Cardiovasc Flashcards
Two main pathophysiology of peripheral artery disease
atherosclerotic PAD and Buerger dz, describe both: pg 70
what is Buerger dz?
thromboangiitis obliterans, “caludication in young smoker”, more common in males/Middle East/Asian, pg 70
exam findings PAD
Muscle atrophy, shiny or scaly skin, evidence of poor wound healing, digital ulcerations, lots of hair follicles, diminished pulses, slowed capillary refill
vascular vs neurgenic claudication
GO!
Leriche Syndrome triad?
Bilateral hip claudication, erectile dysfunction, absent femoral pulses equals aortoiliac occlusive disease
What ABI is diagnostic of PAD? When does claudicatin start? When do rest symptoms start? Descrie ABI
< 0.9, < 0.6, <0.25, cuff and doppler “ankle to arm”
what is only effective therapy for beurger?
smoking cessation
3 layers or arteries
tunica: intima, media, adventitia
most common sites of arterieal aneusrysms
- abdo aorta (AAA)
- popliteal
pathophys of true and pseudo aneurysms, differentiate from a dissection
True aneurysm: constant shear stress weakens the tunica media leading to dilation/ ballooning of all three layers. This shear stress is generally caused by atheros sclerosis and its risk factors.
Pseudo aneurysm: trauma to the vessel wall results in disruption of the intima and the media and communicates with a pseudo aneurysm which is usually a thin wall of tunica adventitia or other surrounding tissue
this is different from a dissection where the tunica intima is disrupted and blood is in a false lumen between the media and the intima
where do AAA most commonly happen?
below renal arteries or inferior SMA
most common location of AAA rupture?
retroperitoneal
what size defines AAA, when is surgery indicated for non-ruptured AAA?
> 3 cm =AAA, if >5 cm in females, 5.5 cm in males
RF for AAA
1st degree relative with same, CAD, PAD, age greater than 65 , , smoking history
symptoms of rapidly expanding/ruptured AAA
Abdominal, back or flank pain. Nausea/vomiting. Syncope or hypertension
Rarely, can also rupture into GI tract leading to GIB or can rupture into IVC and cause AV fistula leading to CHF
** if pt has aortic graft and GIB, need to think AAA
exam finding AAA
pulsatile mass, abdo pain, peritonitis, hypotension/shock
if retroperitoneal rupture can tamponade which may have normal vitals. look for cullen/grey-turner sign
ddx of AAA
Renal colic, muscular back pain, pancreatitis, mesenteric ischaemia, diverticulitis, biliary disease, appendicitis . Rarely, GI bleed or congestive heart failure.
Can also present like a ACS due to hypo perfused coronary is especially impatient with predisposing CAD
what is endoleak?
complication of AAA graft repair. blood gets between graft and aneurysm and aneurysm can continue to grow +/- rupture
complications of AAA graft repair
Acute complications include vascular injury to renal, or mesenteric arteries.
Chronic complications include infection, thrombosis, migration, aortaenteric fistula, pseudo aneurysm at anastamosis site or endo leak
what defines thoracic aortic aneurysm
TAA > 4.5 cm, often an incidental finding
symptoms of thoracic aortic aneurysm
same as AAA, asymptomatic unless ruptures or rapidly expanding or mass effect
if ruptured: chest or back pain, can have hoarsness, cough, wheeze d/t RLN compression
Tx of thoracic aortic aneurysm
similar to dissection: aggressive BP/HR control, pain control, surgical consult STAT
Stanford Classification of Aortic Dissection
A: ascending (or both)
B: descending
RF for aortic dissection
Hypertension, advanced age, connective tissue disease, congenital heart disease, giant cell arteritis, family history, stimulant abuse, iatrogenic [ catheterization or surgery]
complication of dissection
if proximal: MI, aortic regurg, tampondae,
if distal: stroke like symptoms, limb/organ ischemia
chest pain and neuro symptoms, think?
Aortic Dissection
D-Dimer and CXR in dissection?
dimer: 90% sens, poorly specific
CXR abn in 85%, however CTA by far the best test
Initial TX of Dissection:
pain control, SBP 100-120, HR <60
-labetalol, esmolol can then add nitroprusside prn
target time to re-vascularization after acute peripheral artery occlusion
4-6 hrs before limb ischemia requiring amputation, can also cause death
acute artery occlusion pathphys
either embolic or thrombotic, embolic (usually from LV in pt with MI) is worse b/c it is so acute there is no collateral blood flow. thrombotic likely has collateral flow bc atherscleoriss occurs at site pg 78
6 P’s of limb ischemia
pallor, pulselessness, pain out of proportion, paralysis, poikilothermic, paresthesia
treatment of acute peripheral artery occlusion
Heparin! then surgical tx depends on whether embolic or thrombotic.
diagnosis is clinical, can get CTA to confirm
RF for VTE
Trauma, travel, hypercoagulable state, hormone replacement, family history, IVDU, age over 60, malignancy, birth control, obesity, pregnant, recent surgery, smoking, immobilization, sickness… DVT is biggest risk for PE
Homans Sign?
