Cardiovascular Flashcards
Acute chest pain that radiates to back?
Acute dissecting aortic aneurysm; usually initiated by an intimal tear
wide, fixed splitting of S2 that doesn’t vary with respiration
ASD
What may lead to eye problems following treatment for an inferior MI (ST elevation in inferior leads)?
Inferior lead MIs are associated with bradycardia; so, pts are often given atropine to treat the bradycardia. Side effect of atropine = eye problems!
What artery does coronary artery occlusion most commonly occur in?
LAD = Left Anterior Descending artery
=> anterior wall MI
*LAD comes off the LCA (left main coronary artery), supplies the apex and anterior interventricular septum
Which coronary artery supplies the SA and AV nodes?
Majority of time –> SA and AV nodes are supplied by the RCA
Which coronary artery supplies the right ventricle?
Acute marginal artery (comes off the RCA)
Which coronary artery supplies the posterior left ventricle?
CFX = Circumflex artery (comes off the LCA)
PD = Posterior Descending artery is supplied by? supplies?
“Right Dominant” heart –> majority of cases (about 80%), RCA supplies the PD, which supplies the inferior part of the Left ventricle
*20% of the time, the PD arises from the CFX (Circumflex artery, which arises from the LCA)
Most posterior part of the heart? What may it cause if it enlarges?
- most posterior part of the heart is the Left Atrium
- If enlargement of Left Atrium –> dysphagia (d/t esophageal compression) or Hoarseness (d/t recurrent laryngeal nerve compression)
CO (Cardiac Output) = ?
CO = SV X HR
(CO = Stroke Volume X Heart Rate)
***note: if HR is too high –> diastolic filling is incomplete –> get decreased CO (ie ventricular tachycardia)
Fick Principle:
CO = (rate of O2 consumption) / (arterial O2 content - Venous O2 content)
MAP (mean arterial pressure) = P =?
MAP = CO X TPR P = Q X R
*TPR = R = Total Peripheral Resistance
Pulse Pressure = ?
Pulse Pressure = Systolic Pressure - Diastolic Pressure
Pulse Pressure is proportional to?
Stroke Volume
Stroke Volume = ?
SV = CO/HR = EDV - ESV
EDV vs ESV
EDV = End-Diastolic Volume = full heart ESV = End-Systolic Volume = empty heart (after pumping out!)
What maintains the CO during early stages of exercise? late stages of exercise?
- Early stages of exercise –> CO maintained by SV
* Late stages of exercise –> CO is maintained by HR
Which 3 factors affect Stroke Volume?
Increased SV when these factors increase/decrease?:
SV CAP:
- Contractility
- Afterload
- Preload
Increased SV when:
- Increased contractility
- Decreased afterload
- Increased Preload
4 factors that increase contractility (and thus increase SV):
1) Catecholamines –> increase activity of Calcium pump in Sarcomplasmic Reticulum (act on Beta-1 receptors)
2) Increased intracellular Calcium
3) Decreased extracellular Sodium (b/c decreased activity of Na+/Ca2+ exchanger, so more Calcium stay inside cell)
4) Digitalis (b/c blocks Na+/K+ ATPase, so decreased extracellular Na+ –> decreased activity of Na+/Ca2+ exchanger –> more Calcium stays in cell, so –> increased intracellular Calcium)
5 factors that decreased contractility (and thus decrease SV):
1) Beta-1 blockade (decreased cAMP–>decreased Protein Kinase A –> decrease intracellular Ca)
2) Heart failure (systolic dysfxn)–> decreased SV in heart failure
3) Acidosis
4) Hypoxia/Hypercapnea (decreased PO2/increased PCO2)
5) Non-dihydropyridine Ca2+ channel blockers (ie Verapamil, Diltiazem)
3 states in which have increased SV:
- Pregnancy (b/c increased blood volume, so increased preload)
- Exercise (b/c increased pre-load + increased catecholamines)
- Anxiety (b/c increased catecholamines)
4 factors that increase myocardial O2 demand:
1) increased afterload
2) increased contractility
3) increased heart rate
4) increased heart size
What is the preload? What states may increase preload?
Preload = Ventricular EDV Increased preload with: -Exercise (slightly) -Pregnancy -Increased blood volume (ie over-transfusion) -Excitement (ie sympathetics)
***Preload Pumps up the heart!
Mean arterial pressure = ?
