Cardiology Flashcards
when is using troponin not helpful and what should you use instead
during re-infarctions - use CK-MB instead
Acute Coronary Syndrome Tx =
MONA BASH C m- morphine o- oxygen n - nitrates - HOME (if continuous angina) a- aspirin - HOME b - beta blockers - HOME a- ace inhibitor - HOME s- statins- HOME h- heparin - LMWH c- clopridogrel
For ACS tx what are protocols for clopridogrel
- give if stent placed
- if drug eluting stent - tx = 1 year
- if metal stent - tx = 1 month
why are beta blockers important for ACS tx
prevent mortality in first 24 hrs due to ventricular arrythmias
when should TPA be given for ACS
when stents cannot be placed for >60 min
rural settings basically
what type of MI are nitrates contraindicated for
right sided - leads II, III, aVF with ST segment elevation - this is due the RV being pre load dependent and nitrates decrease preload
stable angina basics
due to fixed atherosclerotic lesions that narrow the major coronary arteries
occurs when O2 demand exceeds available blood supply
coronary ischemia due to
imbalance between blood supply and oxygen demand leading to inadequate perfusion
major risk factors for ischemic heart disease
DM HLD HTN Smoking Age: men >45, women<55 FMHX of CAD men <55, women< 65 low levels of HDL
prognostic indicators of CAD
LV function - Ejection Fraction
<50% = increased mortality
vessels involved with severe ischemia
left main coronary artery - poor prognosis - due to covering 2/3 of heart
2 or 3 vessel CAD - worse prognosis
what is the LDL goal in a pt with CAD
<100mg/dL
typical anginal chest pain
substernal
worse with exertion
better with rest or NTG
metabolic syndrome X
combo of: HTN, hypercholesteremia, hypertrigyceridemia, imparied glucose tolerance, diabetes and hyperuricemia
key factor = insulin resistance (due to obesity)
syndrome X
exertional angina with normal coronary arteruigra
pts present with CP after exertion but have no coronary stenosis at catheritization
exercise test and nuclear imagin show evidence of MI
prognosis = excellent
Q Waves are consistent with
prior MI
if ST segment of T wave abnormalities are present during an episode of Chest pain –> tx =
treat as Unstable angina (USA)
how do you calculate a persons max HR
220 - age
what is the best initial test for all forms of CP
ECG
stress testing is used in what situations
- to confirm dx of angina
- to eval response of therapy in patients with documented CAD
- to ID pts with CAD who may have high risk acute coronary events
what makes for a (+) stress test
if any of these occur during exercise
- ST segment depression
- CP
- hypotension
- significant arrhythmias
exercise induced ischemia results in
subendocardial ischemia, producing ST segment depression
pts with a (+) stress test –>
go to get cath
exercise induced ischemia is evidenced by
wall motion abnormalities
stress echocardiography can detect
- can assess LV size and function
- can dx valvular dz
- can be used to ID CAD in the presence of pre-existing ECG abnormalities
pts with (+) stress echo –>
go to cardiac cath
types of stress test
exercise ECG –> ST segment depression
exercise or dobutamine echocardiogram –> wall motion abnormalities
exercise or dipyridamole perfusion study (thallium/technetium) –> decreased uptake of the nuclear isotope exercise)
areas of reversible ischemia may be rescued with
percutaneous coronary intervention or CABG
pharm stress test
IV adenosine, dipyridamole, or dobutamine
- adenosine and dipyridamole - cause generalized coronary vasodilation - further worsening dz arteries
- dobutamine - increased myocardial o2 demand by increasing HR, bp, and cardiac contractility
holter monitor uses
detecting silent ischemia (ECG changes not accompanied by symptoms)
evaluating arrhythmiasm heart rate variability and assess pacemaker and implantable cardioverter-defribillator function
evaluating unexplained syncope and dizziness
- continuous monitoring 24-72hr
definitive test for CAD
coronary angiography
indications for cardiac catheterization
after + stress test
acute MI with intent of performing angiogram and PCI
pt with angina + noninvasive test are non dx
angina that occurs despite medical therapy
angina that occurs soon after MI
any angina that is a dx dilemma
for eval of valuvar dz and to determine need for sx intervention
most accurate method for identifying the presence and severity of CAD
coronary arteriography (angiography)
standard test for delineating coronary anatomy
most accurate method of determining a specific cardiac dx
cardiac catheterization
main purpose of coronary arteriography
ID pts with sever coronary dz and to determine whether revascularization is needed
coronary stenosis > 70%
may be significant
can produce angina
on a arteriography what qualifies as severe and in need of revascularization
left main or three vessel dz
standard of care for stable angina
aspirin
beta blocker
(only ones that lower mortality)
nitrates for CP
diet modifications for ischemic heart disease
reduce intake of saturated fats <7%
reduce cholesterol <200mg per day
side effects of nitrates
HA
orthostatic Hypotension
tolerance
syncope
aspirin basics in CAD
indicated in all pts with CAD
decrease morbidity
reduces risk of MI
beta blockers basics in CAD
block sympathetic stimulation of heart
reduce HR, BP, and contractility , Cardiac work
reduce myocardial oxygen consumption
reduce the frequency of coronary events
first line choices for beta blockers in CAD
atenolol and metoprolol
nitrates in CAD
cause generalized vasodilation
relieved angina - reduce preload myocardial oxygen demand - reduce LVEDV
calcium channel blockers in CAD
cause coronary vasodilation and afterload reduction
reduces contractility
secondary tx when beta blockers and nitrates not fully effective
DO NOT DECREASE mortality
if CHF also present along with CAD tx with
ACE- I and/or diuretics
revascularization basics in CAD
DOES NOT reduce incidence of MI
does result in significant improvement of symptoms
mild CAD disease
normal EF
mild angina
single vessel dz
tx - aspirin, beta blockers and nitrates (+Ca channel blockers if symptoms dont improve)
moderate CAD disease
normal EF
moderate angina
two vessel dz
tx - if nml regiment does work consider arteriography + PCI or CABG
severe CAD disease
decreased EF
severe angina
3 vessel/ left main or left anterior descending dz
tx - coronary angiography and possibly CABG
Percutaneous coronary intervention (PCI)
coronary angioplasty with ballon and stenting
best used for proximal lesions
risk in PCI
higher frequency of revascularization procedures
restenosis is a significant problem - however if it does not occur at 6 months your golden
CABG
standard of care for high risk dz
main indicators:
- 3 vessel dz with >70% stenosis in each vessel
left main coronary dz with >50% dz
- left ventricular dysfunction
unstable angina (USA) pathophysiology
oxygen demand is unchanged - supply is decreased secondary to reduced resting coronary flow
indicates stenosis that has enlarged via thrombosis, hemorrhage, or plaque rupture –> may lead to total occlusion of a coronary vessel
example of pts with USA
- pt with chronic angina with increasing frequency, duration, or intensity of CP
- pts with new onset angina that is severe and worsening
- ts with angina at rest
what is the difference between USA and NSTEMI
NSTEMI - has elevated cardiac enzymes while USA does NOT
stress testing only detects flow limiting high grade lesions so even with a (+) stress test what can be missed
an MI can be missed due to an MI being an acute plaque rupture onto a moderate lesion
pts with USA have a higher risk of adverse events during a
stress test - they should be stabilized with medical management prior to performing one or undergo cardiac cath
tx of USA
admit
MONA BASH C
Clopidogrel for 2 days
glycoprotein IIb/IIIa ihibitors (abciximab, tirofiban) - if pt undergoing stenting
DOC for the H in MONA BASH C
Low molecular weight heparin - specifically enoxaprin
variant angina
prinzmetal
transient coronary vasospasm that is usually accompanied by a fixed atherosclerotic lesion (but can occur in nml coronary ateries as well)
- angina at rest and associated with ventricular dysrhythmias that can be life threating
- angina classically occurs at night
hall mark of prinzmetal
transient ST segment elevation on ECG during CP which represents transmural ischemia
definitive test for prinzmetal
coronary angiography - displaying coronary vasospasm when pt given IV ergonovine or acetylcholine to provoke vasocosntriction
tx of prinzmetal
calcium channel blockers and nitrates and risk modification
MI is due to
necrosis of myocardium as a result of interruption of blood supply –> after thrombotic occlusion of coronary artery previously narrowed by atherosclerosis
most cases of MI are due to
acute coronary thrombosis - atheromatous plaque ruptures into vessel lumen and thrombus forms on top of this lesion –> vessel occlusion
Mortality rate of MI
30% and half of deaths are prehospital
clinical features of MI
intense substernal pressure (crushing elephant on chest)
radiation to neck, jaw, arms, or back (left side)
pain does not respond to NTG
epigastric discomfort
diaphoresis, dyspnea, weakness, fatigue,
N/V, syncope
can be asymptomatic in 1/3 - women, post op pts, elderly, diabetics
ECG markers of ischemia/infarction
Peaked T waves - occur very early
ST segment elevation - transmural injury and can be dx of acute infarct
Q waves - evidence of necrosis - late sign - old infarct
T wave inversion
ST segment depression - subendocardial injury
what comb of symptoms strongly indicates acute MI
substernal CP persisting longer than 30 min
diaphoresis
presentation of a RV infarct
inferior ECG changes hypotension elevated jugular venous pressure hepatomegaly clear lungs
what is contraindcated in RV infarct
nitrates or diuretics as will cause cardiovascular collapse due to RV being preload dependent
anterior infarct ECG changes
ST segment elevation in V1-V4 (acute/active)
Q waves in leads V1-V4 (late changes)
posterior infarct ECG changes
large R waves in V1 and V2
ST segment depression in V1 and V2
upright and prominent T waves in V1 and V2
lateral infarct ECG changes
Q waves in leads I and aVL (late change)
inferior infarct ECG changes
Q waves in leads II, III and aVF (late change)
ST segment elevation infarct indicates
transmural - involves entire thickness of wall tends to be larger
Non ST segment elevation infarct indicates
subendocardial - involves inner 1/3 to 1/2 of the wall - tends to be smaller
CHF pt with EF <35% and not Class IV tx = ?
