiac tumor in adults. 90% occur in atria (mostly left atrium). Myxomas are usually described as a ball valve obstruction in the left atrium (Associated with multiple syncopal episodes)
Cardiac tumors: Rhabdomyomas
Most frequent primary cardiac tumor in children (associated with tuberous sclerosis)
Kussmaul signs
Increased in JVP on inspiration instead of normal decrease;
Inspiration leads to negative intrathoracic pressure not transmitted to heart causing impaired filling of right ventricle leading to blood backs up into venae cavae causing JVD. May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.
Raynaud phenomenon
Decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress. Most often in the fingers and toes. Called raynaud disease when primary (idiopathic), Raynaud syndrome when secondary to a disease process such as mixed connective tissue disease, SLE, CREST syndrome.
Strawberry hemangioma
benign capillary hemangioma of infancy. Appears in the first few weeks of life (1/200 births); grows rapidly and regresses spontaneously at 5-8 years old.
Cherry hemangioma
Benign capillary hemangioma of the elderly. Does not regress. Frequency increase with age.
Pyogenic granuloma
Polypoid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy.
Cystic hygroma
Cavernous lymphangioma of the neck. Associated with turners syndrome.
Glomus tumor
Benign, painful, red-blue tumor under fingernails. Arises from modified muscle cells of glomus body.
Bacillary angiomatosis
Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaken for Kapose sarcoma.
Angiosarcoma
Rare blood vessel malignancy typically occuring in the head, neck, and breast areas. Usually in elderly sun exposed areas. Associated with radiation therapy and arsenic exposure. Very aggressive and difficult to resect due to delay in diagnosis.
Lymphangiosarcoma
Lymphatic malignancy associated with persistent lymphedema (e.g. post radical mastectomy)
Kaposi sarcoma
Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis
Temporal (Giant cell arteritis)
Generally elderly females; Unilateral headache (temporal artery), jaw claudication.
May lead to irreversible blindness due to opthalmic artery occlusion.
Associated with polymyalgia rheumatica;
Focal granulomatous inflammation (do biopsy, may not see it because it is focal) leads to increased ESR, usually affects branches of the aorta,
Treat with high dose corticosteroids
Takayasu arteritis
think asian females
polyarteritis nodosa
young adults; Associated with Hep B (30%) and C, Fever, weight loss, malaise and headache. GI symptoms of melena and abdominal pain. HTN, neuro dysfunction, cutaneous eruptions, renal damage. See increased ESR and CRP. Typically involves renal and visceral vessels but spares lungs. Immune complex mediated. Transmural inflammation of arterial wall with fibrinoid necrosis (likes muscular arterioles). tons of micro-aneurysms. Treat with corticosteroids and cyclophosphamide.
Kawasaki Disease
Asian kids
Buerger disease (thromboangiitis obliterans)
Heavy smokers, males,
Granulomatosis with polyangiitis
weCener disease. Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis. Lower respiratory tract: hemoptysis, cough, dyspnea. Renal: hematuria, red cell casts.
Triad is: Focal necrotizing vasculitis, Necrotizing granulomas in the lungs and upper airway, Necrotizing glomerulonephritis.
Diagnose with PR3-ANCA/c-ANCA (anti-proteinase 3), CXR shows large nodular densities.
Treat with cyclophosphamide and corticosteroids
Microscopic polyangitis
Necrotizing vasculitis commonly involving the lungs, kidneys, skin with pauci-immune glomerulonephritis and palpable purpura. Presentation similar to granulomatosis with polyangiitis but with NO nasal involvement.
No granulomas, MPO-ANCA/p-ANCA (anti-myeloperoxidase). Treat with cyclophosphamide and corticosteroids.
Churg-Strauss syndrome
Asthma, sinusitis, palpable purpura, peripheral neuropathy (e.g. wrist/foot drop). Can also involve the heart, GI, kidneys (pauci-immune glomerulonephritis).
Granulomatous, necrotizing vasculitis with eosinophilia.
MPO-ANCA/p-ANCA (anti-myeloperoxidase), increased IgE
Henoch-Schonlein purpura
Most common childhood systemic vasculitis, follows URIs; Classic triad: Skin (palpable purpura on butt/legs), Arthralgias, GI (abdominal pain, melena, multiple lesions of same age).
Vasculitis secondary to IgA complex deposition. Associated with IgA nephropathy.
Treatment for primary essential HTN
Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), Calcium channel blockers
Treatment for HTN with CHF
Diuretics, ACE inhibitors/ARBs, beta blockers (must be compensated CHF), aldosterone antagonists
HTN with diabetes
ACE inhibitors, ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers (ACEs and ARBs are kidney protective)
Calcium channel blockers: names, mechanism
Dihydropyridines (-dipines, amlodipine, nimodipine, nifidipine); non-dihydropyridines (diltiazem, verapamil);
Mechanism: block voltage gaited L type Ca channels of cardiac and smooth muscle causing reduced muscle contractility.