MAP = 2/3 diastolic pressure + 1/3 systolic pressure
Preload and Afterload: Which is proportional to the mean arterial pressure and total peripheral resistance? to central venous pressure?
- Central venous pressure is about equal to the preload
- Total peripheral resistance is about equal to the afterload
Effect of venodilators (ie Nitroglycerin) on heart?
decrease preload
Effect of vasodilators (ie hydralazine) on heart?
decrease afterload
effect of ACE-inhibitors and ARBs on heart?
decrease preload AND decrease afterload
How to decrease O2 demand in a heart attack? (3 ways)
- decrease afterload –> ACE inhibitors
- decrease contractility –> Beta-blockers
- decrease HR –> Beta-blockers
EF = Ejection Fraction = ?
What is it normally? (%)
EF = what heart can pump out / what heart can hold
EF = SV/EDV = (EDV-ESV)/EDV
EF is an index of ventricular contractility
EF is normally > or = 55%
–>get decreased EF is systolic heart failure
Preload and Afterload: Which is proportional to the mean arterial pressure and total peripheral resistance? to central venous pressure?
- Central venous pressure is about equal to the preload
- Total peripheral resistance is about equal to the afterload
Effect of venodilators (ie Nitroglycerin) on heart?
decrease preload
Effect of vasodilators (ie hydralazine) on heart?
decrease afterload
effect of ACE-inhibitors and ARBs on heart?
decrease preload AND decrease afterload
How to decrease O2 demand in a heart attack? (3 ways)
- decrease afterload –> ACE inhibitors
- decrease contractility –> Beta-blockers
- decrease HR –> Beta-blockers
EF = Ejection Fraction = ?
What is it normally? (%)
EF = what heart can pump out / what heart can hold
EF = SV/EDV = (EDV-ESV)/EDV
EF is an index of ventricular contractility
EF is normally > or = 55%
–>get decreased EF is systolic heart failure
delta P (pressure) = ?
delta P = Q X R
Pressure = Flow X Restistance
Effects of Viscosity and Radius on Resistance?
- Resistance is proportional to Viscosity (increase viscosity –> increase R)
- Resistance is inversely proportional to radius^4 (increase radius –> decrease resistance, and visa versa)
What is the main component that determines viscosity?
Hematocrit
3 states in which have increased Viscosity:
1) Polycythemia
2) Hyperproteinemic states (ie Multiple Myeloma)
3) Hereditary spherocytosis
S1 sound:
Mitral and Tricuspid valve closure
-loudest at mitral area
S2 sound:
Aortic and Pulmonary valve closure
-loudest at left sternal border
S3 sound:
“Ken-Tuc-Key” (key = S3) or “Lub-Dub-Ta”
- in EARLY diastole, during rapid ventricular filling phase.
- Associated with: increased filling pressures (MR, CHF), and more common in dilated ventricles
- Normal in children and pregnant women
When is a S3 sound considered normal?
- Children
- Pregnant women
S4 sound:
="atrial kick" "Ten-Nes-See" (ten=S4) or "Ta-Lub-Dub" -in LATE diastole -High atrial pressure -Associated with ventricular hypertrophy (LA has to push against stiff LV wall)
Mitral and Tricuspid Valves
MitraL –> Left! Bicuspid valve
Triscupid –> Right
Isovolumetric Contraction
Period between mitral valve closure and aortic valve opening; period of highest O2 consumption
Systolic Ejection
period between aortic valve opening and closing
Isovolumetric Relaxation
Period between aortic valve closing and mitral valve opening
Rapid Filling
Period just after mitral valve opens
Reduced Filling
Period just before mitral valve closure
S2 Splitting:
Aortic valve closes before pulmonic (inspiration increases this difference)
What may increase the difference in S2 splitting (when aortic valve closes before pulmonic)? When is S2 splitting normal? When is S2 splitting pathologic?
Inspiration
*Note: split S2 on inspiration = normal; split S2 on expiration = pathologic
Jugular Venous Pulse (JVP)
“At Carter’s Xing Vehicles Yield”
- a wave = atrial contraction
- c wave = RV contraction (closed tricuspid bulges into atrium)
- x descent = atrial relaxation (downward displacement of closed tricuspid during ventricular contraction)
- v wave = increased RA pressure, d/t filling against closed tricuspid
- y descent = blood flow from RA to RV
Wide S2 splitting is associated with?