AICD to prevent sudden cardiac death
tx of CHF exacerbation
LMNOP L - lasix M - morphine N - nitrates O - oxygen P- position
gold standard for myocardial injury test
cardiac enzymes
troponin (trop I and T)
increases within 3-5hrs
peaks at 24hrs
returns to normal 5-14 days
must do serial troponins every 8hrs for 24hrs
how can Troponin I be falsely elevated
in renal failures pts
CK-MB
increases within 4 to 8hrs
reaches peak at 24hrs
returns to normal 48-72hrs - thus making it more helpful in detecting recurrent infarction
the higher the peak and the longer the enzyme levels
the more severe the myocardial injury and the worse the prognosis
In MI what drugs are shown to reduce mortality
aspirin
beta blocker
ace inhibitors
a high frequency of PVCs may predict
VFIB
VT
HTN affects on afterload
increases afterload and thus oxygen demand
tx of an MI patient
admit aspirin beta blockers ace i statins oxygen nitrates morphine sulfate heparin revascularization
aspirin basics for MI
- antiplatelet agent reduces coronary reocclusion by inhibiting platelet aggregation on top of the thrombus
has been shown to reduce mortality
beta blocker basics for MI
block stimulation of HR and contractility to reduce oxygen demand and decrease the incidence of arrhythmias
reduce remodeling of the myocardium post MI
reduce mortality
ace inhibitor basics for MI
initiate within hours of hospitlization
reduce mortality
statins basics for MI
reduce the risk of further coronary events
stabilize plaques and lower cholesterol
statin of choice for MI patients
atorvastatin 80mg
revascularization benefit is highest when
performed <90min of pts arrival
urgent CABGs are performed when
mechanical complications of acute MI
cardiogenic shock
life threatening ventricular arrhythmias
failure of PCI
thrombolytic therapy for MI
outcome is best if given within 6hrs
indications: ST segment elevation in 2 contiguous ECG leads - in pts with pain onset <6hrs who have been refractory to NTG
thrombolytic of choice for MI
alteplase
alternatives - streptokinase, tenecteplase, reteplase, lanotelplase and urokinase
absolute contraindications to thrombolytic therapy
trauma previous stroke recent invasive procedure or surgery dissecting aortic aneurysm active bleeding or bleeding diathesis
papillary muscle infarction/ ischemia leads to
mitral regurgitation - pt presents with new murmur
tx - emergent surgery - with valve replacement + afterload reduction with sodium nitroprusside or intra-aortic ballon pump
pts who suffer an acute MI have a high risk of what developing
stroke for the next 5 years
the lower the EF and the older the pt the higher the risk of stroke
complications of acute MI
pump failure = CHF - mc cause of in hospital mortality - tx if mild ace-i and diuretic
arrhythmias
- PVCs - tx - obs
- Afib
- VT - tx - if stable - IV amiodarone - if unstable = electrical cardioversion
- V fib - immeidate unsynchronized defib and CPR
- sinus tach - worsens ischemia
- av block - if 1st degree or 2nd degree type I = no tx
- but if 2nd deg type II or 3rd degree pacemaker is indicated and IV atropine initially
what arrhythmia is a common occurance in the early stages of an acute MI
sinus bradycardia - especially right sided/ inferior MIs
may be protective - reduces myocardial oxygen demand
- tx - if symptomatic = atropine
if asystole is clearly the cause of an arrest s/p acute MI tx =
transcutaneous pacing - however mortality is very high
if there is repeat ST segment elevation on ECG within the first 24 hrs after infarction suspect
suspect recurrent infarction
mechanical complications of an acute MI
free wall rupture - occurs during 1st 2 weeks post MI - mc 1-4 days s/p MI –> leads to hemopericardium and cardiac tamponade
rupture of interventricular septum - within 10 days of MI
papillary muscle rupture
ventricular pseudoaneurysm - seen by bedside echo
ventricular aneursym
acute pericarditis
dressler syndrome
tx of free wall rupture s/p acute MI
usually fatal
hemodynamic stabilization
immediate pericardiocentesis
surgical repair
MC cause of death in first few days after MI
is ventricular arrhythmia (VTach or VFib)
acute pericarditis s/p MI - tx
aspirin
NSAIDs, corticosteroids are contraindicated (may hinder myocardial scar formation)
dressler syndrome s/p MI
immuno based syndrome - fever, malaise, pericarditis, leukocytosis, and pleuritis occurring weeks to months after MI
tx = aspirin (1st line) and IBU 2nd line
the most common cause of noncardiac chest pain in the ED
GI disorders
if NTG relieves the pain then
a cardiac cause is more likely (although esophageal spasm) is still a possibility
cardiac cause of the pain is highly unlikely if what symptoms appear
if CP changes with respiration (pleuritic) or if there is tenderness of chest wall
CHF overview definition
results from the hearts inability to meet the body’s circulatory demands under nml physiologic conditions
often both systolic and diastolic dysfunction
pathophys of CHF - frank sterling relationship
in nml heart incresing preload -> increase contractility
when preload is low (rest) - there is little difference between nml and failing heart
but –> with exertion a failing heart produces relatively less contractility and symptoms occur
systolic dysfunction
impaired contractility - decreased EF
heart is too flabby to squeeze blood out
causes of systolic dysfunction
ischemic heart dz recent MI HTN - cardiomyopathy valvular dz myocarditis (post viral)
diastolic dysfunction
impaired ventricular filling during diastole
impaired relaxation or increased stiffness of ventricle or both
heart is too thick = no space for blood to fill
echo of a heart with diastolic dysfunction will show
impaired relaxation of LV
in high output HF an increase in cardiac output is needed for
the requirements of peripheral tissues for oxygen
causes of high output HF
chronic anemia pregnancy hyperthyroidism AV fistulas Wet beriberi paget dz of bone Mitral regurg aortic insufficiency
causes of diastolic dysfunction
MCC = HTN leading to myocardial hypertrophy
valvular dz - aortic stenosis, mitral stenosis, and aortic regurg
restrictive cardiomyopathy - amyloidosis, sarcoidosis, hemochromatosis
symptoms of left sided heart failure
dyspnea - secondary to pulm congestion/edema
orthopnea - stack pillows for relief
paroxysmal nocturnal dyspnea - awake 1-2hrs after sleep due to SOB
nocturnal cough
confusion and memory impairment - inadequate brain perfusion
diaphoresis and cool extremities at rest
signs of left sided HF on exam
displaced PMI - due to cardiomegaly
pathologic S3(ventricular gallop) - rapid filling S4 gallop - stiff LV
crackles/rales
dullness to percussion
decreased tactile fremitus
NYHA classification of heart failure
I - symptoms only with vigorous activity
II - symptoms with prolonged or mod exercise - slightly limiting
III - symptoms with usual daily activities extremely limiting
IV - symptoms occur at rest
symptoms /signs of Right sided HF
peripheral pitting edema nocturia - due to increased venous return JVD hepatomegaly/heptojuglar reflex ascites right ventricular heave
Pathologic S3
rapid filling phase into noncompliant LV chamber (LV failure)
nml in kids - pathologic in adults
heard best at apex with bell of stethoscope
S3 follow S2 (kentucky noise)
low freq diastolic sound
tx - diuretics for symptomatic relief
S4 gallop
atrial systole as blood is ejected into a noncompliant or stiff LV chamber
heard best at left sternal border withbell of stethoscope
S4 precedes S1 (tennesse sound)
pathophys behind crackles/rales seen in CHF
caused by fluid spilling into alveoli indicating pulmonary edema
rales heard over lung bases suggest at least moderate severity of LV HF
what is the cause of the dullness to percussion and decreased tactile fremitus seen in pts with HF
pleural effusion
what tests do you want in a new pt with CHF
CXR - pulm edema, cardiomegaly, r/o COPD
ECG + cardiac enzymes - r/o MI
CBC - anemia
Echo- estimate EF, r/o pericardial effusion
normal pulse pressure
pulse pressure change seen in CHF
nml = 30-50 (systolic - diastolic)
CHF < 30
Murmur chart
S D ------------------------------ A - S / A - R P - S . / P - R T - R . / T - S M - R / M - S
grades of murmurs
what needs a workup
I - S1S2 > Murmur II - S1S1 = murmur -------------------------- III - S1S2 < Murmur IV - palpable thrill V - almost 6 - stethoscope half off chest VI - hear without stethoscope
below line need workup = echo and any diastolic murmur
