First Aid Cardio Flashcards
CCB best for
(a) Prevent cerebral vasospasm in subarachnoid hemorrhage
(b) Hypertensive urgency/emergency
(c) AFib/Aflutter
(d) Raynaud’s
(e) HTN
CCB used for
(a) Prevention of cerebral vasospasm as complication of SAH = Nimodipine
(b) Hypertensive urgency = Clevidipine
(c) AFib/Flutter = non-dihydropiridines (act on the heart)- Verapamil, Diltiazem
(d) Raynaud’s = dihydropyridines (amlodipine)
(e) HTN- can use either dihydropyridine or non-dihydropyridine
RF for thoracic aortic aneurysm
Thoracic aortic aneurysms occur 2/2 medial cystic degeneration which is a vascular pathology of large BVs seen in connective tissue d/o (so Marfans, Ehler-Danlos)
Thoracic aortic aneurysm also historically seen in tertiary syphilis
ABCDEs of drug-induced prolonged QT
Drug-induced prolonged QT
Anti-arrthymics: class IA, III Anti-biotics: macrolides Anti-Cycotics: Haldol Anti-depressants: TCAs Anti-emetics: ondansetron (zofran)
Effect of ACEi and ARBs on preload and afterload
ACEi and ARBs both decrease both preload and afterload
Differentiate how receptors in the aortic arch vs. the carotid sinus conveys changes in BP to the CNS
Receptors in the aortic arch send signals via the vagus nerve (CN X) to the solitary nucleus of the medulla
Carotid sinus receptors relay messages thru glossopharyngeal nerve (CN IX) to solitary nucleus of the medulla
Which would present w/ earlier cyanosis: R to L or L to R cardiac shunts
R to L shunt (5 Ts of cyanosis) present earlier than L to R shunt (ex: VSD)
Takayasu arteritis
(a) Populaiton
(b) Clinical presentation
(c) Vessel affected
Takayasu arteritis = large vessel granulomatous vasculitis MC affecting aorta and its branches
(a) See in young (under 40 yo) Asian F
(b) Also called pulselessness disease b/c of weak upper extremity pulses
(c) Also called aortic arch syndrome
Differentiate the physiology of systolic vs. diastolic HF
Systolic HF is due to weakness of contraction (inotropic deficit) while diastolic dysfunction is due to reduced compliance due to myocardial hypertrophy
Systolic = can't properly contract Disastolic = can't properly relax
2 main indications of digoxin
Digoxin (positive inotrope and reduces HR) indications
- HF/LV dysfunction
- AFib b/c reduces AV nodal conduction and depresses AV node
- so reduces ventricular rate in AFib
How does hand grip change murmurs?
Hand grip increases afterload
- increases most murmurs (AS, MR)
- decreases HOCM murmur
Locate the infarct (and which artery is involved) if you see ST elevations or Q waves in the following
(a) V1-V2
(b) V3-V4
(c) V5-V6
(d) I, aVL
(e) II, III, aVF
Location of infarct
(a) Anteroseptal (LAD)
(b) Anteroapical (distal LAD)
(c) Anterolateral (LAD or LCx)
(d) Lateral (LCx)
(e) Inferiorly (RCA)
Name 4 systolic murmurs
4 systolic murmurs = AS, MR, VSD, MVP
Blood test lab value helpful in diagnosing heart failure
BNP (brain naturitic peptide)- released by ventricular myocytes in response to high wall tension, functions to promote diuresis by kidneys
Very good negative predictive value for HF (so if not elevated, can r/o HF)
Kawasaki disease
(a) What population?
(b) Clinical features
Kawasaki disease = medium vessel vasculitis
(a) Children under 4 yo, Asian
(b) Clinically: CRASH and burn
- Conjunctivitis- classically limbic sparing
- Rash
- Adenopathy- cervical
- Strawberry tongue
- Hand/foot changes- edema/erythema
- burn b/c fever for 5/7+ days
Describe the quality of the murmur heard in mitral stenosis
Mitral stenosis = late diastolic murmur following opening snap
Explain physiologic S2 splitting
S2 splits into A2 and P2 physiologically w/ inspiration b/c inspiration drops intrathoracic pressure which increases venous return
Increased venous return = more blood in the right heart, more time needed for RV to empty => delayed pulmonic closure
Describe how an untreated L to R shunt over time can cause late onset clubbing (Eisenmengers)
Eisenmengers = untreated L to R shunt causes eventual R to L shunt => late-onset cyanosis, clubbing, polycythemia
L to R shunt increases blood flow into pulm vasculature => pulm HTN => RVH => R to L shunt
Drug to decrease mortality in CAD pts
Statins (HMG CoA reductase)
Child 1 wk s/p URi p/w belly pain and red rash on buttocks and legs
(a) Dx
(b) Mechanism of disease
(a) HSP = Henoch-Schonlein purpura
- Clinical triad: skin-palpable purpura on butt/legs, arthralgias, abd pain
- following URI
- associated w/ IgA nephropathy => blood/protein in urine
(b) IgA complex deposition
What is the most common coronary artery to get occluded?
LAD (widow makerrrr)
Lab values to check in pt on amiodarone
Amiodarone is a dirty antiarrhythmic, w/ features of all 4 classes of drug (but is technically class III b/c it’s a K+ channel blocker)
Monitor 2 lab values: TFTs and LFTs q6 mo
-and EKG at baseline
What makes S1 and S2?