- Pulmonic stenosis
- R bundle branch block
*kind of just an exaggeration of normal splitting
Fixed S2 splitting is associated with?
ASD
Paradoxical S2 splitting is associated with?
- Aortic stenosis
- L bundle branch block
*hear pulmonic closure before aortic!
Systolic murmurs:
- Aortic or Pulmonic stenosis
- Mitral or Tricuspid Regurg
Diastolic Murmurs:
- Mitral or Tricuspid stenosis
- Aortic or Pulmonic Regurg
Which murmurs are worse with inspiration? Worse with expiration?
- Tricuspid = worse with inspiration (b/c increased blood in RA)
- Mitral = worse with expiration (b/c increased blood into LA)
Holosystolic Murmur:
- Tricuspid Regurg
- Mitral Regurg
- VSD
Holosystolic murmur that increases in intensity during inspiration?
-Tricuspid Regurgitation
Murmur that is loudest at apex, radiates toward axilla?
- Mitral Regurgitation
- -> enhanced by: expiration, squatting, hand grip
Murmur that is loudest at tricuspid area and radiates to Right sternal border?
Tricuspid Regurgitation:
–>enhanced by inspiration
Pulsus parvus et tardus
pulse is weak compared to heart sounds
-Aortic stenosis
Bicuspid aortic valve –> what kind of murmur?
Aortic stenosis
Systolic ejection murmur following ejection click
Aortic stenosis
-ejection click is d/t abrupt halting of valve leaflets
holosystolic, harsh-sounding murmur; loudest at tricuspid area (over L sternal border in 3rd or 4th intercostal space)
VSD
Midsystolic click
- Mitral Prolapse
- click is d/t sudden tensing of chordae tendineae
- loudest at S2
- can predispose to infective endocarditis
Diastolic murmur, bounding pulses, head bobbing
-Aortic regurgitation
Murmur with an opening snap
Mitral Stenosis
- snap is d/t abrupt halt of leaflet motion in diastole, after rapid opening d/t fusion at leaflet tips
- enhanced by expiration
continuous machine-like murmur; loudest at S2
PDA
Speed of conduction through heart: fastest –> slowest:
Fastest “Park At Ventura Avenue” Slowest
Purkinje > Atria > Ventricles > AV node
inverted T wave on ECG
indicates recent MI
presence of U wave on ECG?
caused by hypokalemia or bradycardia
Conduction pathway through heart:
SA node –> atria –> AV node –> common bundle –> LAF –> Bundle branches –> Purkinje fibers –> ventricles
Torsades de pointes
- What can it progress to?
- What may predispose to it?
= Ventricular tachycardia; fast, wide QRS of varying amplitudes.
- Can progress to V-fib
- anything that prolongs QT interval can predispose to torsades
Jervell and Lange-Nielsen syndrome
- autosomal recessive
- Torsades de pointes + severe congenital sensorineural deafness
Drugs that can prolong QT interval (and thus predispose to Torsades de pointes)?
- Macrolides
- Antimalarials
- Haloperidol
- Risperidone (atypical antipsychotic)
- Methadone
- Protease inhibitors
- Class 1A antiarrhythmics
What drug can be given to treat torsades de pointes?
Magnesium!
WPW = Wolf-Parkinson White Syndrome
Ventricular pre-excitation syndrome - have an accessory excitation pathway from atria to ventricle that bypasses AV node; so, get early ventricular depolarization and see a Delta wave
- -> may lead to SVT
- -> Treat with Procainamide and Amiodarone
Delta wave
seen with WPW syndrome
Irregularly irregular ECG with no discrete P waves; see irregularly spaced QRS complexes
Atrial fibrillation (no distinct SA node; have several SA nodes acting at once, so no coordinated atrial contractions)
- -> get pooling of blood in atria –> can lead to pulm embolism, stroke, SVT
- Treat with: beta blockers, Ca-channel blockers, or digoxin (plus prophylaxis against thromboembolism with warfarin)
Sawtooth appearance on ECG
Atrial flutter -treat with class IA, IC or III antiarrhythmics, or beta-blockers
PR interval is prolonged by >200 msec on ECG
1st degree AV block
-asymptomatic
ECG with progressive lengthening of PR interval until a beat is “dropped” (so, have a P wave, not followed by a QRS complex)
2nd degree AV block = Mobitz type I = Wenckebach AV block
-asymptomatic
ECG with sudden dropped beats (QRS complexes) after a P wave; no change in PR interval prior to the dropped beat.