mitral stenosis basics
blood backs up in LA -> LA dilation -> blood in lungs
path - Rheumatic heart disease - young pt 20-30s
atrial stretch –> possible A FIb
mitral stenosis auscultation =
diastolic murmur - best heard at cardiac apex - 5th ICS MCL
opening snap followed by low pitched diastolic rumble
aortic insufficiency (regurgitation) basics
weak floppy valve -> blood backs up into LV –> dilated floppy heart
path - infection or infarction, aortic dissection
head bobbing, uvula bobs
widened pulse pressure
tx - medical emergency - replace valve
acute and chronic presentation of aortic insufficiency (regurgitation)
acute - cardiogenic shock, flash pulmonary edema, tearing chest pain (if aortic dissection) radiating to back
chronic - CHF and CP
auscultation of aortic insufficiency (regurgitation)
diastolic murmur - best heard at base of heart - 2nd ICS right sternal border
pistol shots heard over the femoral arteries
aortic stenosis basics
stiff valve –> little blood gets through –> LV dilates -> big loose floppy heart –> HF symptoms
path - atherosclerosis, calcium deposits
bicuspid valve - speeds up stenosis
presentation of aortic stenosis patient
old man with atherosclerosis
CP, HF symptoms, syncope
auscultation of aortic stenosis
systolic murmur - best heard at the base of the heart right sternal border a crescendo decresendo murmur that radiates to carotid arteries aorit
S4
diminished and delayed carotid upstrokes
mitral insufficiency basics
leaflets dont come together -> increased pressure in LA –> blood backs up into lungs -> left atrial sketch -> afib + CHF symptoms
endocarditis - staph, papillary rupture s/p MI, Rheumatifc fever
mitral insufficiency presentation acute vs chronic
acute - cardiogenic shock, flash pulmonary edema,
Chronic - CHF, afib
mitral insufficiency auscultation
holostyolic murmur - high pitched blowing murmur
best heard at apex 5th ICS MCL
MS, MR , AS, AR
what worsens these murmurs
what improves these murmurs
increasing venous return - squatting, leg lifting - worsens murmur
decreasing venous return - valsalva maneuver - improves murmur
hypertrophic cardiomyopathy murmur (HCOM) basics
unilateral septum hypetrophy -> covers the aortic opening -> left ventricular outflow obstruction
pt with HCOM
ppl with sarcomere mutations
young athlete with sudden death or SOB or Syncope with exertion
FMHX is signficant
auscultation of HCOM
sounds like AS (systolic murmur)
but more blood improves the murmur opposite of AS
tx of HCOM
avoid dehydration
beta blockade
maintain preload
no exercise
mitral valve prolapse basics
leaflets too big donnt touch well due to excessive or. redundant mitral leaflet tissue due to myxomatous degeneration of leaflets and/or chordae tedineae
congenital young women, pregnant women
auscultation of mitral valve prolapse
murmur gets better with more blood - mitral regurg but better with more blood
midsystolic or late systolic click
mid to late systolic murmur
tx of mitral valve prolapse
avoid dehydration
beta blockade
tx of NYHA classifications
I = ace-I + beta blocker II = ^^ + diuretics (furosemide, bumetanide) III = ^^ + spironolactone or hydralazine and isosorbide dinitrate (BiDil) IV = ^^ + LVAD, transplant
initial test of choice for CHF
echocardiogram - determines whether systolic or diastolic - determines the cause - estimates EF shows chamber dilation/hypertrophy
BNP
released from the ventricles in response to ventricular volume expansion and pressure overload
useful for differentiating between dyspnea caused by CHF and COPD
BNP levels >150
a NT pro-BNP <300
correlate strongly with the presence of decompensated CHF
virtually excludes a dx of HF
what is a common cause of CHF that can be treated by reducing preload and afterload
HTN
systolic dysfunction HF - tx =
sodium restriction <4g/ fluid restriction 1.5 to 2.0 L
weight loss/smoking cess/exercise
diuretics spironolactone ace -i beta blockers digitalis hydralazine
role of diuretics in HF tx
most effective means of providing symptomatic relief
DONT REDUCE MORTALITY
diuretic of choice for HF
loop diuretics - furosemide - most potent
thiazides - hydrochlorothiazide - modest potency
role of spironolactone in HF tx
(aldosterone antagonist)
PROLONG SURVIVAL
effective only in advanced stages of HF - III and IV
monitor K+ and renal function
what is an alternative to spironolactone that does not cause gynecomastia
eplerenone
role of ACE-I in HF tx
cause venous and arterial dilation —> decreased preload and decreased afterload
REDUCE MORTALITY
prolong survival and alleviate symptoms in all grades of CHF
what is a contraindication for spironolactone in the tx of patients with HF
renal failure
what combo is the initial tx for HF patients who are symptomatic
diuretics (loop) and ACE- I (prils)
standard also includes beta blocker
what is an indication for the use of ACE-I in HF
LV systolic dysfunction with EF <40%
why do you always start pts with a low dose on ACE-I
to prevent hypotension
if patients have a persistent cough while on ACE-I what med do you switch to
ARBS - angiotensin II receptor blockers (artans)
what signs are you monitoring in a pt with CHF
weight - unexplained weight gain can be an early sign of worsening CHF
peripheral edema
electrolytes, K, BUN, dig levels
MCC of death from CHF =
sudden death from ventricular arrhythmias
ischemia -> provokes ventricular arrhythmias
role of beta blockers in tx of CHF
DECREASE MORTALITY in pts with post MI HF
slow the progression by slowing down tissue remodeling
beta blocker of choice for HF
carvedilol
digatlis
+ inotropic agent
useful in pts with EF <40%, severe CHF, AFib
short term relief - no change to mortality
serum digoxin levels should be checked periodically
role hydralazine and isosorbide dinitrates play in CHF tx
used in pts who dont tolerate ACE-I
COMBO IMPROVES MORTALITY in African americans with CHF
what meds are contraindicated in CHF
metformin - potentially lethal lactic acidosis
thiazolidinediones - fluid retention
NSAIDs - increase risk of CHF exacerbation
role of an ICD in CHF tx
LOWERS MORTALITY - prevents sudden death cardiac death
indicated for pts - >40 days post MI with EF <35% and class II or III CHF not controlled
cardiac resynchronization therapy role in CHF tx
biventricular pacemaker
indications > 40 days post MI with EF <35% class II or III CHF not controlled + prolonged QRS >120msec
diastolic dysfunction HF tx
NO MEDS DECREASE MORTALITY
beta blockers
diuretics
DIGOXIN AND SPRIONOLACTONE SHOULD NOT BE USED
signs of digoxin toxicity
GI - N/V and anorexia
Cardiac - ectopic (ventricular) beats, AV block, A Fib
CNS - visual disturbances, disorientation
Calcium channel blockers (CCB) role in CHF tx
no role -may increase mortality
BUT amlodipine and felodipine are safe to use in CHF (if another indication like HTN exists that needs controlling)
what is the overall 5 year mortality rate of CHF
50%
tx of class I and II HF (mild)
mild restriction of sodium intake and physical activity
start loop diuretic if volume overload or pulmonary congestion is present
use an ACE-I as first line agent
tx of class II and III HF (moderate)
start a diuretic (loop) and ACE-I (pril)
add a beta blocker if mod dz is present and the response of nml tx is suboptimal
tx of class III and IV HF (mod -severe)
add digoxin (to loop and ACE-I)
in pts with class IV symptoms who are still symptomatic despite above tx - add Spironolactone
ventricular assist device (VAD) role in CHF tx
used to support LV and RV or both
pump is implanted in the abdominal cavity with cannulation to the hart
system controller and battery worn externally
lifelong anticoagulation with heparin or warfarin is required without exceptions due to the devices being so thrombogenic
acute decompensated HF signs and causes
acute dyspnea - elevated left sided filing pressure with or without pulmonary edema
MC - due to lV systolic or diastolic dysfunction
flash pulmonary edema - severe form of HF with rapid accumulation of fluid in the lungs
tx of acute compensated HF
oxygenation and ventilatory assistance with nonrebreather face mask, NPPV, or intubation
diuretics to tx volume overload and congestive symptoms (MOST IMPORTANT) ^^^
nitrates
pts in acute compensated HF with pulmonary edema despite use of oxygen and diuretics and nitrates may benefit from what tx
dobutamine (inotropic agent) -works much quicker then digoxin which takes weeks