S1 = closing of AV valves (tricuspid and mitral)
S2 = closing of aortic and pulmonic valves
Key to management of cardiac glycoside toxicity
Management of glycoside toxicity
- pacer or management of any arrhythmias
- gradually normalize K+
- -Anti-dig Fab fragments = Dig-specific antibody
- Mg2+
Types of shock where skin is cold and clammy
Skin is cold and clammy in most shock (cardiogenic, hypovolemic)
Skin is warm/dry in distributive = neurogenic/anaphylactic
What is coarctation of the aorta?
(a) Location of defect
(b) Associated conditions
(c) CXR finding
(d) Clinical findings
Coarctation of the aorta = critical narrowing of the aorta
(a) Often juxtaductally (near the ductus arteriosus)
(b) Associated w/ bicuspid aortic valve and Turners syndrome
(c) CXR: rib notching, collaterals expand and erode ribs
(d) HTN in arms, weak delayed pulse w/ low BP in legs (brachial-femoral delay)
Name the 4 parts of Tetrology of Fallot
PROV
- Pulmonary infundibular stenosis
- RVH
- Overriding aorta
- VSD
Embryologic cause of
(a) persistent truncus arteriosus
(b) transposition of the great vessels
(c) tetrology of fallot
Embryology (gahhh Rindler no)
(a) Persistent truncus from failure of truncus division from lack of aorticopulmonary septum formation
(b) TGA due to failure of the aorticopulmonary septum to spiral
(c) ToF from anterosuperior displacement of the infundibular septum
How long after MI do you expect
(a) Neutrophils vs. macrophages to come on the scene
(b) Free wall rupture
(c) Dressler syndrome
Post-MI
(a) Neutrophils come first (w/in 4-12 hrs), then macrophages later around 3 days
(b) Highest risk of free wall rupture at 3-10 days
(c) Dressler syndrome (autoimmune post-MI pericarditis) several weeks post-MI
Ductus arteriosus
(a) How to keep open
(b) How to shut
Ductus arteriosus
(a) Keep open w/ prostaglandin E2
“kEEp opEn w/ E2”
(b) Shut w/ indomethacin (NSAID)
Function of ANP
ANP (atrial naturitic peptide) functions to promote diuresis in the setting of high blood volume and atrial volume
- released by atrial myocytes in responseto high volume and high atrial pressures
- causes vasodilation and decreased Na+ reabsorption in kidney => promoting diuresis
- contributes to aldo escape mechanism (aldo high but still diures)
Name the 4 locations of fetal erythropoiesis
“young liver synthesizes blood”
Yolk sac for first 3-8 weeks
Liver from 6 weeks to birth
Spleen from 10-28 weeks of life
Bone marrow from 18 weeks to adulthood
What does it mean to be right heart dominant?
PDA (posterior descending artery/interventricular artery) arises from the right carotid artery- 85% of the population
While 8% are L. dominant where the PDA arises from the LCx
Describe coronary steal syndrome and how it explains pharmacologic stress tests
Coronary steal syndrome: at rest the post-stenotic arterial segment is maximally dilated, so upon administrating vasodilator (dipyridamole, regadenoson) blood is actually shunted towards already well perfused areas of the heart, causing loss of flow to the areas that need it (and just can’t dilate anymore b/c already maximally dilated at rest)
What embryologic structure gives rise to the ascending aorta
Truncus arteriosus => ascending aorta and pulmonary trunk
VSD
(a) Describe the quality of the murmur
(b) Location of the murmur
VSD
(a) Harsh holosystolic murmur
(b) Typically heard loudest at the tricuspid area
MC primary cardiac tumor in
(a) Adults
(b) Children
MC primary cardiac tumors in
(a) Adults = myxomas- usually in the LA
Rheumatic fever
(a) Early vs. late valvular finding
(b) Tx
(c) Major criteria
Rheumatic fever
(a) Early lesion is MR, late lesion is MS
(b) Penicillin
(c) Major criteria = JO(heart shaped)NES for clinical findings of rheuamtic fever
Joints- migrating polyarthritis
Cardiac
Nodules in skin (subcutaneous)
What do the following embryologic structures become
(a) Allantois
(b) Ductus arteriosus
(c) Foramen ovale
(d) Notochord
(e) Umbilical arteries
(f) Umbilical vein
Embryologic derivatives
(a) AllaNtois => urachus (connects bladder and umbilicus) => mediaN umbilical ligament
(b) Ductus arteriosus => ligamentum arteriosum
(c) Foramen ovale => fossa ovalis
(d) Notochord => nucleus pulposis btwn vertebrae
(e) UmbilicaL arteries => mediaL umbilical ligament
(f) Umbilical vein => falciform ligament
Differentiate effects of venodilators vs. vasodilators on preload and afterload
vEnodilators (ex: nitroglycerin) decrease prEload
-explains why to not give pts w/ inferior MI sublingual nitro, b/c they’re preload dependent to maintain CO
vAsodilators (hydrAlAzine) decrease Afterload
What is isovolumetric relaxation?
