Step Up to medicine - Cardiovascular Flashcards
stable angina pectoris is due to __________ narrowing of _________ vessels
fixed
atherosclerotic
what are the top 5 risk factors for stable angina pectoris
DM HLD HTN Cigarette smoking age FHx
what are the two prognostic indicators for CAD
Left ventricular function
vessels involved
which of the vessels involved in CAD purports the worst prognosiss
left main
T/F multiple vessel disease is worse that single vessel
T
T/F ischemic pain changes with changes in body positioning and breathing
F ( does not change with these changes, these would indicate a different pathology for the pain)
Any combination of Hypercholesterolemia
Hypertriglyceridemia impaired glucose tolerance
diabetes hyperuricemia
HTN
Key underlying factor is insulin resistance
Metabolic syndrome X
exertional angina with normal coronary arteriogram
exercise testing and nuclear imaging show evidence of myocardial ischemia
syndrome X
T/F physical exam in patients with CAD is often normal
T
what is the typical outcome of resting ecg in patients with stable angina
normal
Q waves present on resting ECG indicate
prior MI
how does the diagnosis of angina change with presence of ST elevations or segmeental changes
unstable
useful test for patients with an intermediate pretest probability of CAD based upon age gender and symptoms
stress test
quick and dirty method for finding a persons maximum HR
220 - age
patients with a positive stress test should undergo
cardiac cath
what is the parameter by which a stress test is considered postive
ST segment depression
ventricular arrhythmia
hypotension
stress test is 75% sensitive if patients can complete what task during the test
increase HR to 85% maximum
when is the echo performed in stress echo
after exercise
patients with a positive stress echo should undergo
cardiac cath
what cardiac pathology does not allow radioactive testing in cardiac workup
left bundle branch block
what should be done in cardiac workup if patient cannot exercise
pharmacologic testing
how do IV adenosine and dipyramidole work with pharmacologic testing
cause coronary vasodilation which means that the vessels supplying ischemic portions of the heart are already maximally dilated therefore the shunting of blood to the areas of the heart in which the vessels still have vasodilatory capacity will lead to ischemic changes in the vessels that supply ischemic portions of the heart
how does dobutamine work in pharmacologic testing in cardiac workup
increases HR, strength of contraction, increases BP
can be useful for detecting silent ischemic, arrhythmias, heart rate variability and assess pacemaker/ ICD function
holter monitoring
useful testing for unexplained dizziness and syncope if cardiovascular cause suspected
holter monitoring
definitive test for CAD
cardiac catheterization
most accurate test for detecting CAD
cardiac angiography
if CAD is severe typically with three vessel disease what should be done
surgical (CABG) repair
what medication is commonly employed in lowering cholesterol and decrease risk for CAD
statins (HMG CoA reductase inhibitors)
what types of fats should be avoided in patients with CAD
saturated
what medical therapy is indicated for all patients with CAD
aspirin
first line therapy that has been shown to decrease the number of coronary events in patients with CAD
beta blocker
relieve angina by reducing preload myocardial O2 demand
VERY COMMON
nitrates
medical therapy that induces coronary vasodilation and afterload reduction
calcium channel blockers
If CHF is present in patients with CAD then what two medications can be added on to the typical therapeutic options of aspirin beta blockers and CCbs
diuretics and ACE inhibitors
Mild disease
normal EF
mild angina
single vessel
what should be done in terms of management on top of aspirin therapy
beta blockers and nitrates
consider CCBs if symptoms persist
normal EF moderate angina and two vessel disease
coronary angiography to assess for revascularization
decreased EF
severe angina
three vessel of left main or LAD disease
angiography to consider CABG
T/F oxygen demand is increased in unstable agina
F (only the supply is diminished)
significant because it indicates stenosis that has enlarged via throbosis hemorrhage or plaque rupture
unstable angina
chronic angina with increasing frequency duration or intensity of chest pain
new onset that is severe and worsening
angina at rest
unstable angina
what is the only test that determines the difference between unstable angina and NSTEMI
cardiac enzymes
in what order should testing and management be carried out in patients with unstable angina
medically stabilize symptoms first before stress testing or angiography to assess for two/three vessel disease
patients with unstable angina should undergo what global management in terms of placement, nuts and bolts medical management
admission to hospital for continuous cardiac enzyme monitoring
establish IV access and give 2L fluids initially
give supplemental oxygen
control pain with nitrates and morphine