premature atrial complexes
early beat arises within atria firing on its own
early P waves that differ morphology
nml QRS
may be a precursor of ischemia in a diseased heart
causes and tx of symptomatic premature atrial complexes
causes: adernergic excess, drugs, alcohol, tobacco, electrolyte imbalances, ischemia and infection
tx if symptomatic = beta blockers
premature ventricular complexes
early beat fires on its own from ventricle then spreads to other ventricle
since conduction is not going thru nml pathways but thru ventricular muscle = slower than nml –> WIDE QRS complex that is bizarre with compensatory pause
buried P wave
presence in nml hearts - associated with increased mortality
PVCs causes and tx
can occur in pts with and without structural heart disease
causes: hypoxia, electrolyte abnormalities, stimulants, caffeine, meds, structural heart dz
tx - beta blockers if symptomatic - dizziness, palpitations
pts with frequent, repetitive PVCs and underlying heart disease are at increased risk for
sudden death due to VFib
the use of antiarrhythmic drugs to suppress PVCs after MIs increases
the risk of death
PVCs
couplet
bigeminy
trigeminy
couplet - 2 successive PVCs
bigeminy - sinus beat followed by a PVC
trigeminy - 2 sinus beats followed by a PVC
atrial fibrillation pathophys
multiple foci in the atria fire continously in a chaotic pattern - totally irregular, rapid ventricular rate
atrial rate >400 bpm but most of these impulses are blocked at the AV node so ventricular rate = 75-175
pts with AFib and underlying heart disease are at increased risk for
thromboembolism
hemodynamic compromise
causes of AFib
heart dz - CAD, MI, HTN, surgery pericarditis and pericardial trauma pulm dz - PE hyperthyroidism or hypothyroidism systemic illness stress excessive alcohol intake sick sinus syndrome pheochromocytoma
clinical features of afib
fatigue and exertional dyspnea
palpitations, dizziness, angina syncope
irregularly irregular pulse
blood stasis
blood stasis mechanism in afib
- secondary to ineffective contraction - leads to formation of intramural thrombi which can embolize to the brain
dilated cardiomyopathy
chambers are dilated - thin walled - floppy
little actin and myosin overlap - decreased contractiliy
problem pumping so systolic HF
some causes of dilated cardiomyopathy
viruses
wet beriberi
alcohol
ischemia
hypertrophic cardiomyopathy (HCM)
asymmetric septal wall thickening -> left ventricle outlet obstruction -> covers aortic opening
genetic mutation in sarcomeres
presentation of HCM
young athlete syncope, SOB, sudden death
murmur sounds like AS but gets better with increased venous return
tx of HCM
etoh ablation - for poor surgical candidates
myectomy - remove obstruction in muscle
ACID for pts with increased risk of death (prior ventricular arrhythmias)
concentric hypertrophy cardiomyopathy
diastolic HF
filling problem
causes of restrictive cardiomyopathy
sarcoidosis
amyloid
hemachromatosis
cancer and fibrosis
sarcoidosis in cardiomyopathy
- echo = patchy all over
- pt with pulmonary disease
- african american
Dx - cardiac MRI –> endomyocardial biopsy
tx - glucocorticoids
amyloidosis in cardiomyopathy
echo - bright and speckled pattern
peripheral neuropathy
fat pad biopsy (gingival biopsy)
hemachromatosis in cardiomyopathy
cirrhosis and bronze diabetes
screen with ferritin which will be elevated –> genetic testing
tx - phlebotomy or deferoxamine
definitive tx for cardiomyopathy
transplant
causes of pericardial dz
infections - virus (coxsackie) bacteria (staph/strep), fungal, TB
autoimmune - RA, lupus, dressler, Uremia
penetrating trauma > blunt trauma
aortic dissection
cancer - breast, lung, esophageal, lymphoma
pericarditis
viral, urimia
CP, pleuritic, positional (leaning forward better, leaning back worse)
dx of pericarditis
ECG - diffuse ST segment elevation everywhere
and depressed PR segment is key
tx of pericarditis
NSAIDs and Colchicine - best
no NSAIDs if - CKD, thrombocytopenia, peptic ulcer dz
no colchicine if - dose limiting due to diarrhea
steroids - worst due to increasing the recurrence of pericarditis (especially viral)
tx of pericarditis if the cause is uremia
dialize - diaylsis is curative
dx test of choice for pericardial effusion
echo - see the fluid
tx of pericardial effusion if refractory
pericardial window - allowing fluid to drain into a body cavity to be absorbed
presentation of pericardial tamponade
CHF symptoms - specifically Right sided HF –>
becks triad - hypotension, JVD, decreased heart sounds
pulsus paradoxus >10mmHg
clear lungs
tx of pericardial tamponade
pericardiocentesis - if cant be done right away then IVF to increase BP temporarily
constrictive pericarditis
recurrent pericarditis –> scaring forming a rigid box
as the heart expands in diastole –> pericardial knock is heard
diastolic CHF presentation
dx test of choice for constrictive pericarditis and tx
dx - echo
tx - pericardiectomy - remove rigid portion
dx of afib
ECG - irregularly irregular rhythm - irregular RR intervals
NO P WAVES
tx of afib
if hemodynamically unstable –> immediate electrical cardioversion
if stable –> rate control (60-100) beta blockers or CCBs –>
- if <48hrs –> cardioversion
- if >48 hours –> either TEE or anticoagulate for 3wks –> cardioversion
cardioversion basics
delivery of shock that is in synchrony with QRS complex
terminates certain dysrhythmias - PSVT or VT
an electric shock during a T wave can cause
V fib
indications for cardioversion
afib
atrial flutter
VT with plse
SVT
defibrillation basics
delivery of shock that is not in synchrony with QRS complex
purpose is to convert a dysrhythmia to a normal sinus rhythm
indications for defribillation
vfib
VT without a pulse
indications for automatic implantable defribillator
vfib
VT that is not controlled by medical therapy
in afib if LV systolic dysfunction is present what should you consider adding to the tx regiment
digoxin or amiodarone
candidates for cardioversion in afib
hemodynamically unstable
those with worsening symptoms
those having first ever case of afib
if pharmacologic cardioversion is going to happen for afib what drugs do you use
parenteral ibutilide procainamide flecainide sotalol amiodarone
anticoagulation in afib pts
prevents embolic CVA
if >48hrs risk for embolization = 2-5%
anticoagulate pts 3wks before and 4wks after
INR of 2-3 is goal
how to avoid anticoagulating 3wks before cardioversion
TEE - transesophageal echocardiogram - images LA if no thrombus –> start IV heparin and perform cardioversion within 24hrs then 4wks of anticoagulation
chronic afib anticoagulation
> 60 tx with warfarin
risk is increased in pts with heart dz as well
in afib what is superior rate or rhythm control
rate control
aflutter pathophys
one irritable automaticity focus in atria fires 250-350bpm –> the longer refractory period in the AV node allows only 1/2 1/3 flutter waves to conduct to the ventricles
causes of atrial flutter
heart failure (MC association)
RHD
CAD
COPD
atrial flutter ECG
saw tooth baseline with a QRS after every 2nd or 3rd tooh
best seen in inferior leads - II, III, and aVF
multifocal atrial tachycardia
occurs in COPD pts
ecg - variable p wave morphology at least 3 different types of P waves
tx of multifocal atrial tachcardia
if LV function is not preserved use digoxin diltiazem or amiodarone
if LV function is preserved - CCB, beta blockers, digoxin amiodarone, IV flecainide and IV propafenone
paroxysmal supraventricular tachycardia pathophys
most often due to reentry
two pathways within AV node one fast one slow so the reentrant circuit is within the AV node
initiated or terminated by PACs
most common cause of SVT
PSVT
ECG of PSVT
narrow QRS complexes with no discernible P waves since they are buried in QRS complexes
causes of PSVT
ischemic heart disease
digoxin toxicity - most common arrhythmia associated with digoxin toxicity
narrow QRS complexes suggest that the arrhythmia originates
at or above the level of the AV node
wide QRS complexes suggest that the arrhythmia originates
outside of the normal conducting system or there is a supraventricular arrhythmia with coexisting abnormality in the HIS-purkinje system
side effects of adenosine
HA flushing SOB chest pressure nausea
tx of PSVT (nonpharm)
maneuvers that stimulate the vagus delay AV conduction and thus block the reentry mechanism
- valsalva manuever, carotid massage, breath holding, head immersion in cold water (ice bag to face)