Isovolumetric relaxation = time between when pulmonic/aortic valves close and the AV valves open
Name the mechanism of the classes of antiarrhythmis
(a) I
(b) II
(c) III
(d) IV
Antiarrhtyhmics
(a) I = Na+ channel blockers, reduces the slope of phase 0
(b) II = beta-blockers, reduces slope of phase 4, reduces SA and AV node activity
(c) III = K+ channel blockers
Mitral valve prolapse
(a) Describe the quality of the murmur
(b) Location of the murmur
MVP
(a) Late systolic crescendo murmur w/ midsystolic click
(b) Over the apex, heard best just before S2
Bacterial endoarditis
(a) Most frequently involved valve
(b) Valve associated w/ IV drug use
(a) Mitral- almost most frequently involved in rheumatic fever
(b) “dont TRI drugs”- tricuspid valve vegetations associated w/ IVDU
Differentiate S3 and S4
(a) Timing
(b) Implications
S3 happens in early diastole
- indicates elevated filling pressures (HF, MR) and in dilated ventricles
- can be normal in children and pregnant F
S4 happens in late diastole
- indicates high atrial pressure and ventricular hypertrophy
- LA pushing against a stiff LV wall
How does inspiration change heart sounds?
Inspiration decreases intrathoracic pressure => increases venous return => increases preload so increases right sided heart sounds (like S1)
Clinical manifestations of bacterial endocarditis
“FROM JAME”
FROM JANE
Fever
Roth spots = round white spots on retina surrounded by hemorrhage
Osler nodes = tender raised lesions on finger or toe pads
Murmur- of new onset
Janeway lesions = small, painless, erythematous lesions on palm or soles
Anemia
Nail-bed (splinter) hemorrhage
Emboli (septic arterial or pulmonary)
Define
(a) HTN
(b) Hypertensive urgency
(c) Hypertensive emergency
(a) HTN = over 140, over 90
(b) hypertensive surgery: severe HTN (over 180, over 120) w/o e/o end organ damage
(c) Over 180, over 120 w/ evidence of end organ damage
- stroke, MI, retinal hemorrhage, papilledema, encephalopathy, aortic dissection, eclampsia
What is the Starling curve?
Starling curve = compares preload to cardiac output/SV
So at any given preload, how much of it will the heart output
-shows how HF will have much lower CO at a given preload
Name some positive inotropes
Inotropes increase contractility
- Digoxin (Na/K channel blocker) increases contractility by increasing intracellular Ca2+
- Catecholamines (Dopamine, epi, norepi)
- exercise
What is Brugada syndrome?
(a) EKG pattern
(b) Risk
(c) Prevention
Brugada syndrome = aut dom d/o w/ characteristic EKG and increased risk of sudden cardiac death from VF
-MC in asian males
(a) EKG: pseudo-right bundle branch block w/ ST elevations in V1-V3
(b) Risk = sudden cardiac death
(c) ICD = implantable cardioverter-defibrillator
Name 2 etiologies of wide S2 splitting
Wide S2 splitting caused by things that delay closure of the pulmonic valve
- pulmonic stenosis
- RBBB
Differentiate baroreceptors and chemoreceptors
Both are located at the carotid body (swelling at the bifurcation of common carotid artery) and in the aortic arch
Baroreceptors repsond to stretch (carotid massage, pressure due to elevated ICP) while chemoreceptors respond to change in pCO2 and pH (and peripherally to low pO2)
Differentiate the 4 types of AV block
1st degree block = benign, prolongation of PR interval to over 200 ms
2nd degree
- Mobitz Type I (Wenckebach): progressive lengthening of PR interval until dropped beat, regularly irregular
- Mobitz Type II: dropped beats not preceded by PR prolongation, may progress to 3rd degree so often tx w/ pacemaker
3rd degree = presence of P-waves and QRS complexes but completely independent of each other
What is a J point on EKG?
J point = junction btwn the end of the QRS and the start of the ST segment
Unique feature of pulmonary vasculature
Pulmonary vasculature is the one place that vasoconstricts in response to hypoxia
- high CO2 in brain/heart causes vasodilation, while in lungs high CO2 causes vasoconstriction so that only well-ventilated areas are perfused
- selective vasoconstriction to make the best V/Q match
Which lipid lowering agent increases the risk of cholesterol gallstones
Fibrates (best at reducing TG) can cause cholesterol galstones
Name 3 shunts found in utero not found in the fetus
- Ductus venosus connecting umbilical vein to IVC
- Foramen ovale connecting RA and LA
- bypass the lungs - Ductus arteriosus shunts from pulmonary artery (R. heart) into the descending aorta
- 2/2 high fetal pulmonary artery resistance
Describe the quality of the murmur heard in aortic regurgitation
Aortic regurg = early diastolic decrescendo murmur, high pitched
Predictor of mortality in cardiac glycoside activity
In digoxin toxicity, hyperkalemia (presence and degree) determines prognosis and is associated to mortality
Tetrology of fallot
(a) most important factor for prognostic determination
(b) CXR finding
(c) Classic clinical feature
(d) Response to squatting
(e) Tx
ToF
(a) Degree of pulmonary stenosis determines prognosis
(b) Boot shaped heart 2/2 RVH
(c) Tet spells (blue spells) where baby hugs knees into chest (squatting to increase SVR)
(d) Squatting improves cyanosis b/c increases SVR and decreases the R to L shunt
(e) Tx is early surgical correction