Targets for smooth muscle: amlodipine=nifidipine > diltiazem > verapamil
Target for heart: verapamil > Diltiazem > amlodipine=nifedipine
Calcium channel blockers: clinical use
Dihydropyridine (-dipines, except nimodipine): HTN, angina (including prinzmental), Raynaud
non-dihydropyridine (verapamil, diltiazem): HTN, angina, atrial fib/flutter
Nimodipine: Subarachnoid hemorrhage (prevents cerebral vasospasm)
Calcium channel blockers: side effects
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation.
Hydralazine
mechanism: increases cGMP causing smooth muscle relaxation. Vasodilates arteries > veins (kinda opposite of nitro); afterload reduction;
Uses: severe HTN, CHF. 1st line for HTN in pregnancy, with methyldopa. co-administered with beta blocker to prevent reflex tachycardia.
Toxicity: compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus like syndrome.
Hypertensive emergency: treatment
Commonly used drugs are nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.
Nitroprusside
short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity; used for hypertensive emergency
Fenoldopam
Dopamine D1 receptor agonist: coronary, peripheral, renal, and splenic vasodilation. decreased BP and increased natriuresis. Used in hypertensive emergencies.
Nitroglycerin, isosorbide dinitrate
Mechanism: vasodilate by increased NO in vascular smooth muscle causing increased cGMP and smooth muscle relaxation. dilates veins»_space; arteries. Decreases preload.
Uses: angina, acute coronary syndrome, pulmonary edema
Toxicity: reflex tachycardia (treat with beta blockers), hypotension, flushing, headacne
What is Monday disease in industrial exposure to Nitroglycerin?
Development of tolerance for the vasodilating effects during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon re-exposure
What do nitrates do to cardiac function measurements: End-diastolic pressure, blood pressure, contractility, heart rate, ejection time, MVO2
End-diastolic pressure decreases, blood pressure decreases, contractility increases (reflex), heart rate increases (reflex), ejection time (Decreases), MVO2 (Decreases)
What do beta blockers do to cardiac function measurements: End-diastolic pressure, blood pressure, contractility, heart rate, ejection time, MVO2
End-diastolic pressure (increase), blood pressure (decreases), contractility (decrease), heart rate (decreases), ejection time (increases), MVO2 (decrease)
What do nitrates + beta blockers do to cardiac function measurements: End-diastolic pressure, blood pressure, contractility, heart rate, ejection time, MVO2
End-diastolic pressure (no effect or decreased), blood pressure (Decrease), contractility(no effect), heart rate (decreased), ejection time (no effect), MVO2 (massive decrease)
HMG-CoA reductase inhibitors
-statins; massively decrease LDL, decrease triglycerides, increase HDL; inhibit conversion of HMG-CoA to mevalonate which is a cholesterol precursor;
Side effects: Hepatotoxicity (increases LFTs), rhabdomyolysis (esp. when used with fibrates and niacin)
Niacin (Vit B3)
decreased LDL, really increase HDL (why we give it), decrease triglycerides; inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis;
Side effects: red flushed face which in decreased by taking aspirin, hyperglycemia (acanthosis nigricans), hyperuricemia (gout)
Bile acid resins
(Chole-) cholestyramine, colestipol, colesevelam; Big LDL decrease; prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more; Patients hate it, tastes bad, GI problems, cholesterol gall stones, decreased fat soluble vitamin absorption
Fibrates
(-fibrate), clofibrate, bezafibrate, fenofibrate, gemfibrozil; decreases LDL, increases HDL, massive decrease in triglycerides; upregulates LPL leading to increased TG clearance; activates PPAR-alpha to induce HDL synthesis.
Side effects: myositis (increased risk with concurrent statins), hepatotoxicity (increased LFT), cholesterol gallstones
Cardiac glycosides (digoxin): mechanism and uses
Direct inhibition of Na/K ATPase, leading to inhibition of Na/Ca exchanger, increased intracellular Ca levels, positive inotrope. Stimulates vagus nerve causing decreased HR.
Used for CHF (increases contractility); atrial fib (decreased conduction at AV node and depression at SA node)
Digoxin toxicity
Cholinergic: nausea, vomiting, diarrhea, blurry yellow vision; ECG shows increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block/
Can lead to hyperkalemia which indicates poor prognosis.
Factors predisposing to toxicity: renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K binding site on Na/K ATPase), verapamil, amiodarone, quinidine (decreased digoxin clearance; displaces digoxin from tissue binding sites). Don’t give with K wasting diuretics.