Pain in calf or posterior knee with passive dorsiflexion of foot…. looks for DVT
3 complications of DVT
PE, chronic venous insufficieny, SVC sydrome (with upper extremity clot), postphlbetic syndrome
2 severe manifestations of DVT
Phlegmasia cerulean dolens = painful blue leg –> massive clot, causes massive edema to venous insufficieny
phlegmasia alba dolens= painful whit leg, massive venous clot causes arterial spasm
W/U of DVT
Wells 2 or less = dimer
wells 3 or more = u/s
timeframe of surgery/trauma that confers biggest VTE risk?
within last 4 weeks
PE wells: 2-tier model?
wells 4 or less = dimer
wells 5 or more = CTA
2 cxr findings in PE
Hamptom hump, Westermark sign (rare)
when to use PERC
in a patient with low pretest probability
indications for thrombolysis in PE
hypotension (SBP <90 for >15 minutes or SBP 60 pts below baseline), severe hypoxemia, cardiac arrest, evidence of right heart strain
RBBB ECG findings?
QRS > 0.12, rSR’ in V1, slurred S in V6 and discordant T waves
LBBB ECG findings
QRS > 0.12 s, big S wave in V1, monophasic or notched R in lateral (somtimes looks like M), discordant T waves
conduction path in BBB
through opposite side of heart
Can RBBB and LBBB occur in healthy heart?
RBBB can but usually not, LBBB cannot
causes of RBBB
acute or chronic rt heart strain ( pulm HTN, PE, COPD, cardiomyopathy)
Causes of LBBB (same as fasicular blocks)
HTN, valve dz, IHD, cardiomyopathy, myocarditis, CHD, post cardiac sx
what are bifasciular blocks? what to do for them?
LBBB (according to some, but maybe not)
,RBBB + LAFB (manifested as LAD)
RBBB+LPFB (manifested as RAD)
temporary then permanent pacing if symptomatic brady (syncope etc)
LAFB and LPFB ECG findings:
normal QRS for both:
LAFB: big S in inf leads, R in Lat leads
LPFB: big R in inf leads big S in lat leads
RVH causes?
anything increasing rt sided pressures chronically eg Pulmonic stenosis, pulm HTN, chronic PE,
LVH ECG findings?
left axis,
S in v1 + R in V5 > 35 mm or R in aVL > 11mm
ECG signs of rt sided heart strain?
inverted Ts in V1-3
RVH ECG findings?
-Right axis deviation
-Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
-Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
-QRS duration < 120ms (i.e. changes not due to RBBB).
ECG findings in hyperK, and at what levels
6.5-7.5 –> Tall peaked T’s (EARLIEST), PR prolongation
7.5-8 –> P wave flattens, QRS widens
>9.0 –> sine wave, anticipate arrest
ECG findings of hypokalemia
flattening of T wave (earliest), U wave following T wave, ST depression, PR prolongation
hypercalcemia ECG
short QT, depressed and short ST
hypocalcemia ECG
long QT
dig effect vs dig toxicity on ECG
dig effect = common in dig users (not indicative of toxicity) = depressed ST, short QT, flat T, prominent U AKA similar to hypo K
dig toxic: any arrythmia –> PVC, a fib, AVB,
hypothermia ECG
everything prolongs and J wave (aka Osborn wave)
defn hypothermia = T < 35, biggest risk of arrhythmia < 30.
progressino is often : sinus brady –> afib –> Vfib
SACPE (aka flash pulm edema, aka severe hypertensive HF) features?
-Rapid onset of respiratory distress (e.g., usually within <6 hours).
-Marked tachypnea and dyspnea.
-Hypoxemia.
-Hypertension (generally SBP>160 mm and/or MAP>120 mm).
-Diffuse rales on auscultation.
-Pink, frothy sputum may be seen.
-Clinical features of sympathetic activation:
Diaphoresis, pallor, appearing extremely unwell.
Tachycardia.
Agitation.