Name the congenital heart defect(s) associated w/ the following d/o
(a) Fetal alcohol syndrome
(b) Congenital rubella
(c) Down syndrome
(d) Maternal diabetes
(a) FAS => VSD, ASD, ToF, PDA
(b) Congenital rubella => pulmonary artery stenosis and patent ductus
(c) Down => endocardial cushion defect (causing AV septal defect)
(d) Maternal diabetes => transposition of great vessels
Name 3 places in the body where lipid-laiden histiocytes are MC to deposit 2/2 hyperlipidemia
Xanthomas = lipid-laiden histiocytes deposit in nodules/plauqes
- skin, especially eyelides (xanthelomas)
- also in the cornea, causing earlier onset of corneal arcus (rim around cornea)
Main features of cardiac glycoside toxicity
Cardiac glycoside (digoxin) toxicity
- -cardiac arrhythmias (really can cause any)
- -electrolyte abnormalities: mainly hyperkalemia
- visual changes
- cholinergic: nausea/vom/dio
Etiologies of right HF
MC cause of R HF is left HF
R HF w/o L HF = cor pulmonale- due to pulm HTN and other lung pathology
Differentiate physiologic cardiac action potential from pacemaker action potential
Talking physiologic pacemaker (not external) so like SA and AV node
Similar (obvs) except for fast-gated Na+ channels (responsible for rapid depolarization in step 0) are permanently inactivated
-phase 0 done by opening of voltage-gated Ca2+ channels => slow conduction velocity used by AV node to delay transmission from A to V
Then Ca2+ inactivated and K+ activated (same as non-pacemaker regions)
Stage 4 is a slow spontaneous depolarization (upstroke)
-slope of this stage 4 at the SA node determines HR
3 clinical manifestations of aortic stenosis
AS- SAD
syncope
angina
dyspnea on exertion
Bacteria implicated in endocarditis and
(a) acute rapid onset w/ no previously abnormal valves
(b) congenitally abnormal or diseased valve w/ gradual onset
(c) colon cancer
(d) prosthetic valves
(e) after dental procedure
Bacterial endocarditis
(a) Acute, staph aureus
- high virulence
(b) Gradual onset on diseased valve (subacute)- strep viridans
(c) Colon cancer- think strep bovis (gallolyticus)
(d) Prosthetic valve- staph epidermis
(e) Post-dental procedure = strep viridans => subacute
How is cardiac output maintained
(a) Early in exercise
(b) Later in exercise
Cardiac output
(a) Early in exercise both stroke volume and HR increase to maintain
(b) Then SV plateaus and elevated HR maintains CO the rest of exercise
What can cause fixed S2 splitting?
Fixed S2 splitting (aka doesn’t change w/ inspiration) caused by ASD, b/c left to right shunt makes pulmonic valve close super delayed regardless
Name some negative inotropes
Negative inotropes = decrease cardiac contractility (thereby decrease myocoardial O2 demand)
- Beta1-blockers transiently (atenolol, metoprolol) by reducing cAMP
- loss of cardiac tissue: like infarction seen in MI
- non-dihydropyridine CCB = Verapamil, Diltiazam
- Acidosis (elevated PCO2)
Differentiate microscopic polyangiitis from eosinophilic granulomatosis w/ polyangiitis
Both are p-ANCA small vessel vasculitides
Microscopic polyangiitis = no granulomas, mostly lung kidney and skin involvement
Eosinophilic granulomatosis w/ polyangiitis = asthma/sinusitis, skin nodules or purpura, granulomatosis and IgE
-mechanism = IgE deposition
Mitral regurgitation
(a) Describe the quality of the murmur
(b) Location of the murmur
(c) Most common cause
MR
(a) Holosystolic high pitched blowing murmur
(b) Heard best at the apex radiating towards the axilla
(c) MC cause = MI (ischemic heart disease)
EKG findings of Prinzmetal angina
Prinzmetal angina = coronary vasospasm, CP at rest not due to occlusion
EKG shows transient ST elevations
Name 2 etiologies of paradoxically split S2
Paradoxically split S2 means the split goes away w/ inspiration, really P2 coming before A2 w/ inspiration
Caused by things that delay closure of aortic valve
-aortic stenosis
-LBBB
MC cause of
(a) aortic regurg
(b) mitral stenosis
MC cause of
(a) Aortic regurg = bicuspid aortic valve, aortic root dilation, endocarditis
(b) MS 2/2 RF
Polyarteritis nodosa
(a) What is it? Vessels affected?
(b) Associated condition
(c) Classic finding on renal arteriogram
(d) Tx in addition to corticosteroids
Polyarteritis nodosa = medium-vessel vasculitis
(a) Medium vessel vasculitis affecting mostly renal and visceral vessels, sparing pulmonary vasculature
(b) Around 30% of pts have chronic HepB
(c) Rosary appearance of renal arteries b/c of tons of small renal aneurysms strung like beads
(d) In addition to corticosteroids, tx w/ immunosupression (cyclophosphamide) b/c it’s immune complex mediated
Mechanism of digoxin
Digoxin = cardiac glycoside = Na/K ATPase inhibitor
- Indirectly inhibits Na/Ca2+ exchanger to increase intracellular calcium => positive inotrope
- stimulates vagus nerve => reduces HR
Recombinant form of what natural peptide is useful in tx of HF
Recombinant form of BNP (released by ventricular myocytes in response to high wall tension to promote diuresis by kidneys) is available in the tx of HF
Differentiate clinical signs of L vs. R heart failure
LHF- orthopnea, PND, pulmonary edema
-fluid backs up into lungs
RHF- JVD, hepatomegaly, peripheral edema
Kawasaki disease
(a) What is it?