acute tx of PSVT (pharm)
IV adenosine - DOC - short duration of action and effectivess in terminating SVTs
IV verapamil (CCB) and IV esmolol (BB) or digoxin are alternatives for pts with preserved LV function
prevention of PVST
verapamil or beta blockers
radiofrequency catheter ablation of either AV node or accessory tract
wolf parkinson white syndrome pathophys
accessory conduction pathway from atria to ventricle through the bundle of kent –> causes premature ventricular excitation because it lacks the delay seen in the AV node
wolf parkinson white syndrome may lead to
paroxysmal tachycardia
dx of wolf parkinson white
ecg - delta wave (upward deflection seen before QRS complex)
narrow complex tachycardia
short PR interval
tx of wolf parkinson white syndrome
radiofrequency catheter ablation of one arm of the reentrant loop
procainamide or quinidine
what drugs should you avoid in wolf parkinson white syndrome
drugs that are active on AV node (digoxin, verapamil, beta blockers) –> they accelerate conduction through the accessory pathway
ventricular tachycardia
rapid and repetitive firing of 3 or more PVCs in a row at a rate of 100-250bpm
originate below bundle of HIS
causes of VTach
CAD with prior MI = MCC active ischemia, hypotension cardiomyopathies congenital defects prolonged QT
sustained Vtach
> 30seconds
always symptomatic
associated with hemodynamic compromise
life threatening
can progress to vfib
nonsustained vtach
brief self limited runs of vtach
asymptomatic
when CAD and LV dysfunction are present - risk factor for sudden death
VTach after an MI
poor prognosis especially if it is sustained
what cause 75% of cardiac arrests
vfib
Vtach
torsades de pointes
rapid polymorphic Vtach
can lead to afib
associated with factors that prolong QT interval
tx - IV magnesium
clinical features of Vtach
palpitations, lightheadedness, dyspnea
sudden cardiac death
cardiogenic shock
cannon A waves in neck
dx of vtach
wide and bizarre QRS complexes
monomorphic or polymorphic
does NOT respond to vagal maneuvers or adenosine
the presence of VT or PVCs in pts with underlying heart dz and LV dysfunction are at high risk for
risk for sudden death
pt with wide (>0.12) QRS tachycardia suspect
VTach
tx of sustained vtach
hemodynamically stable pts - IV amiodarone, IV procainamide or IV sotalol
unstable pts - immediate synchronous DC cardioversion followed bby IV amiodarone
ICD (unless EF = nml)
tx of unstained vtach
no underlying heart dz - dont tx
if underlying heart dz - ICD placement
pharm therapy = 2nd line - amiodarone
wide complex tachycardia in adults with hx of structural heart dz is much more likely to be due to
Vtach than SVT
cardiac arrest definition
sudden loss of output
potentially reversible if circulation and oxygen delivery are promptly restored
sudden cardiac death definition
unexpected death within 1hr of symptom onset secondary to cardiac cause
narrow complex tachycardias originate
above ventricles
wide complex tachycardias originate
within ventricles and are more ominous because they are more likely to progress to vfib
vfib basics
multiple foci in ventricles fire rapidly leading to chaotic quivering of the ventricles and no cardiac output
most episodes begin with vtach except acute ischemia
if vfib develops ,48hrs of an acute MI
long term prognosis is favorable and recurrence rate is low
causes of vfib
ischemic heart dz = mcc
antiarrhythmic drugs - especially those that cause torsades de pointes
afib with very rapid ventricular rates in pts with wolf parkinson white syndrome
clinical features of afib
cannon measure bp
absent heart sounds and pulse
dx of vfib
ecg - no atrial p waves, no QRS complexes
tx of vfib
medical emergency - immediate defribillation and CPR
give up to 3 sequential shocks
if persists –> CPR - intubate - epi 1mg every 3-5 min (decreases defribillation threshold by increasing myocardial and cerebral blood flow
IV amiodarone followed by shocks
if cardioversion is successful maintain IV infusion of effective agent - typically amiodarone
sinus bradycardia
Clinically significant <45
caused: ischemia, increased vagal tone
tx of sinus bradycardia
atropine - elevates sinus rate by blocking vagal stimulation to the Sinoatrial node
sick sinus syndrome
sinus node dysfunction characterized by persistent spontaneous sinus bradycardia
elerly, dizzy, confused, syncope, fatigue, CHF
defribrillation and asystole
doesnt really work
epi and CPR
pulseless electrical activity (PEA)
electrical activity on the monitor but no pulses even with doppler
grim prognosis
first degree AV block
PR interval is prolonged (>0.20sec)
a QRS follows each P wave
no tx
second degree AV block type I (wenckebach)
progressive prolongation of PR interval until a P wave fails to conduct (qrs dropped)
no tx
second degree AV block type II
P wave fails to conduct suddenly without preceding PR interval prolongation
QRS just drops suddenly
often progresses to complete heart block
site block is in His-purkinje system
tx - pacemaker
third degree complete AV block
absence of conduction of atrial impulses to the ventricles - no communication between the 2
characterized by AV dissociation
tx - pacemaker
chemo drugs that cause dilated cardiomyopathy
doxorubicin
adriamycin
infectious causes of dilated cardiomyopathy
viral
chagas dz
lyme dz
HIV
vasovagal syncope
vagus nerve stimulation –> dumps Ach –> bradycardia and vasodilation
decrease in systolic BP of 50mmhg
typically there is a prodrome (they know its coming)
causes of vasovagal syncope
visceral organ stimulation - (cough, defecation, micturition)
carotid bodies - (turning head, shaving, tie too tight)
psychogenic - (site of blood)
dx and tx of vasovagal syncope
dx - tilt table test (not really necessary)
tx - beta blockers
orthostatic syncope
systolic drop >20
diastolic >10
HR >10
causes of orthostatic hypotension
volume down causes:
- diarrhea
- dehydration
- diuresis
- hemorrhage
ANS issues:
- diabetes
- parkinson’s
- advanced age
tx of orthostatic hypotension
volume down - IVF
ANS - doesnt respond to fluids - get up slowly
cardiogenic syncope
mechanical:
- valve problem - rest no issue - issue with exertion
young athlete - HCOM
old person random exertion - Aortic Stenosis
Arrhythmia:
- sudden no prodrome
- dx halter monitor or event recorder
neurogenic syncope
posterior circulation issue - vertebrobasilar insufficiency
dx CT angiogram
LDL
brings cholesterol to the periphery – if too much accumulates there it leads to plaque formation
HDL
bring cholesterol back to liver for processing
who needs statin
1 - vascular dz- MI, CVA, PVD, CS
2- LDL >190
3 - LDL 70-189 + age (40-75) + DM
4 - LDL 70-189 + age (40-75) + calculated
ppl who dont need statins
LDL <70
high intensity statins
atorvastatin 40-80
rosuvastatin 20, 40
those who should be on moderate intensity statins
age >75
liver dz
renal dz
moderate intensity statins
atorvastatin 10, 20 rosuvastatin 5,10 simvastatin 20,40 pravastatin 40,80 lovastatin 40
how often should lipids be assessed
annually
if signs of statin toxicity
stop statins and when symptoms get better start them again
basline studies needed before statins
lipid panel
A1c
CK
LFTs
ADR of statins
myositis and hepatitis –> if pt develop these stop statins and then restart on lower doses
if you cant use a statin next best drug
fibrates - same ADR profile (myositis and increased LFTs)
fibrates
decrease TGLs and increase HDL
lipoprotein lipase inhibitor
ezetimibe
decrease LDL
prevent cholesterol absorption
ADR - fatty stool osmotic diarrhea
niacin
increase HDL and decrease LDL
decrease FA release
Decrease LDL synthesis
ADR - flushing tx with prophylactic aspsirin
bile acid resins
decrease LDL
decrease bile acid resorption
adr - diarrhea
ST segment elevation in inferior leads II, III, aVF
inferior wall MI - most commonly RCA 4:1 (LCX)
ST elevation in V1-v6
anterior MI - LAD
posterior wall MI
ST depression in v1-v3
ST elevation I and aVL (LCX)
ST depression in I and aVL (RCA)
ST elevation I, aVL, V5, V6
ST depression II, III, aVF
lateral wall MI LCX
right ventricle MI signs
RCA
ST elevation in V4-V6r
decreased CO in CHF –>
increase in RAAS –> increased ADH –> increase angiotensin II
increase in angiotensin II leads to
vasoconstriction of afferent and efferent glomerular arterioles (more so in efferent)
increased intraglomerular pressure to maintain GFR
decreased Na delivery to distal tubules
ST depression in V1-v3
ST elevation I and aVL = ?