- Mobitz type II AV Block (2nd degree AV block)
- pathologic –> may progress to 3rd degree AV block
ECG with both P waves and QRS complexes, but P waves bear no relation to the QRS complexes.
- 3rd degree = Complete AV block
- ->atria and ventricles beat independently of one another
*Lyme disease may result in 3rd degree heart block
What microbiology disease may lead to 3rd degree heart block?
Lyme disease may result in 3rd degree heart block
ECG with completely erratic rhythm and no identifiable waves
V-fib (fatal arrhythmia without immediate CPR and defibrillation)
ANP = Atrial Natriuretic Peptide:
- Released from atria in response to increased blood volume and atrial pressure
- leads to generalized vascular relaxation
- lowers BP by:
- ->peripheral vasodilation
- ->natriuresis
- ->diuresis
- contstricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated) which promotes diuresis (and “escapes from aldosterone”)
Responses to BP changes in the aortic arch? carotid sinus?
- aortic arch –> only responds to increased BP; transmits signal via vagus nerve to medulla
- Carotid sinus –> responds to increased and decreased BP; transmits signal via glossopharyngeal nerve to solitary nucleus of medulla
Carotid massage:
Carotid massage increases cardiac PARASYMPATHETIC tone –> get increased AV node refractory period
carotid massage –> increased pressure on carotid artery –> increased stretch –> increased afferent baroreceptor firing –> decreased HR
SO: massage–> Increased BP –> decreased HR
Cushing Reaction:
increased ICP –> constricts arterioles –> cerebral ischemia –> HTN (sympathetic response) –> reflex bradycardia
Cushing’s Triad
1) HTN
2) Bradycardia
3) Respiratory depression
***get Cushing’s triad when: intracranial hemorrhage with increased ICP
PCWP = Pulmonary Capillary Wedge Pressure (mmHg): Approximates what?
-LA pressure
Swan-Ganz catheter:
- used to measure PCWP (pulm capillary wedge pressure); so used to approximate LA pressure
- mechanism: venous catheter into internal jugular or subclavian vein –> SVC –> RA –> RV –> Pulm artery –> stops somewhere along here, balloon is wedged into a branch of the pulm artery; measures pressure on opposite side of ballon –> so, = pressure in LA
What does hypoxia do to vasculature throughout the body?
- In majority of organs: hypoxia –> vasodilation
- In pulmonary vasculature: hypoxia –> vasoconstriction (this way, only well-ventilated areas are perfused)
- **so, lungs = unique in hypoxia
“blue babies” vs “blue kids”
- blue babies = early cyanosis; R–> L shunts (the 5 Ts)
- blue kids = late cyanosis: L–> R shunts (VSD, ASD, PDA) (then, get Eisenmenger’s syndrome, eventually, leading to late cyanosis…)
Early Cyanosis/ R–>L shunts causes:
5 T’s:
- TOF (= most common cause)
- Transposition of Great Vessels
- Truncus arteriosus
- Tricuspid atresia
- Total anomalous pulmonary venous return (TAPVR)
Persistent truncus arteriosus:
- failure of truncus arteriosus to divide into pulmonary trunk and aorta; so just have 1 vessel!
- causes cyanosis at birth
Tricuspid atresia
absent tricuspid valve, and hypoplastic RV
- cyanotic at birth
- requires both ASD + VSD for viability
TAPVR = Total Anomalous Pulmonary Venous Return
pulmonary veins drain into right heart circulation (similar to transposition…)
- must have a patent foramen ovale or an ASD to be viable.
- babies cyanotic at birth
Causes of L–>R shunts (late cyanosis)
1) VSD (most common)
2) ASD (loud S1; wide, fixed split S2)
3) PDA (machinery murmur; most close on own w/in first 24 hours; otherwise, close with indomethacin)
*L–>R shunts: VSD, ASD, PDA may lead to Eisenmenger’s syndrome if not corrected
Eisenmenger’s syndrome:
-uncorrected VSD, ASD, PDA –> causes compensatory pulmonary vascular hypertrophy –> results in progressive pulmonary hypertension
increased pulmonary resistance –> shunt reverses from L–>R to R–>L; get late cyanosis (clubbing + polycythemia)
Cyanosis + Clubbing (swollen finger tips) + Polycythemia:
Eisenmenger’s syndrome
Tetralogy of Fallot
1) Pulmonary stenosis (most important determinant for prognosis)
2) RVH (causes boot-shaped heart on x-ray)
3) Overriding aorta (overrides VSD)
4) VSD
What causes Tetralogy of Fallot?
anterosuperior displacement of infundibular septum
Why do pts with TOF squat to relieve symptoms?