(b) Tx
(c) Coronary complication
Kawasaki disease
(a) Medium vessel vasculitis of children under 4 yo p/w fever for multiple days
(b) Tx = IVIG and aspirin
(c) Risk of coronary artery aneurysm
ANP vs. BNP
(a) Where are they released from?
(b) Function
ANP vs. BNP
(a) ANP from atrial myocytes (in response to high atrial pressure and high blood volume), BNP from ventricular myocytes (in response to high wall tension)
(b) Both function to cause vasodilation and reduce renal Na+ reabsorption => promote diuresis (ex: elevated in HF)
Differentiate Romano-Ward syndrome from Jervell/Lange-Nielson syndrome
Both are congenital ion channel defects that cause congenital long QT syndrome => increased risk of sudden cardiac death
Romano-Ward: aut dom, pure cardiac phenotype (no deafness)
Jervell/Lange-Nielson: aut rec, sensorineural hearing loss
What is Kussmal’s sign (not breathing…)
(a) Associated conditions
Kussmal’s sign - paradoxical increase in JVD w/ inspiration (usually JVD decreases w/ inspiration)
-occurs b/c there is an obstruction preventing RV filling
(a) RA/RV tumors, constrictive pericarditis, restrictive cardiomyopathy
Differentiate granulomatosis w/ polyangiitis from microscopic polyangiitis
Granulomatosis w/ polyangiitis = c-ANCA small vessel vasculitis involving kidneys, upper and lower airways
Microscopic polyangiitis = p-ANCA small vessel vasculitis involving kidneys, lung, and skin (w/o nasopharyngeal involvement)
-no granulomas
MC
(a) congenital heart defect
(b) cause of early childhood cyanosis
MC
(a) Congenital heart defect = VSD
(b) Cause of earlihood cyanosis = ToF
Temporal arteritis
(a) Clinical presentation
(b) Vessels MC affected
(c) Tx and why to tx fast
(d) Associated condition
(e) Pathology on biopsy
Temporal arteritis = large vessel vasculitis
(a) Unilateral headache and ipsilateral jaw claudication
(b) Carotid artery and its branches (temporal artery, opthalmic artery)
(c) Tx w/ corticosteroids before temporal artery biopsy comes back b/c want to prevent vision loss 2/2 opthalmic artery occlusion
(d) Associated w/ polymyalgia rheumatica (pain of girdles- shoulder and hips/pelvis)
(e) Focal granulomatous inflammation
Name the 5 T’s that cause blue baby
5 T’s (use fingers 1 through 5)
- Truncus arteriosus- persistence of single vessel comprising of aortic and pulmonic trunk
- Transposition of the great vessels
- Tricuspid atresia
- Tetrology of Fallot
- TAPVR = total anomalous pulmonary venous return- pulmonary veins drain into the r. heart
What is isovolumetric contraction?
Isovolumetric contraction = the period between the time that the mitral valve closes and the aortic/pulmonic valve opens
-first little bit of systolic
Mechanism of CCBs in tx of HTN
CCBs block voltage-dependent L-type calcium channels of cardiac and smooth muscle to decrease contractility
Relationship of pulse pressure to
(a) Stroke volume
(b) arterial compliance
(c) Aortic valve function
(d) thyroid hormone levels
Pulse pressure = SBP - DBP
(a) directly proportional to stroke volume
(b) inversely proportional to arterial compliance
- more elastic vessels causes narrower pulse pressure
(c) Aortic stenosis causes narrowing of pulse pressure, while aortic insufficiency/stiffening (w/ age)
(d) Hyperthyroid can cause widened pulse pressure
Cherry hemangioma vs. strawberry hemangioma
Both are benign capillary hemangiomas, but just dif age groups
Cherry hemangiomas in the elderly, incidence increases w/ age
Strawberry hemangiomas in infancy, regress spontaneously by ages 5-8
Differentiate the two categories of CCB
Dihydropyridines act on vascular smooth muscle: amlodipine, clevidipine, nicardipine, nifedipine, nimodipine
Non-dihydropyridines act on the heart: verapamil, diltiazem
Name 2 large vessel vasculitides
Large vessel vasculitides = temporal/giant cell arteritis and Takayusu arteritis
Cushings triad
HTN, bradycardia, respiratory depresison
Describe 2 things that happen to fetal circulation w/ the first breath
- Reduced resistance of the pulmonary vasculature causes increased LA pressure => closing of the foramen ovale (now the fossa ovalis)
- High O2 (from respiration) and decreased prostaglandins (from placental separation) closes ductus arteriosus
- now the ligamentum arteriosum
HF tx
(a) Symptomatic
(b) Decrease mortality
Tx of HF
(a) For symptomatic tx only: diuretics
(b) Drugs that have mortality benefit =
What is the funny current?