Patients may have a history of recurrent episodes of SCAPE.
mortality of HF
50% die in 5 yrs of dx
precipitants of AHF
non-adherence (meds or excessive fluid/salt), renal failure, drugs (meth, cocaine, etoh), HTN, IHD, iatrogenic (meds)
6 phenotypes of AHF
SCAPE, cardiogenic shock, pulm edema, acute on chronic, high-output, right sided
My approach: Is it SCAPE? Is it cardiogenic shock? or is it “regular” HF
if regular: what is BP, what TX can they tolerate, what Tx do they need, what Tx are they on already.
if SCAPE: bipap or cpap and nitro, these usually reduce BP if not add something else
cardiogenic shock:
- Optimize oxygenation with NIPPV
-Optimize blood pressure with vasopressors (eg. norepinephrine) to maintain cardiac/end-organ perfusion targeting a MAP of 65-80
Optimize contractility with ionotropes (eg. dobutamine, milrinone)
-Optimize volume status (crystalloid or diuretics)
** norepi 1st!!, most inotropes are vasodilators, so can worsen things if pressor not on board.
indications of bipap in AHF
hypoxia, tachypnea/resp distress, pulm edema
5 types of non-ischemic cardiomyopathy –> names, pathophys, some causes
this means structural or functinoal dz in the absence of CAD, HTN, valve dz
ischemic cardiomyopathy is also a thing tho?
- dilated, myocyt death leading to chamber dilation and systolic dysfunction, 40% are genetic rest are d/t drugs (cocaine, etoh), myocarditis (NOT ISCHEMIA) etc, presenet like Lt sided HF
- resitrictive (leat common), infiltrates that impair fillin and cause diastolic dysfunction, systolic function retained, eg amyloid, sarcoid, hemochromatosis,
- hypertrophic –> often autosomal dom (ask about famhx SCD), causes asymetric LV thickening, will lead to LV outflow tract obstruction (aka HOCM)
- ARVC(H) –> auto dom, common in italy, right ventricular dysplasia, leading to ventricular arrythmias
- unclassified (eg takutsubos LV dysfunctino caused by stress hormones/microvasc spasm) –>mimics stemi (HAS ST ELEVATION AND ELEVATED TROP) but has normal angiocath. treat like ACS, can only diagnose after normal cath
when to consider restrictive cardiomyopathy
pt with HF and no cardiomegaly and no systolic dysfunction (eg preserved EF)
ECG finding for ARVC
T-wave inversion in V1,V2, V3 AND EPSILON WAVE (EXACT OPPO OF DELTA, AKA DOWN SLOPING AND ON OTHER SIDE OF QRS)
ECG finding for Brugada
coved or DOWN sloping ST segments in V1-2
ECG finding for HCM
dagger-like q waves in lateral and inferior, LVH criteria
ECG finding for WPW
delta wave (upsloping QRS)
Who presents atypically with ACS?
Women, diabetics, elderly, racial minorities, psych pts, altered mental status
Immediately life threatening CP causes?
PE, esophageal rupture, tension pneumo, mi, aortic dissection, cardiac tamponde
Also consider pma, pericarditis/myocarditis
Non ACS causes of elevated trop
Cardiac contusion, cardiac procedures, acute or chronic HF, dissection, aortic valve dz, HCM, arrhythmia, PE, pulm htn, myocarditis, resp failure, burns, sepsis, among others
Most common cause of myocarditis in developed vs worldwide
Viral illness
Chagas disease
Common viral triggers for myocarditis
Cocksackie virus
Adenovirus
Covid
Hep B and C
HIV
Bacterial causes of myocarditis
Strep
Mycoplasma
Diphtheria
Lyme (borrelia burgdoferi)
Mycobacterium
Myocarditis symptoms
Flu like symptoms, CP, new chf ,
Syncope
Two sensitive, but not specific blood tests in myocarditis
Trop, Crp
General causes of myocarditis
Virus
Bact
Fungi
Parasite eg chagas
Tox eg pcn, sulfas, cocaine
Autoimmune eg Kawasaki, sarcoidosis, SLE
Mgmt of myocarditis
Subclinical -> trend trop
Stable —> ace, BB, MRA
Unstable—> inotropes, balloon pump, ecmo etc
Complications of myocarditis
Sudden death
Dilated cardiomyopathy
Heart failure
Mural thrombus
Dysrhythmia
Echo in myocarditis
Dilated chambers
Global or focal hypokinesis
Note mri: is helpful too
three principal presentations of unstable angina
rest angina, new-onset angina, increasing angina
describe coronary artery anatomy
tintins 334
what %age of ACS has cc other than CP?