Squatting–> compress femoral arteries –> increased TPR–> decreased R–>L shunt and thus directs more blood from RV to lungs
Cause of Transposition of great vessels?
Failure of aorticopulmonary septum to spiral
Infantile vs Adult coarctation of the aorta:
Infantile–> preductal aortic stenosis (proximal to insertion of ductus arteriosus); assoc w/Turner’s
Adult: postductal aortic stenosis; distal to ligamentum arteriosum
Notching of ribs
Coarctation of aorta (adult type/post-ductal)
Paradoxical hypertension in upper extremities; hypotension in lower extremities
Coarctation of aorta (adult type/post-ductal)
22q11 syndromes associated with what cardiac defects?
(ie DiGeorge syndrome)
- Truncus arteriosus
- TOF
Congenital rubella is associated with what cardiac defects?
- PDA
- pulmonary artery stenosis
- septal defects
What cardiac defect is associated with Turner’s syndrome?
Coarctation of aorta (preductal/infantile type)
Cardiac defect associated with infants born to diabetic mothers?
Transposition of great vessels
Monckeberg arteriosclerosis
- calcification of MEDIA of arteries (intima not involved); usually benign
- “pipestem” arteries
Arteriolosclerosis
hyaline thickening of small arteries in essential HTN or DM
-hyperplastic “onion skinning” in malignant HTN
Atherosclerosis (what layer of arterial wall is involved?
fibrous plaques and aterhomas in INTIMA of arteries
Abdominal aortic aneurysms: associated with what precursor condition?
-Associated with atherosclerosis of the abdominal aorta
mediastinal widening on CXR
Aortic dissection (have intraluminal tear, forming a false lumen)
DX of MI:
- first 6 hours: ECG = gold-standard
- 4 hrs - 7-10 days: Cardiac troponin (=most specific)
- CK-MB = nonspecific, but good for dx reinfarction on top of acute MI
most specific marker of MI and lasts longest
Cardiac troponin I (rises after 4 hours, stays elevated for 7-10 days)
ST elevation on ECG after MI
Transmural infacts (non-STEMI = subendocardial infarcts; get ST depression on ECG)
Dressler’s syndrome
autoimmune process several weeks post-MI –> get fibrinous pericarditis
S3, balloon appearance on CXR, laterally displaced apical pulse:
-Dilated Cardiomyopathy
S4, increased sized of apical pulse, systolic murmur
Hypertrophic cardiomyopathy
Possible etiologies of Dilated Cardiomyopathy:
ABCCCD
- Alcohol (chronic)
- wet Beriberi
- Coxsackie B virus myocarditis
- Cocaine (chronic)
- Chaga’s
- Doxorubicin toxicity (anti-cancer drug)
- also: hemochromatosis and peripartum cardiomyopathy
Most common cause of Right heart failure?
Left heart failure
*isolated R heart failure is usually d/t cor pulmonale
signs of Left heart failure:
- pulmonary edema (have hemosiderin-laden macrophages = heart failure cells in lungs)
- paroxysmal nocturnal dyspnea
- orthopnea (shortness of breath while supine)
signs of Right heart failure:
- Hepatomegaly –> nutmeg liver
- ankle, sacral edema
- Jugular venous distention
Valsalva meanuever effect on vasculature/murmurs:
decreases venous return
- most murmurs decrease in intensity
- increased intensity of hypertrophic cardiomyopathy murmurs
Hand grip effect on vasculature/murmurs:
increases systemic vascular resistance
-increases mitral regurg, VSD systolic murmurs
Rapid squatting effect on vasculature/murmurs:
increases venous return, increases afterload
-decreases intensity of hypertrophic cardiomyopathy murmurs
VSD vs Tricuspid regurgitation murmurs:
Both:
- holosystolic
- loudest at tricuspid area
Differentiate by clinical:
- newborn–> prob VSD
- adult IV drug user –> prop Tricuspid regurgitation
***also: tricuspid = worse with inspiration; VSD = not usually worsened with inspiration
Causes of Tricuspid regurgitation?