Funny current is the current thru funny channels on cardiac pacemaker cells- slightly different type of conduction potential that causes spontaneous depolarization
-spontaneous depolarization during diastole to create the funny current, forming a natural pacemaker
Define sudden cardiac death and name some causes
SCD = death from cardiac cause w/in 1 hour of symptom onset
Etiologies
- arrhythmia
- large obstruction
- congenital: long-QT, Brugada (channelopathies)
- HOCM
Local metabolites of the
(a) Heart
(b) Brain
that help maintain blood flow during low perfusion states
Local metabolites to increase perfusion (autoregulation), aka local factors that cause vasodilation
(a) Heart- adenosine, NO, CO2, hypoxia
(b) Brain- CO2
- this is why hyperventilation (CO2 to 30) temporarily causes vasoconstriction in attempt to reduce ICP
Give a brief overview of atherosclerotic plaque formation
Pathophysiology of atherosclerotic plaque: macrophages eat up LDL and turn into foam cells and form fatty streaks, PDGF and FGF attract smooth muscle cells which deposit proliferate and form fibrous plaque over cholesterol deposits
Hydralazine
(a) Mechanism
(b) Indications
(c) Why often coadministered w/ beta-blocker
Hydralazine
(a) Smooth muscle relaxation (vasodilation) viaincrease in cGMP
- Vasodilates arterioles much more than veins => reduces afterload
(b) Used for severe HTN (and safe in pregnancy) and HF tx
(c) Prevents reflex tachycardia seen w/ beta-blockers
What is pulsus paradoxus?
(a) Seen in what?
Pulsus paradoxus = drop in systolic BP of 10 or more mmHg during inspiration
(a) Seen in cardiac tamponade, asthma, OSA, pericarditis, croup
What does a T wave represent on EKG?
T wave is ventricular repolarization
-expect it to be in the same direction as the QRS (unless there is a bundle branch block)
Inverted T waves (as in in a different direction than the QRS w/o BBB) may indicate recent MI
Keys to treating HTN in pts w/ DM
ARB/ACEis help prevent diabetic neuropathy
Differentiate peripheral vs. central chemoreceptors for BP
Central chemoreceptors respond to changes in pH and pCO2 in the brain
-so not directly, but these reflex body arterial pO2
Peripheral chemoreceptors respond to change in pH, pCO2, and very low pO2 (under 60 mmHg)
Describe how baroreceptors are involved in the following
(a) Response to carotid massage
(b) Cushings reflex
Baroreceptors
(a) Carotid massage increases pressure on the carotid baroreceptors which increases firing, increasing the refractory period and slowing HR
- basically know it slows HR
(b) Cushing’s triad (HTN, bradycardia, respiratory depression): elevated ICP vasoconstricts cerebral vasculature => ischemia which activates central reflexive increase in sympathetic tone (hence the HTN)
- this HTN then increases stretch on the baroreceptors => bradycardia
How to treat HTN in HF
- diuretics for symptoms
- ACEi and ARBs to decrease mortality
- beta-blockers cautiously, only in compensated (not acute) HF
Describe what ion is in charge of causing cardiac myocyte contraction
Ultimately it is intracellular calcium that stimulates calcium release from SR that causes contraction
First line anti-anginals
(a) Physiology
Anti-angina = nitrate plus beta-blocker
(a) Act to decrease myocardial oxygen demand
Describe the pathway of blood from placenta to fetal heart
Blood leaves the placenta out the umbilical vein, then into ductus venosus (only present embryologically, allows bypass of portal circulation) into the IVC
So umbilical vein –> ductus venosus –> IVC
What embryologic structure gives rise to the valves of the heart
Endocardial cushions
Differentiate physiology of nitrates vs. hydralazine
Both vasodilate
- nitrates vasodilate veins over arteries => reduce preload
- hydralazine vasodilates arteries over veins => reduces afterload
What is the ST segment on EKG?
ST segment = ventricles are depolarized, haven’t started to repolarize yet
Segments don’t include waves while intervals do
Risk factor for Ebstein’s anomaly
Mothers taking Lithium in first trimester
EF value in systolic vs. diastolic HF
EF is normal in diastolic, but reduced (under 55%) in systolic HF
Small vessel vasculitides
(a) c-ANCA
(b) p-ANCA
Small vessel vasculitides
(a) c-ANCA = granulomatosis w/ polyangiitis
(b) p-ANCA = both microscopic polyangiitis and eosinophilic granulomatosis w/ polyangiitis
Differentiate the components of embryonic, fetal, and adult Hgb
Embryonic = zeta2epsilon2 Fetal = alpha2gamma2 Adult = alpha2beta2
“Alpha always, gamma goes and becomes beta”
Treatment of
(a) Afib
(b) Aflutter
(c) Vfib
Tx
(a) Afib:
rate control: beta-block, no-dihy CCB, digoxin
rhythm control w/ class Ic and III antiarrhythmics
anticoagulate w/ warfarin
(b) Aflutter- same tx as Afib or definitive therapy of catheter ablation
(c) Vfib- defibrillate immediately
How does valsalva change murmurs?
Valsalva decreases preload
- decreases most murmurs (AS, MR)
- increases HOCM murmur
Dx if you hear pericardial friction rub
(a) 1-3 days post-MI
(b) 3 weeks post-MI
Pericardial friction rub post-MI
(a) 1-3 days = postinfarction fibrinous pericarditis
(b) 3 weeks = Dressler syndrome = autoimmune phenomenon causing fibrinous pericarditis
Name the congenital heart defect(s) associated w/ the following d/o
(a) Marfan syndrome
(b) Lithium exposure
(c) Turner syndrome
(d) Williams syndrome
(e) 22q11 syndromes
(a) Marfan => MVP, thoracic aortic aneurysm, aortic insufficiency
(b) Lithium exposure => Ebstein anomaly (severe TR)
(c) Turner => coarctation of aorta, bicuspid aortic valve
(d) Williams => supravalvular aortic stenosis
(e) 22q11 syndromes => truncus arteriosus, ToF
Of the 3 types of cardiomyopathies (dilated, hypertrophic, restrictive) which is associated w/
(a) systolic dysfunction
(b) S3
(c) S4
(d) chronic EtOH/chronic abuse
(e) Doxorubicin toxicity
(f) Sarcoidosis
(g) Amyloidosis
(h) Friedreich ataxia
(i) B1 deficiency
90% of cardiomyopathies are dilated (so majorly the most common)
(a) Systolic dysfunction seen in dilated, while diastolic dysfunction seen in hypertrophic and restrictive
(b) S3 heard in dilated
(c) S4 heard in hypetrophic
(d) EtOh/Cocaine => dilated
(e) Doxorubicin (amikacin, chemo drug) => dilated
(f) Sarcoidosis => usually restrictive but can cause dilated
(g) Amyloid => restrictive
(h) Friedreich ataxia => hypertrophic
(i) Wet beriberi => dilated
Wolff-Parkinson-White
(a) What is it?