ST depression I and aVL = ?
elevation in I and aVL = LCX
depression in I and aVl = RCA
ST depression in V1-v3
ST elevation I and aVL = ?
ST depression I and aVL = ?
elevation in I and aVL = LCX
depression in I and aVl = RCA
S4 indicates
a stiff LV which occurs in the setting of:
-restrictive cardiomyopathy
or
- hypertrophy from prolonged HTN
ascending aortic aneurysm leads to –>
aortic regurgitation (diastolic murmur)
severe Aortic stenosis signs
- delayed (slow rising) and diminished (weak) carotid pulses
- single and soft S2
- mid to late peaking systolic murmur with max intensity at 2nd R ICS radiating to the carotids
pulsus parvus and tardus
- delayed (slow rising) and diminished (weak) carotid pulses
prominent capillary pulsations in the fingers or nail beds is seen in
aortic regurgitation - due to the widened pulse pressure
Most common side effect of amiodarone
pulmonary toxicity - longer term use months to years
acute limb ischemia causes
- cardiac/ arterial embolus (severe and sudden)
- arterial thrombus
- iatrogenic/ blunt trauma
clinical signs of acute limb ischemia
pain pallor parethesias pulselessness poikilothermia (cool extremity) paralysis (late sign)
management of acute limb ischemia
anticoagulation - heparin
thrombolysis vs sx
DVT presentation
dull aching pain
swelling
tenderness of LE
pulse is present
cause of ascending aortic aneurysms
cystic medial necrosis
connective tissue disorders
cause of descending aortic aneurysms
atherosclerosis
CXR of thoracic aortic aneursyms
widened mediastinal silhoutte
increased aortic knob
tracheal deviation
decreased left ventricular preload can be seen in
cardiac tamponade
septic shock cardiac findings
hypotensive, tachy
reduced cardiac afterload – decreased systemic vascular resistance –> due to overall peripheral vasodilation
decreased pulmonary capillary wedge pressure
increased mixed venous O2 saturation
what is the initial tx of choice for a hyperthyroidism pt with afib
beta blockers
meds for stable afib pt
beta blockers
diltiazem
digoxin
CHA2DS2-VASc score = thromboembolic risk
C- CHF H- HTN A2 - age >75 (2pts) D- Diabetes mellitus S- stroke/TIA/thromboembolism (2pts) V-vascular dz (prior MI, periph artery dz, plaques) A- age 65-74 (1pt) S- sex category female
max score = 9
major side effects for amiodarone
cardiac - sinus brady, heart block QT prolongtion
pulm - chronic interstitial pneumonitis
endocrine - hypo/hyperthyroidism
GI/hepatic - elevated transaminases, hepatitis
occular - corneal microdeposits, optic neuropathy
derm = blue gray skin discoloration
neuro - peripheral neuropathy
MCC of mitral regurgitation in a developed country
mitral valve prolapse
lifte style modifications recommended for HTN
diet: <2.4g salt per day, K supplements, DASH, no etoh
exercise: 30min/day or 2hrs per week
Weight: lost weight if obese, or BMI>25
stage 1 HTN
systolic < 140
diastolic <90
LSM or if 10% risk LSM + 1 drug
stage 2 HTN
systolic >140
diastolic >90
LSM + 2 drugs
hypertensive urgency vs emergency
> 220 systolic + >120 diastolic
only difference is that emergency has end organ damage
papilledema, HA, AMS
tx for HF or CAD + HTN
beta blocker (carvedilol, metoprolol) - ACE-I
tx for stroke + HTN
thiazide + ACE-I
tx for CKD + HTN
ACE-I or ARB (except in stage IV)
tx for diabetes + HTN
ACE-I
tx for new onset HTN alone
thiazides, ACE-I (except if your black), CCB
dihydroperidine CCB (dipines) basics
ADR - peripheal edema
anti anginal
ACE- ARBS basics
ADR- increased creatinine and K
other ADR for ACE-I = dry cough + angioedema
tx of HTN during angioedema caused by ACE-I
ARBs
thiazides basics
HCTZ - works on the collecting duct - ADR - decreased k+
will also decreased urinary Ca which helps prevent kidney stones
beta blockers basics for HNT
useful for HF with decreased EF
ADR - decreased HR, Obstructive lung disease
Spironolactone
epleronone
ADR - increased K and sprinolacotne (gynecomastia) so use epleronone instead
CHF class III
Hydrazaline
arteriolar dilator - useful for CKD V - ADR - reflex tachycardia and drug induced SLE
isosorbide nitrate
venous dilator
dont use with other nitrates or PDE I
alpha antagonist
useful if also treating BPH but can cause orthostatic hypotension
ADR of clonidine
rebound hypertension
tx of hypertensive emergency
IV nitrates or CCB to get MAP down 25% in first 2-6hrs
hyperaldosteronism (primary aldosteronism)
refractory HTN or HTN and hypokalemia
renin > 20
CT pelvis
hypercalcemia and HTN
polyuria, AMS, “moans, bones, groans”
kidney stones
check free Ca
aortic coarctation
children = warm arms, cold legs, claudications
adults = rib notching, BP differential in legs and arms
CXR, angiogram, CT angio
renovascular HTN
DM or glomerulonephritis
young woman = FMD
old guy RAS
renal bruit, hypo K
pheochromocytoma HTN
pallor palpitations pain perspiration pressure
24hr urinary metanephrines
CT
cushings
diabets, HTN, central obesity, Moon facies
low dose Dexa, ACTH level
high dose DEXA
fast arrhythmia with narrow QRS
either SVT or AFib
SVT basics
no P waves
HR > 150 and regulr
tx - adenosine 6mg –> 12mg –> 12mg
afib basics
no p waves irregularly irregular
heart rate <150
CCBs = beta blockers for rate control except in CHF use digoxin or amiodarone
saw tooth pattern =
atrial flutter
fast arrhythmia with wide QRS
torsades or V tach
torsades basics
changing amplitude (ribbon like)
tx magnesium (amiodarone too)
v tach basics tx
stable - amiodarone
unstable - shock
in valvular afib DOC for anticoagulation =
warfarin
Slow rhythm and wide QRS
3rd degree AV block or idioventricular rhythm
no atropine for either rhythm but pace them
slow rhythm and narrow QRS
sinus brady - atropine and pace
1st degree block - atropine and pace
2nd degree type I block - atropine and pace
2nd degree type II block - pace
differences between AV blocks
1st - just PR prolongation - no dropped beats
2nd type I - PR prolongation with drop after
2nd type II - nml PR length with random dropped beats
fast and narrow rhythm tx =
adenosine
fast and wide rhythm tx =
amiodarone
squatting increases the intensity of all murmurs except
MVP and HCM
clinical manifestations of acute pericarditis
chest pain
pericardial friction rub
diffuse ST elevation and PR depression
pericardial effusion without tamponade
diastole dysfunction in constrictive pericarditis
early diastole - rapid filling
late diastole - halted filling
constrictive pericarditis - when intracardiac volume reaches the limit set by the noncompliant pericardium
ventricular filling is halted abruptly
in cardiac tamponade ventricular filling
is impeded throughout diastole
if pat has clinical signs of cirrhosis (ascites, hepatospleomegaly) and distended neck veins perform tests to r/o out
constrictive pericarditis
imaging test of choice for dx of pericardial effusion and cardiac tamponade
echo
CXR findings of pericardial effusion
cardiac silhoutte - water bottle appearance
enlarged heart without pulmonary vascular congestion
cardiac tamponade causes
rapid accumulation of. 200ml or slow accumulation of 2L
mechanically impairs diastolic filling
pressures in RV, LV, RA, LA equalize
decreased stroke volume
decreased cardiac output
becks triad
hypotension
muffled heart sounds JVD
pulsus paradoxus
systolic bP drop >10mmHg on inspiration
complications of mitral stenosis
hemoptysis - due to elevated LA pressure ruptures anastomoses of small bronchial veins
thromboembolism - afib
tricuspid regurg
IV Drug users, LV failure - mcc
blowing holosystolic murmur at LLSB
pt with new murmur and unexplained fever or bacteremia suspect
endocarditis
acute endocarditis
MCC - staph aureus
nml heart valves
subacute endocarditis
strep viridans and enterococcus
damaged heart valves
prosthetic valve endocarditis