- endocarditis (IV drug users…)
- RV dilation
- Rheumatic fever
Causes of Mitral regurgitation?
- Ischemic heart disease
- Mitral valve prolapse
- LV dilation
- Rheumatic fever
Main causes of aortic stenosis?
- Bicuspid aortic valve
- Age-related calcification
Murmur that is normally benign, but can predispose to infective endocarditis:
- Mitral Prolapse
* **can predispose to infective endocarditis ONLY if also have mitral regurgitation associated with it.
Murmurs associatd with endocarditis:
- mitral regurg and mitral stenosis
- aortic regurg and aortic stenosis
- tricuspid regurg
Splitting of S2 that doesn’t change with inspiration?
=Fixed splitting
–> ASD
Roth’s spots
round white spots on retina, surrounded y hemorrhage; seen in bacterial endocarditis (but, rare)
Janeway lesions
painless lesions on palms or soles; bacterial endocarditis
Osler’s nodes
painful lesions on fingers or toes; bacterial endocarditis
splinter hemorrhages on nail bed
bacterial endocarditis
Signs/Symptoms of Bacterial Endocarditis (X8)
“FROM JANE”
- Fever
- Roth’s spots
- Osler’s nodes
- new Murmur
- Janeway lesions
- Anemia
- Nail-bed hemorrhage = splinter hemorrhages
- Emboli (Pulm embolism if Tricuspid EC; Stroke if Mitral EC)
Most common cause of Acute Bacterial Endocarditis? Subacute Bacterial Endocarditis?
- Acute–> S. aureus (rapid; on previously normal heart valves)
- Subacute: Viridans Strep (ie Strep sanguis, mutans) –> more insidious; on previously abnormal/diseased valves (ie mutans, after dental procedures)
Aschoff bodies
Area of fibrinoid necrosis/granuloma surrounded by mononuclear and multinucleated giant cells
Sydenham’s chorea
Chorea related to Rheumatic fever
- ->most common acquired chorea of childhood and only nuero manifestation of acute rheumatic fever; CNS autoimmune rxn, precipitated by GAS pharyngitis, after latency of 203 months
- ->pts have increased risk for chronic rheumatic heart disease
Signs/Symptoms of Rheumatic Fever (X7):
“FEVERSS”
- Fever
- Erythema marginatum
- Valvular damage (vegetation and fibrosis)
- ESR elevated
- Red hot joints (migtatory polyarthritis)
- Subcutaneous nodules
- St. Vitus’ dance = Sydenham’s chorea
- **also:
- Aschoff bodies
- Anitschkow’s cells (activated histiocytes)
- Elevated ASO titers
- Antibodies to M protein
What type of hypersensitivity rxn is Rheumatic Fever?
Type II hypersensitivity
Acute pain, worse with inspiration, relieved by sitting up and leaning forward:
Acute pericarditis
ST elevation in ALL ECG leads?
Pericarditis
Friction rub
Fibrinous pericarditis (ie with Dressler’s syndrome)
Pulsus Paradoxus
seen in cardiac tamponade
-exaggerated decrease in systolic BP during inspiration (by >10 mmHg)
Hypotension + increased JVD + distant heart sounds + increased HR + really decreased systolic BP during inspiration?
Cardiac tamponade
“Tree Bark” appearance of the aorta
seen with Tertiary Syphilis –> calcification of the aortic root and ascending aortic arch
- -> tertiary syphilis disrupts vaso vasorum of the aorta
- -> may result in aortic aneurysm….
“ball-valve” obstruction in left atrium; and multiple syncopal episodes
Myxoma = primary cardiac tumor in adults
primary cardiac tumor associated with tuberous sclerosis?
Rhabdomyomas
–> most frequent primary cardiac tumors in kids
Most common heart tumor?
Metastasis…
Kussmaul’s sign:
increased jugular venous pressure on inspiration
Most common vasculitis?
Temporal/Giant Cell Arteritis
unilateral headache, jaw claudication, elevated ESR, mostly in elderly females:
Temporal/Giant Cell Arteritis
Weak upper extremity pulses, younger females (<40 yo), elevated ESR
Takayasu’s arteritis
Vasculitis associated with Hepatitis B?
Polyarteritis nodosa
Which vessels are NOT affected in Polyarteritis nodosa?