(b) EKG pattern
(c) Risk
WPW
(a) Ventricular pre-excitation, presence of abberant fast accessory pathway from the A to V (bundle of Kent) that bypass the rate-slowing by the AV node
(b) Ventricles depolarize earlier => characteristic delta wave (concave upward slope of P to R), widened QRS, shortened PR
(c) Can result in reentry circuit => supraventricular tachycardia
Clinical findings of end organ damage in hypertensive emergency
Signs of end organ damage
- Neuro: encephalopathy, stroke
- HEENT: papilledema, retinal hemorrhage
- CV: MI, aortic dissection
- Renal: kidney injury
- eclampsia
Formula for MAP
MAP = 2/3(diastole) + 1/3(systole)
Antiarrhythmic that is best for
(a) post-MI ventricular tachycardia
(b) Digitalis induced arrhythmias
(c) diagnose and abolish SVT short-term
(d) Afib rate control
Antiarrhtyhmic for
(a) post-MI ventricular arrythmias = Class IBs (Na+ channel blockers) = Lidocaine, Mexiletine
(b) Digitalis induced arrhtyhmias = Mg2+, Class IBs
(c) Diagnose and abolish SVT = adenosine, very short acting (like 15 seconds)
(d) AFib rate control- lots of options
- beta-blockers (class II)
- CCBs (class IV)
What is Ebstein’s anomaly
Inferiorly displaced tricuspid valve, causes severe tricuspid regurgitation (backflow into the RA)
Aortic stenosis
(a) Describe the quality of the murmur
(b) Location of the murmur
(c) Associated physical exam finding
Aortic stenosis
(a) Holosystolic crescendo- decrescendo ejection murmur
(b) Heard best at RUSB (base of the heart), radiating to the carotids
(c) Pulsus parvus et tardus = pulse weak and w/ delayed peak
Statins
(a) Mechanism of action
(b) Lab value to monitor
(c) Effect on LDL, HDL, and TG
(d) Clinical side effect
Statins = lipid lowering agent
(a) HMG CoA reductase inhibitor to reduce precursor production into cholesterol in hepatocytes
(b) Monitor LFTs, can cause hepatotoxicity
(c) Great at reducing LDL, increase HDL, reduces TG
- yay to all 3
(d) Myopathy
- especially when taken w/ fibrates or niacin
Which cyanotic congenital heart lesions require VSD
Out of the 5 cyanotic heart lesions
- Truncus arteriosus usually w/ VSD
- Transposition of the great vessels REQUIRES shunt (VSD, PDA, PFO)
- Tricuspid atresia- requires both ASD and VSD for viability
- Tetrology of fallot- has VSD
- TAPVR often ASD (not VSD)
Explain how LA enlargement could cause
(a) dysphagia
(b) hoarseness
(a) LA is just anterior to the esophagus => esophageal compression
(b) left recurrent larygneal nerve compression
Name 2 causes of U-waves on EKG
U waves = waves after T wave before P wave
Caused by hypokalemia and bradycardia
Tx of Raynaud’s phenomenon
CCB b/c it’s arteriolar vasospasm
Risk factors for prolonged QT
RF for prolonged QT
- tons of drugs (macrolides, haldol, zofran)
- hypomag and hypophs
Describe 4 mechanisms by which edema can occur given capillary pressure, interstitial fluid pressure, plasma colloid osmotic pressure, and interstitial fluid colloid osmotic pressure
Edema = excess fluid outflow out of capillaries into the interstitium
- increased capillary pressure: HF
- loss of plasma proteins (reduced plasma colloid osmotic pressure): nephrotic syndrome, liver failure
- increase in capillary permeability: toxins, infections,burns
- increase in intertitial fluid colloid osmotic pressure (pulls fluid out of capillaries) such as in lymphatic blockage
Cardiac tamponade
(a) Clinical findings
(b) EKG finding
Cardiac tamponade
(a) Beck’s triad = muffled heart sounds, JVD, hypotension
(b) EKG: electrical alternans and low-voltage QRS
MC heart tumor
Mets
Nitroprusside
(a) Mechanism
(b) Indication
(c) Risk
Nitroprusside
(a) Direct release of NO causes increase in cGMP
(b) Hypertensive emergency
(c) Risk of cyanide poisoning b/c releases cyanide
How does rapid squatting change murmurs?
Rapid squatting increases preload
- increases most murmurs (AS, MR)
- decreases HOCM
What is congenital long QT syndrome?