staph epidermidis > staph aureus
endocarditis in IV drug users
staph aureus is MCC other causes include streptoccoci, enteroccocci, candida and pseudomonas
dx of endocarditis
DUKE criteria (2 maj, 1 maj + 2min, 5 min) TEE
situations that require prophylactic tx for endocarditis
proesthetic heart valves
hx of infective endocarditis
congenital heart dz
dental procedures
nonbacterial thrombotic endocarditis (1)
nonbacterial verrucous endocarditis (2)
1 - metastic cancer - deposits of fibrin and platelets along closure line of cardiac valve leaflets
2- aortic valves in SLE pts - small warty vegetations on both side sof valve leaflets
first step if pt has severe HA and markedly elevated BP
lower Bp(hydraazine) then CT –> if CT neg –> LP
managment of hypertensive crisis
reduce mean arterial pressure by 25% in 1-2 hrs
if severe - IV hydralazine, esmolol, nitroprusside, labetalol, NTG
types of aortic dissections and dx
type a = ascending - anterior chest pain - tx surgical + IV beta blockers, IV sodium nitroprusside
type b = descending - interscapular back pain - tx medical
dx - cxr - widened mediastinum >8mm on AP view + TEE
presentation of. aortic dissection
severe tearing/ripping/stabbing pain
abrupt onset
anterior chest or back of the chest
pulse or bP asymmetry between limbs
predisposing factors for aortic dissections
long standing HTN
cocaine, trauma
Connective tissue diseases (marfans, ehlers danlos)
3rd trimester of pregnancy
AAA
located between renal arteries and iliac bifurcation
more common in. men 65-70 (women more likely to tear)
multifactorial - atherosclerotic weakening of aortic wall, HTN, trauama, vasculitis, smoking
syphillis, and CT diseases marfasn - thoracic more tho
clinical features of AAA
sense of fullness
pulsatile mas on abd exam
ecchymoses on back and flanks, around umbilicus
presentation of ruptured AAA
abd pain
hypotension
palpable pulsatile abdominal mass
emergency laparotomy indicated
test of choice for AAA
US of abdomen
meds that improves long term survival in pts with LV systolic dysfunction
beta blockers
ACE-I
ARBs
mineralcorticoid receptor antagonists
hydralazine + isosoribide nitrates in black
symmetric duskiness and coolness of all fingertips can be caused by
pressers such as NE - lead to ischemia of distal fingers and toes secondary to vasospasm not painful
raynauds phenomenom
finger ischemia that is typically painful and due to cold exposures or stress
Formation of AV fistulas can occur from
trauma –> leading to high output cardiac failure by shunting blood from arterial side to venous side –> increasing cardiac preload –>HF
CHA2DS2-VSAc score interpretation
0 - no tx
1- aspirin or more
2 - blood thinner (wafarin, -bans)
drugs that inhibit cyp450 –> increasing warfarin effect
acetominophen, NSAIDs ABX, antifungals amiodarone thyroid hormones cimetidines cranberry juice + vit E omeprazole SSRIs
drugs that induce cyp450 –> decreasing warfarin effect
st johns wort, ginseg carbameapine, phenytin rifampin OCPs phenobarbital
dx test of choice for cardiac tamponade
echo
some causes of. low pulmonary capillary wedge pressure
acute PE due to impaired blood flow
sepsis
hypovolemic shock
complication of mitral stenosis
afib –> thromboembolic stroke –> hemiparesis
beta blocker overdose
bradycardia
AV block
hypotension
diffuse wheezing
antidote = glucagon
in cardiogenic shock what happens to the pulmonary capillary wedge pressure
pulmonary capillary wedge pressure will be elevated
SVR in sepsis, hypovolemia, cardiogenic shock
sepsis - decrease SVR
hypovolemia - increase SVR
cardiogenic shock - increase SVR
non selective beta blockers can trigger
bronchoconstriction in patients with underyling asthma
late complication of radiation therapy
constrictive pericarditis
pts with endocarditis with abnormal conduction on ECG –> think
perivalvular abscess
fibromuscular dysplasia
women, internal carotid artery stenosis -> recurrent headaches, pulsatile tinnitus, TIA, stroke
renal artery stenosis -> secondary HTN
subaruicular systolic bruit, abd bruit
tx - antiarrhythmias (ACE-I or ARBs)
pheochromocytoma presentation
secondary HTN - due to secretion of catecholamines
episodes of HA sweating, diaphoresis
primary hyperaldosternism
secondary HTN
decreased K+
metabolic alkalosis
conditions associated with AFIB
HTN, CAD, CHF, valvular dz, hypertrophic cardiomyopathy
obstructive sleep apnea, PE, COPD, acute hypoxia
obesity, hyperthyroidism, DM, Alcohol
cushing syndrome
central obesity glucose intolerance hirsutism abdominal striae elevated BP
digoxin toxicity
GI - anorexia, N/V, abd pain
cardiac - life threatening arrhythmias
neuro - fatigue, confusion, weakness, color vision alterations
viral myocarditis
young pt
viral prodrom
causes - parvovirus B19, coxsackie, HSV -6, adenovirus, HIV, influenza
eho - 4 chamber dilation, impaired contractile function
renovascular dz clues
HTN resistant to tx
malignant HTN (end organ damage)
onset of severe HTN > 55y/o
asymmetric renal size
abdomial bruit
unexplained increase in serum creatinine >30% after starting on ACE-I or ARBs
renin pathway
low bp or low volume -> JGC -> converts angiotensinogen –> angiotensin I –> ace converts it into –> angiotensin II –> vasoconstriction + increased aldosterone
management of symptomatic bradycardia and/or complete heart block
transcutaneous pacing
supravalvular aortic stenosis
aortic outflow obstruction - develop LV hypertrophy and can have exertional anginal due to subendocardial ischemia -> increased myocardial oxygen demand during exercise
primary hyperparathyroidism
muscle weakness recurrent kidney stones neuropysch problems hypercalcemia secondary HTN
MEN type I
hyperparathyroidism
pancreatic tumors
pituitary tumors
MEN type II a
medullary thyroid carcinoma
pheochromocytoma
parathyroid hyperplasia
MEN type IIb
medullary thyroid carcinoma
pheochromocytoma
mucosal neuromas
marfanoid habitus
ADR of dihydropyridine Ca channel antagonist
peripheral edema
peristent AFIB in WPW syndrome patient should be treated with
if unstable - electrical cardioversion
if stable - rhythm control with ibutilide or procainamide
pain relief from NTG is due to
decreased LV wall stress
inf wall MI with delayed presentation followed by sudden onset hypotension, dyspnea, tachypnea, pulm edema and a soft systoli cmurmur is indicative of
acute MR due to posteromedial papillary muscle rupture
clinical presentation of amyloidosis in cardiomyopathy
unexplained CHF
proteinuria
left ventricular hypertrophy in the absence of HTN hx
ADR of class IC anti arrhythmics (fleicande)
increase in QRS duration
statins MOA
inhibit HMG CoA reductase -. intracellular synthesis pathway
decrease coenzyme q10 synthesis
ACE-I moa
extracellular enzyme blocker and increase levels of bradykinin
the strongest predictor of AAA expansion and ruputre =
smoking
diameter of AAA and speed of expansion of AAA
younger pt has exertional dyspnea
pounding heart sensation when lying on left side
widened pulse pressure
dx=
AR - increase in LV size bring the ventricular apex close to the chest wall
the most common cause of AR in developed countries =
aortic root dilation or congenital bicuspid valve
complication of aortic dissection
AR and cardiac tamponade
most common ectopic foci in afib
pulmonary veins
underlying pathophys of atrial flutter
involves reentreant circuit around the tricuspid annulus
murmurs that require workup
diastolic and continous murmurs
ECG –> echo
murmur that does nOT require workup
midsystolic murmur in otherwise young asymptomatic adult
decreased tracer uptake in technetium 99 scan at rest and with exercise indicates
fixed defect - likely scar issue with decreased perfusion and CAD
decreased tracer uptake in technetium 99 scan only with exercise indicates