Pulmonary arteries are NOT typically involved in Polyarteritis nodosa
1 case when kids can be given Aspirin?
Kawasaki disease (to prevent coronary aneurysms)
Coronary aneurysms in kids?
Kawasaki disease
strawberry tongue + lymphadenitis + peeling skin in kid?
Kawasaki disease
Vasculitis in a heavy smoker; usually male < 40 yo:
Buerger’s disease
p-ANCA
- Microscoppic polyangitis (purpura/vasculitis + glomerulonephritis)
- Churg-Strauss syndrome
Vasculitis with asthma and eosinophilia?
Churg-Strauss syndrome
most common childhood systemic vasculitis?
-Henoch-Schonlein purpura
Palpable purpura on butt/legs + Arthralgia (esp knees) + GI symptoms
- -> in kids, following an URI
- -> IgA immune complexes
Henoch-Schonlein purpura
2 types of Vasculitis with immune complexes:
- Polyarteritis Nodosa
- Henoch-Scholein Purpura (IgA immune complexes)
Port-wine stain on face; seizures, early-onset glaucoma
Sturge-Weber Disease (congentical vascular disorder; affects capillary-sized blood vessels)
Strawberry and Cherry Hemangiomas:
- Both are benign capillary hemangiomas (little red lesions)
- Strawberry–> infants; regresses spontaneously at 5-8 yo
- Cherry–> Elderly (little red mole); doesn’t regress; increase frequency with increase age
Cystic hygroma
red lesion on neck; seen with Turner syndrome
Red-Blue tumor under fingernails
- Glomus tumor
- ->benign, but painful
Bacillary angiomatous (caused by? may be mistaken for?)
- benign capillary red skin papules in AIDS pts
- caused by Bartonella henselae
- may be mistaken for Kaposi’s sarcoma
What should Beta-blockers be used cautiously in pts with DM?
beta-blockers can mask symtpoms of hypoglycemia in diabetic pts
first-line therapy for HTN in pregnancy?
-Hydralazine with Methyldopa
Hydralazine mechanism:
-Toxicity?
Vasodilates areterioles > veins
–> decreases Afterload!
*Toxicity: reflex/compensatory tachycardia; Drug-induced SLE
Prinzmetal’s angina
- -> occurs at rest, secondary to coronary artery vasospasm
- -> see ST elevation on ECG
anti-hypertensive drug that can cause cyanide toxicity?
Nitroprusside
anti-hypertensive drugs that decrease Preload AND Afterload?
Nitroprusside and ACE-inhibitors/ARBs
Calcium Channel Blockers: Which are dihydropyridines? Non-dihydropyridines?
- Non-Dihydrogpyridines –> act directly on the heart: Verapamil and Diltiazem
- Dihydropyridines: act on vascular smooth muscle: Nifedipine, Amlodipine…
- **Dihydropyridine CCBs act like nitrates: dilate veins and decrease preload
- **Non-dyhydropyridine CCBs act like Beta-blockers (increase preload; decrease afterload)
Nitrates mechanism? Effect on preload?
Dilate veins»_space; arteries
-decrease preload
non-cardiac clinical use of nitrates?
aphrodisiac and erection enhancer
side effects of nitrates?
- reflex tachycardia
- throbbing headaches
- cutaneous flushing
- tolerance/”Monday disease”
Drugs that decrease BP that are safe in pregnancy?
- Hydralazine
- Methyldopa
- Nifedipine
- Labetolol (mixed alpha/beta blocker; anti-HTN)
Drug of choice to decrease LDL? Side effects?
- HMG-CoA Reductase Inhibitors = Statins
- Side effects: Hepatotoxicity, Myopathy/Rhabdomyolysis
Side effects of Statins?
- Hepatotoxicity (elevated LFTs)
- Myopathy/Rhabdomyolysis
Drug of choice to increase HDL?
Side effects?
- Niacin = Vitamin B3
- Side effects:
- red, flushed face (can combat with aspirin)
- Hyperglycemia (acanthosis nigricans)
- Hyperuricemia (may exacerbate gout)
What may be given to combat side effects of Niacin therapy?
Aspirin (b/c red/flushed face may be d/t PG’s; so, give Aspirin to decrease PGs)
Which lipid-lowering drug may cause hyperglycemia and hyperuricemia?
-Niacin (Vitamin B3)
Drug of choice to decrease TGs?