(a) Why it’s concerning
Congenital long QT syndrome = inherited ion channel defect causing disorder of myocardial repolarization => increased risk of sudden cardiac death due to torsades de pointes (polymorphic VT)
35 yo heavy smoker w/ Raynaud’s phenomenon and auto-amputation of 2 toes
(a) Possible dx
(b) Mechanism of disease
(a) Dx = Buerger disease = Thromboangiitis obliterans = medium vessel vasculitis seen in smokers
(b) Recurring progressive inflammation and clotting in hands/feet => gangrene, autoamputation
Tx = smoking cessation
What are angiosarcomas?
Angiosarcomas = malignant tumors of vasculature, can be of the walls of blood vessels or lymphatic vessels
-often aggressive and hard to treat
What two arrhythmias indicate tx w/ Mg2+
Give Mg2+ in Torsades de pointes and digoxin toxicity
PDA
(a) Quality of murmur
(b) Location of murmur
(c) 2 MC etiologies
Patent ductus
(a) Machine like continuous murmur loudest at S2
(b) Best heard at the L infraclavicular area
Differentiate ASD from PFO
ASD = actual lack of atrial septal tissue
PFO = failure to fuse
Differentiate function of troponin I and CK-MB as cardiac markers
Troponin I elevates after 4 hrs, remains elevated for 7-10 days. Most specific marker b/c only released by cardiac myocytes
CK-MB elevated after 6-12 hrs and normalizes w/in 48 hrs. Not as specific b/c also can be released by skeletal muscle, but good for marker of reinfarction b/c normalizes much faster
Acute pericarditis
(a) Clinical features
(b) Physical exam finding
(c) EKG findings
(d) MC cause
Acute pericarditis
(a) Pain worse w/ inspiration, improves on sitting up and leaning forward
(b) Pericardial rub
(c) Classically- diffuse ST elevations w/ PR
(d) MC cause = idiopathic, which then is assumed to be viral
Describe the EKG findings of
(a) Afib
(b) Aflutter
(c) Vfib
EKG findings
(a) Afib- irregularly irregular sporadic baseline w/ no discrete P waves
(b) Aflutter- rapid identical atrial depolarizations giving appearance of sawtooth
(c) Vfib- completely erratic w/ no identifiable waves
Differentiate EKG findings of
(a) transmural
(b) subendocardial infarcts
EKG findings
(a) Transmural infarct = ST elevations, Q waves
(b) Subendocardial infarcts (less than 50% of the ventricular wall infarcted) = ST depression
What is torsades de pointes?
Tosades de pointes = polymorphic ventricular tachycardia (waves all look dif, fast HR with wide QRS)
Dangerous b/c can turn into Vfib => sudden cardiac death
Describe phases 0 through 4 of a myocardial action potential
Myocardial action potential
Phase 0 = INa = opening of voltage-gated Na+ channels to go from -85mV to +10ish
Phase 1 = initial repolarization, Na+ channels inactivated and voltage-gated K+ channels begin to open
Phase 2 = Ica and Ik) Plateau, Ca2+ influx thru voltage-gated Ca2+ channels balances K+ efflux
-Ca2+ influx triggers Ca2+ release from SR and myocyte contraction
Phase 3 = IK = rapid repolarization- quickly drops from 0mv back down to -85 2/2 massive K+ efflux due to opening of voltage-gated slow K+ and closure of voltage-gated Ca2+
Phase 4 = resting potential, high K+ permeability through K+ channels
AV node
(a) Exact location
(b) Blood supply
(c) Duration and significance of conduction delay
AV node
(a) Posterior inferior part of the intra-atrial septum
(b) Usually supplied by the RCA
(c) Conduction delay of about 100ms to allow for ventricular filling
Why don’t we see atrial repolarization on EKG?
Masked by QRS (ventricular depol)
Possible etiologies of mitral valve prolapse
MVP
- myxomatous degeneration: primary or secondary to CT disease (Marfans, Ehlers-Danlos)
- RF
- chordae rupture
Duration of
(a) QRS interval
(b) PR interval
Duration of
(a) Ventricular depolarization = 120 ms or shorter (so 3 small boxes)
(b) PR interval- time from start to atrial depol to start of ventricular depol (start of P wave to start of Q) under 200ms
Describe paradoxical emboli and their cause
Cause = PFO = patent foramen ovale- foramen secundum not completely covered by the septum secundum
When venous clot ends up in the arterial circulation (so out the aorta by getting shunted RA to LA) instead of in the lungs
What is PCWP used to approximate?
(a) Name a disease state where PCWP > LV diastolic pressure
PCWP used to approximate LA pressure
-measured w/ Swan-Ganz catheter
(a) Mitral stenosis
Most common etiologies of aortic stenosis
AS
- calcification w/ age
- bicuspid aortic valve
When does coronary blood flow peak?
Coronary blood flow peaks in early diastole
-heart relaxes so less mechanical pressures on the arteries so they can fill
Why is ASD often seen in TAPVR?
TAPVR = total anamalous pulmonary venous return where the pulmonary veins drain freshly oxygenated blood into the RA (instead of the LA)
-so need ASD to shunt oxygenated blood to the left heart
What percent of HTN is secondary?
(a) Name two causes of secondary HTN
10% of HTN is secondary
(a) 2 big causes
- renal artery disease: stenosis, fibromuscular dysplasia (vasculopathy)
- pheo
- primary hyperaldosteronosim