47%!
new systolic murmur in ACS could mean?
papillary muscle rupture and resultant mitral regurg
time frame for ECG upon presentation for any ?ACS
< 10 mins
next step in inferior STEMI?
rt sided leads, get lead V4R looking for rt ventricular infarct
right sided ECG - put precordial leads in mirror image on right sie, can usually leave V1,2 in place an just get v3-6R, alternatively, just get V4R as it is most useful.
anatomical localisation of ST elevation?
Anteroseptal = LAD, V1-V4
Anterolateral = Cx V1-V6, aVL, 1
Inferior = RCA 2, 3, aVF
Posterior = Cx or PDA (off RCA), posterior ECG –> V7-9 elevation.
STEMI minimum criteria:
≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
≥ 1.5 mm ST elevation in V2-3 in women
≥ 1 mm ST elevation in other leads
New LBBB (LBBB should be considered new unless there is evidence otherwise)
** note recirpocal changes are not required, but certainly make it more likely (ie help differentiate benign early repol most prominent in v2-5)
posterior lead placement?
v7, 8, 9 get wrapped around left chest wall –> different from right sided placement
inferior wall MI can result from damage to which to vessels
LCx or right main
if ST elevation in 3>2, predicts right main
if inferior with any lateral lead STE (v6, 1, aVL) more likely LCx
STE in aVR > v1 suggests?
LAD occlusion (strangely)
what is wellens syndrome?
T wave abn (usually deep T wave inversion in V2-3), indicative of critical LAD stenosis
T wave abn often resolve when pain goes away, check ECGs when in pain and pain free
de winter T wave?
upsloping ST depresiion with peaked T in precordial leads –> anterior MI/STEMI equivalent
LBBB in ? ACS
look for concordant STE or STD (both suggest infarct) use sgarbossa and assume its new unless documented otherwise
how long is trop + after MI
usually at least 10 days
NSTEMI ED cocktail
ASA, ticag or plavix, enox or fonda SC
STEMI cocktail
depends on reperfusion strategy, go through both
time to needle goal for lytics?
time to balloon for PCI?
30 mins
90-120 mins
indication for lytics
<6-12 hrs of symptoms onset, >=1mm STE in 2 or more contiguous leads and no CI
list CI to lytics
tints 346
failure rate of lytics in STEMI
40-50%
when to start BB after STEMI?NSTEMI
start PO (not IV) within 24 hrs, if no CI (HF, brady, hypotension, etc)
suspect posterior MI when
inferior or lateral ischemia, OR when big ST depression in V1-3 (can flip it upside and it looks like posterior ECG, get the post though and look for STE in v7-9
isoloated poterior is rare, (3-11%), but if posterior MI along with either inferior or lateral, suggests greater damage/ higher M&M
ae of MI
acute: CHF, cardiogenic shock, dysrhymia (any really), wall rupture, papillary muscle rupture, pericarditis
longer term: LV thrombus, LV aneurysm, pleuropericarditis (Dressler syndrome)
Dressler syndomre?
pleuropericarditis, presents with CP and fever 2-10 weeks post MI, tx is NSAIDs and steroids
causes of pericarditis?
idiopathic (80%), infectious (mostly viral), then meds, autoimmnue dz, dressler’s, uremia, malignancy, trauma
ECG changes, 4 stages of pericarditis,
1 (first hours-days): PR depression, diffuse STE
2. PR and ST normalize, then T waves flatten
3. diffuse t wave inversion
4. back to normal
is pericarditis made better leaning forward or backwards
Better leaning forward!
most specific finding for pericarditis
PR depression
complications of pericarditis
tamponade
constrictive pericarditis
etiologies of pericardial effusion
malignancy, trauma, post infection, radiation, post cardiac Sx, pericarditis, renal failure
Becks triad for tamponde
hypotension, muffled HS, JVD
what does electrical alternans signify
pericardial EFFUSION
effusion vs tamponade
effusion: fluid in sac, generally develops slowly
tamponade= generally develop quicker, hemodynamic compromise from effusion, RV collapses during diastole (seen on echo)
finding in tamponade
electrical alternans, low voltage QRS, kaussmaul sign, pulsus parodoxus >10 mmhg, narrow pulse pressure, pericardial friction rub
types of hypertensive emergency
head to toe: PRES (aka hypertensive encephalopathy), ICH,, aortic dissection, MI, pulm edema, HELLP, acute renal failure, retinopathy
immediate mgmt of HTN emergency?
reduce MAP 10-20% in 30-60 mins or to DBP of about 110
can cause ischemia if reduction >20% dt relative hypotension.
some meds for HTN emergencies
labetalol/esmolol/hydralazine,
esmolol onset 60 sec, offset 10-20mins. bolus 250-500mcg/kg ( probs 250?) then infusion.