- Fibrates
- -> side effects include hepatotoxicity and myositis (so, don’t give with statins, b/c exacerbate side effects)
- **can also give omega-3-FAs to decrease TGs
Ezetimibe
Cholesterol absorption blocker (lipid-lowering drug)
- not used much, b/c may increase plaque thickness
- prevent cholesterol reabsorption at small intestine brush border
Cholestyramine
Bile acid resin, decreases TGs (lipid-lowering drug)
-not used much, b/c tastes bad, causes GI discomfort, decreased absorption of fat-soluble vitamins
2nd line therapy if LDL is still high, despite Statins?
Ezetimibe (cholesterol absorption blocker)
Charcoal may be used as an antidote for?
-Digoxin toxicity!
Best anti-arrhythmic drug post-MI?
Class IB antiarrhythmics (Lidocaine, Tocainide, Mexiletine (Phenytoin))
Anti-arrhythmic that’s contra-indicated post-MI?
Class IC (Flecainide, Propafenone)
Effect of Class I antiarrhythmics on cardiac action potential and ECG?
- Decrease slope of Phase 0
- IA –> increase AP duration, increase ERP, increase QT
- IB –> decrease AP duration
- IC –> no effect on AP duration
Effect of Class II antiarrhythmics on cardiac Action Potential and ECG?
- decrease slope of phase 4
- increase PR interval (so slows AV conduction) –> takes longer to travel from SA node to ventricles via AV node, bundle of His, and fascicles)
List the Class IA antiarrhythmics:
“Double Quarter Pounder”
- Disopyramide
- Quinidine
- Procainamide
List the Class IB antiarrhythmics:
“Lettuce, Tomato, Mayo (Pickles)”
- Lidocaine
- Tocainide
- Mexiletine
- (Phenytoin)
List the Class IC antiarrhythmics:
“Fries, Please”
- Flecainide
- Propafenone
List the Class III antiarrhythmics:
“K IS BAD”
- Ibutilide
- Sotalol
- Bretylium
- Amiodarone
- Dofetilide
Anti-arrhythmics used to treat WPW syndrome?
- Procainamide (IA)
- Amiodarone (III)
List the Class IV antiarrhythmics
- Verapamil
- Diltiazem
Effect of Class II antiarrhythmics on cardiac Action Potential and ECG?
- decrease slope of phase 4
- increase PR interval (so slows AV conduction) –> takes longer to travel from SA node to ventricles via AV node, bundle of His, and fascicles)
List the Class IA antiarrhythmics:
“Double Quarter Pounder”
- Disopyramide
- Quinidine
- Procainamide
List the Class IB antiarrhythmics:
“Lettuce, Tomato, Mayo (Pickles)”
- Lidocaine
- Tocainide
- Mexiletine
- (Phenytoin)
List the Class IC antiarrhythmics:
“Fries, Please”
- Flecainide
- Propafenone
List the Class III antiarrhythmics:
“K IS BAD”
- Ibutilide
- Sotalol
- Bretylium
- Amiodarone
- Dofetilide
Anti-arrhythmics used to treat WPW syndrome?
- Procainamide (IA)
- Amiodarone (III)
List the Class IV antiarrhythmics
- Verapamil
- Diltiazem
child with weakened femoral pulses, systolic ejection murmur, higher BP on one arm than the other?
Coarctation of the Aorta - Infantile/Preductal type
Why increased coronary blood flow in aortic stenosis?
Blood flow through coronary arteries is regulated almost entirely by the metabolic requirements of the cardiac muscle. When have increased oxygen consumption by heart muscle, increased proportion of ATP is broken down to adenosine. Adenosine causes dilation of coronary arteries, which increases oxygen delivery to coronary arteries. So, in this sense, coronary blood flow increases proportionally to heart oxygen consumption.
***So, in aortic stenosis –> get increased Left Ventricular pressure –> increased oxygen consumption by Left Ventricle, because has a higher work load in pumping.
Capillary fluid exchange equation (Starling Force Equation):
Direction of flow?
Pnet = [(pc-pi) - (nc-ni)] where: pc = capillary pressure pi = interstitial fluid pressure nc = plasma colloid osmotic pressure ni = interstitial fluid colloid osmotic pressure
If Pnet = positive –> net flow OUT of capillary
If Pnet = negative –> net flow IN to capillary