Digoxin antidote
Slowly normalize the K levels, cardiac pacer, antidigoxin Fab fragments, Mg2+
Na channel blockers Class IA: name them
Quinidine, Procainamide, Disopyramide “the Queen Proclaims Diso’s pyramid”
Na channel blockers Class IA: Mechanism and use
Mechanism: Increase AP duration, increased effective refractory period.
Uses: Both atrial and ventricular arrhthmias, especially re-enterant and ectopic SVT and VT
Na channel blockers Class IA: Toxicity
Conchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), Heart failure (disopyramide), thrombocytopenia, torsades de pointes due to increased QT interval
Na channel blockers Class IB: Names
Lidocaine, mexiletine, Phenytoin can also fall into this category.
Na channel blockers Class IB: Mechanism, uses
Mechanism: decreases AP duration, Preferentially affects ischemic or depolarized purkinje and ventricular tissue.
Uses: acute ventricular arrhythmias (Especially post MI), digitalis induced arrhythmias, 1B is Best post MI
Na channel blockers Class IB: Toxicity
CNS stimulation/depression; cardiovascular depression
Na channel blockers Class IC: Names
Flecainide, Propafenone (Can i have Fries Please)
Na channel blockers Class IC: Mechanism and uses
Mechanism: Significantly prolongs refractory period in AV node, minimal effect on AP duration;
Uses: SVTs, including atrial fib. Only used as last resort in refractory VT
Na channel blockers Class IC: Toxicity
Proarrhythmic; 1C is Contraindicated post MI and ischemic heart disease.
Na channel blockers Class 1: Give me an overview of what they do
Slow or block conduction (especially in depolarized cells). Decrease slope of phase 0 and increased threshold for firing in pacemaker cells. Are state dependent (act more on depolarized cells so they will target tachycardic areas); Hyperkalemia causes increased toxicity for all Type 1 drugs.
Antiarrhythmics Type II (Beta blockers): names
-olol (and carvedilol)
Antiarrhythmics Type II (Beta blockers): Mechanism
Decrease SA and AV node activity by decreasing cAMP, and Ca currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV especially sensitive, increases PR interval. Esmolol is very short acting
Antiarrhythmics Type II (Beta blockers): Clinical uses
SVT, slowing ventricular rate during atrial flutter and fibrillation
Antiarrhythmics Type II (Beta blockers): Toxicity
Impotence, Makes COPD and asthma worse, heart block, bradycardia, sedation, sleep alterations. May mask the signs of hypoglycemia. Metoprolol can cause dyslipidemia, Propranolol can cause vasospasm in Prinzmetal angina. Contraindicated in cocaine users (unopposed alpha receptor agonist activity), treat overdose with glucagon
Beta blockers can cause heart block: how will this normally present on ECG
ECG may show mobitz type II AV block (Some P waves will not be followed by QRS, but every QRS has a P wave before it)
Antiarrhythmics Type III K channel blockers: names
Amiodarone (has class 1, 2, 3, and 4 effects), Ibutilide, Dofetilide, Sotalol (AIDS)
Antiarrhythmics Type III K channel blockers: Mechanism
Increase AP duration, Increase ESR. Used only when other antiarrythmics fail. Increases QT interval.
Antiarrhythmics Type III K channel blockers: Clinical use
Atrial Fib, atrial flutter, Ventricular tachycardia (amiodarone, sotalol)
Antiarrhythmics Type III K channel blockers: Toxicity
Sotalol: Torsades de pointes, excessive Beta blockade;
Ibutilide: Torsades de pointes;
Amiodarone: pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine), corneal deposits, skin deposits (blue/gray), resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF
Antiarrhythmics Type IV Calcium channel blockers: Names
Verapamil, Diltiazem (non-dihydropyridines)
Antiarrhythmics Type IV Calcium channel blockers: Mechanism, uses
Mechanism: decrease conduction velocity, increase ERP, increase PR interval;
Uses: Prevention of nodal arrhythmias (e.g. SVT), rate control in atrial fib.
Antiarrhythmics Type IV Calcium channel blockers: Toxicity
Constipation, flushing, edema, CHF, AV block, sinus node depression
Adenosine
Anti-arrythmic;
Increases K outside of cells leading to hyperpolarization and decreased Ca entering cell. Drug of choice for diagnosing and treating supraventricular tachycardia. Very short acting (15 seconds). Adverse effects are hypotension, chest pain, and flushing. Effects blocked by theophylline and caffeine
Mg2+ as an anti-arrythmic
Effective in torsades de pointes and digoxin toxicity.
What does the heart do when you have severe anemia
The decrease hemoglobin and decrease hematrocrit (hematocit is more important) cause decrease viscosity of blood. You get decreased peripheral resistance. The heart has increased HR, Stroke Volume, Pulse Pressure, and CO. you may get high output cardiac failure.