HTN urgency?
controversial. >180/110, but best Tx is oral meds, if no end organ damage, no need to tx IV.
can use captopril or losartan,
if on acei/ARB, can add HCTZ/increase dose, add beta blocker etc.
Most common valve lesion
Mitral prolapse
Complications of LVH
LVH -> Dec cardiac output -> dilated cardiomyopathy -> can lead to CHF, arrhythmias, sudden death, (also can drop SBP)
When is aortic stenosis symptomatic, classic triad?
70% stenosis, angina, syncope, CHF
Aortic stenosis: causes, murmur
Calcific valve degen (>65), bicuspid valve (<65)
Crescendo decrescendo systolic
Management considerations for aortic stenosis
Gentle diuresis, cautious fluid, rule out ACS, ?prophylaxis for IE, IABP which can bridge to definitive tx
Avoid preload and afterload reducers (no nitro)
Causes of acute aortic regurg? Mgmt of acute aortic regurg? Presents like?
IE, aortic dissection, trauma
Mgmt: surgical emergency, need aggressive after load reduction
Presents like pulmonary edema, CV collapse
Mitral stenosis causes,,, most common and a few other causes
Rheumatic dz (common)
Atrial myxoma, congenital abn, calcific valve degen
valve indicaitons for IABP
Acute AS, MR, BUT NOT acute AR
acute MR tx:
surgical emergency IABP as bridge, afterload reduction and tx of pulm edema
what other valve dz does MVP cause
MR
2 broad categories of prosthetic valves
mechanical and bioprosthetic
complications of prosthetic valves:
failure, thrombosis +/- systemic embolization, paravavular leak, endocarditis
RF for IE
CHD, rheumatic dz, IVDU, prosthetic valves, pacemaker
most common causative organisms in IE
Staph and strep
what are HACEK organisms
difficult to isolate bugs that can cause IE in immunocomp pts
Hemophilus, actinobacillus, Cardiobacterium, Eikenlla, Kingella
Rt sided endo, think?
IVDU
duke criteria for IE
2 major findings, 1 major and 3 minor or 5 minor findings = IE
major: 2 or more + BCx, major echo findings
minor: fever, minor echo findings, RF, embolic dz, immunologic phenomeneeon (osler’s nodes osler = ouch), 1 + BCx
exam findings in IE
murmur, immuno: osler’s, roths spots
vasc: splinter hemm, Janeway lesions, signs of emboli
categories of syncope
First rule out catastrophic bleeds: subarachnoid hemorrhage, ectopic pregnancy, massive GI bleed, ruptured AAA (USUALLY THESE HAVE OTHER symptoms)
-Reflex syncope – vasovagal, carotid sinus syndrome, situational
-Orthostatic syncope – drug induced, volume depletion, neurogenic
-Cardiovascular syncope – mechanical (PE, tamponade, aortic stenosis), dysrhythmias, MI
clues for cardiac syncope
-Cardiovascular risk factors
-Structural heart disease (especially HCM, aortic stenosis)
-Pacemaker
-Sudden syncope with no prodrome
-Exertional syncope
-Prodrome that includes palpitations, shortness of breath or chest pain
-Associated facial injury (including dental injury, eye glasses damage, tip of tongue bite)
-Family history of unexplained sudden death, drowning or single MVC <50 years of age
-Aortic stenosis murmur – high mortality rate in patients with critical aortic stenosis and syncope
seizure vs syncope 10:20 rule
<10 myoclonic jerks = syncope, >20 seizure, between ?
what %age of pts with seizure have post ictal state
96% usually 5-30 mins
7 step approach to syncope ECG
tachy/brady, bifasciular blocks, WPW, HCM, ARVC brugada, long qt
drugs that commonly cause syncope
Erectile dysfunction medications, antihypertensive, beta blockers, cardiac glycosides, diuretics, antiarrhythmics, anti psychotics, antiparkinson drugs, antidepressants common nitrates, alcohol, cocaine
4 tips to distinguish SVT from VT
These suggest VT:
Fusion beats
Capture beats
Precordial concordance (if all are going same direction in v1-3 suggests vt)
Av dissociation
+ qrs in AvR suggests VT
syncope ddx