ischemia and CAD (reversible)
dx test of choice for aortic dissection causing hemopericardium and rapidly progessing cardiac tamponade
CT angiography
increased incidence of orthostatic hypotension in the elderly is due to
progressively decreasing baroreceptor sensitivity and defects in the myocardial response to this reflex
GFR changes in the elderly
decreases -> promotes sodium retention
common causes of pulm HTN
LV systolic or diastolic dysfunction
tx - loop diuretics and (ACE-I or ARBs)
ventricular aneursym
late complication of MI (wks to months)
ECG - persistent localized ST seg elevation and eep Q waves in the leads correspondingto previous MI
modification with greatest benefit on decreasing high BP
1) weight loss
2 DASH diet
3 exercise
4 sodium
tx of hypertrophic cardiomyopathy
neg inotropic agents:
beta . bockers, verapamil, disopyramide (not first line due to ADR)
situational syncope
neurally mediated syncope associated with micturition, cough, defecation
what is the tx for acute thormbotic occlusions
heparin
MOA of dihydropyridiine CCBs
decreases afterload by systemic vasodilation
exertional heat stroke
strenous activity in hot humid weather
dehydration, obesity
core temp >104, AMS, organ/tissue damage
management of exertional heat stroke
rapid cooling
fluid resuscitation
electrolyte correction
management of end organ complications
cardiac sarcoidosis
dz of noncasseating granuloma infiltration of the myocardium and can result in
serios arrhythmias
cardiomyopathy HF
sudden cardiac death
lyme carditis
1-2 months after borrelia burgdorferi inf
AV block is the MC abnormality seen
common cardiac issues in marfans syndrome
mitral valve prolapse
aortic dilation -> aortic dissection -> aoritc regurgitation = early diastolic murmur
hypovolemic shock cardiac values
decreased CO
decreased BP
decreased PCWP
increased SVR
abrupt onset of regular tachycardia that resolves with cold water immersion =
PSVT - can be treated with vagal maneuvers
MOA of vagal maneuvers to terminate AV nodal reentrant tachycardia
increase parasympathetic tone -> temporary slowing of conduction in the AV node –> increase in the AV node refractory period –> termination
MCC of sudden cardiac arrest in the immediate post infraction period in pts with acute MI
reentrant ventricular arrhythmias (vfib)
tricuspid regurgitation affect during inspiratioin
murmur increases
dobutamine moa
strong affinity for beta 1-r, weak affinity for beta-2-r + alpha 1-r
stimulate increased myocardial contractility -> increased EF -> reduced LV end systolic volume
improvement of symptoms of decompensated HF
clinical signs of acute decompensated HF
acute dyspnea, orthopnea
HTN, Hypotension(if severe)
accessory muscle suse, tachycardia, tachypneic
diffuse crackles with possible wheezes
JVD, peripheral edema
tx of acute decompensated HF
O2 and furosemide +
NTG - HTN
NE or dobutamine - hypotension
cardiac signs of cor pulmonale
tricuspid regurgitation murmur
ECG - RBBB, RAD, RVH, RA enargment
echo - pulm HTN, dilated RV,
right heart cath (gold standard) - RV dysfunction, elevated pulmonary artery systolic pressure >25mmHg
abnormal causes of S3
HF
restrictive cardiomyopathy
high output states
abnormal causes of S4
acute MI
young adults, kids
ventricular hypertrophy
MCC of aortic stenosis > 70 y/o and <70 y/o
> 70 - senile calcific aortic stenosi
< 70 - bicupsid aortic valves
pulsus paradoxus can be seen in
cardiac tamponade
severe asthma
severe COPD
chagas disease
preceded by megacolon
dilated carditis
protozoal infection
diptheria myocarditis
preceded by URI
underdeveloped country
no vaccine hx
MC site of occlusion in peripheral vascular dz
superficial femoral artery (hunter cannal)
smoking = biggest risk factor
calf claudication
buttock and hip claudication + cave claudication
femoral or popliteal
aortoilliac occlusive
Normal ABI is between
0.9 - 1.3
>1.3 - is due to noncompressible vessels and indicates severe disease
cholesterol embolization syndrome
due to showers of cholesterol crystals
triggered by surgical or radiographic intervention
blue/black toes
superficial thrombophlebitis
local tenderness, erythema, along course of superficial vein
UE - site of IV infusion
LE - varicose vein association
tx - analgesics - monitor for spread or cellulitis
cardogenic shock
decreased CO
increased SVR
increased PCWP
hypovolemic shock
decreased CO
increased SVR
decreased PCWP
neurogenic shock
decreased CO
decreased SVR
decreased PCWP
Septic shock
increased CO
decreased SVR
decreased PCWP
afterload reducing agents
NTG
nitroprusside
what is the best indicator that tht etx of shock is effective
monitoring urine output as well as a pulmonary artery catheter and/or central venous line
septic shock is asociated with
severe peripheral vasodilation (flushing, warm skin)
hypovolemic shock is associated with
peripheal vasoconstriction (cool skin)
most common cause of. death in ICU
septic shock
SIRS
2 or more: Fever > 38 or hypothermia <36 hyperventilation or PaCO2 <32 tachy increased WBCs
ADR of nitroprusside
cyanide toxicity especially in those with continouse infusions
lactic acidosis, AMS, Seizure Coma
tx of vasospastic angina
CCB for prevention and NTG for abortive tx
long standing systemic HTN ECG signs
high voltage QrS complexes
lateral ST segment depression
lateral T wave inversion
when is metoprolol C/I in the tx of an acute MI
when pulmonary edema is present along with acute decompensated HF
MCC of constrictive pericarditis in developing countries
tuberuculosis
presentation of interventricular septum
3-5 days after MI
suddent onset cardiogenic shock with hypotension
biventricular failure
new harsh holosystolic murmur with palpable thrill at the. left sternal border
what lifestyle modification can greatly decrease TGLs
reducing or no longer consuming alcohol
ventricular aneursyms
5days to 3 months post PI
thin and scarred fibrotic myocardium
ecg - presents with persistent ST segment elvation after recent MI
can eventually lead to –> MR
ECG findings that suggest an arrhytmia that can cause syncope
inappropiate sinus brady sinoatrial block sinus pauses AV block nonsustained ventricular arrhthyias short or prolonged QTc interval
symptomatic management of carotid stenosis is. required whwen
TIA CVA, stenosis 70-99%
digoxin and furosemides role in CHF
provide symptomatic relief but will not decrease mortality
MCC of isolated AR in a young adult in developed countries
congenital bicupsid aortic valves
uremic pericarditis
BUN levels >60
no classical pericarditis ECG findings
tx- hemodyialysis
pathphys behind the ADR of niacin
high dose niacin -> flushing - due to prostaglandin induced periheral vasodilation and can be reduced by low dose aspsirin
primary mitral valve abnormality in pts with hypertrophic cardiomyopathy is the presence of
systolic anterior mitral valve - > anterior motion of the mitral valve leaflets towards the interventricular septum and when connected to thickened septum during systole to LV outflow tract obstruction
what is the most common finding associated with HF and an elevated BNP
S3 - sign of increased cardiac filling pressures
hemodynamics in HF
decreased contractility
decreased CO
increased afterload
increased SVR
the goals of the initial therapy of aortic dissection
pain control
reduction of systolic bp to 100-120
decreased CV contractility to reduce aortic wall stress
(tx of these 2 beta blockers)
most important predisposing factor associated with the development of aortic dissection
systemic HTN
if <40 y/o 50% are due to marfans syndrome
electrical alternans + sinus tachy
large pericardial effusion
poor prognostic factors for CHF
hyponatremia resting tachycardia s3 mod to severe MR LBBB severe LV dsyfunction pulm HTN