what is the aggressive medical management employed in a patient with unstable angina
supplemental oxygen IV fluid resuscitation beta blockers (if no contraindications) aspirin/clopidogrel LMWH nitrates K+ and Mg+ replacement (to avoid arrhythmia)
duration of aspirin and clopidogrel dual therapy in patients presenting with unstable angina
9 to 12 months
PERCENTAGE of patients that recover following initial aggressive medical management in the case of unstable angina
90%
what should be done in the management of a patient with USA that responds to initial medical management
stress ECG to assess need for catheerization
what is the immediate management in an individual that fails initial medical management in the setting of USA
immediately proceed to the cath lab
what is continued following acute treatment of USA
aspirin beta blockers and nitrate
what are the two beta blockers typically employed in the treatment of USA
metoprolol and atenolol
on top of continuing medical management what should be done in individuals with USA following acute treatment
reduce risk factors
smoking cessation
treat DM HTN HLD
t/F following USA a patient should be started on statin regardless of LDL level
T
transient ST segment elevation classically occuring at night associated with ventricular dysrhythmia
prinzmetal (variant) angina
what two medications are proven helpful with variant angina
CCBs and nitrates (those that vasodilate)
due to necrosis of myocardium as a result of an interruption of blood supply
MI
most cases of MI are due to
acute coronary thrombosis
mortality rate associated with MI
30%
what are the two medications that are utilized in the coronary angiography when looking for variant angina
ergonovine or acetylcholine
intense substernal pressure sensation
radiation to neck jaw arms back
pain typically unresponsive to nitro
epigastric discomfort
MI
T/F MI can be asymptomatic in up to one third of patients
T
painless infarcts or atypical MI more likely in these 4 demographics
women
postoperative
elderly
diabetics
less common symptoms of MI
dyspnea diaphoresis weakness fatigues nausea vomiting snese of impending doom syncope
very early sign of MI that is often missed
peaked T waves
ECG sign indivating transmural injury and diagnostic of acute infarct
ST segment elevation
evidence for necrosis usually seen late and typically absent acutely
Q waves
T/F T wave inversion is specific for MI
F (sensitive not specific)
ECG finding associated with subendocardial ischemia
ST segment depression
currently the diagnostic gold standard for MI versus USA
cardiac enzymes
time period over which troponins return to normal
5-14 days
when do troponins reach their peak
24-48 hours
what is the utility of CKMB enzymes
reinfarction measurement
PROVE IT TIMI 22 trial proved starting this agent should be part of maintenance therapy in MI management
statin (specifically atorvastatin 80mg)
what are the 7 agents that should be initiated in the acute treatment of MI
morphine oxygen nitrates aspirin ace inhibitor statin heparin
this ultimate treatment should be incorporated to the treatment of all patients being managed for acute MI
revascularization ASAP
what is the time period in which revascularization should be attempted in any patient presenting with acute MI
within 90 minutes
this outcome occurs with rupture of papillary muscle infarction ischemia
mitral regurg
length of time with which patients receiving a bare metal stent should be on dual platelet therapy
one month
how long should a patient be on dual platelet therapy following the placement of drug eluting stents
12 months
what is the most common cuase of inhospital mortality following MI
CHF
what is the treatment for PVCs following acute MI
conservative management (no need for antiarrhythmic agent)
what should be done in a stable patient that shows VTach that is sustained
IV amio
what should be done in an unstable patient that shows Vtach that is sustain
electrical cardioversion
what is the treatment for vfib following MI
immediate desynchronized defibrillation and CPR
sinus bradycardia management in the setting of acute MI
observation
if severe atropine may be helpful in increasing HR
asystole management in the setting of acute MI
elecrtrical defibrillation if thought to be 2/2 VFIB
transcutaneous pacing if asystole is clearly the cause
what is the typical cause for AV block in the setting of MI
infarction of the conduction tracts
second or third degree block has a terrible prognosis in the setting of what type of MI
anterior
what should be done in second or third degree heart block in the setting of anterior MI
temporary pacing (transcutaneous or transvenous)
initial management for heart block secondary to inferior MI
atropine
treatment for heart block 2/2 inferior MI that is refractory to initial treatment with atropine
pacemaker
T/F recurrent infarction is not as bad in prognosis as initial MIA
F (worse in both acute and long term prognosis)
catastrophic mechanical complication of MI that occurs within the first TWO WEEKS after MI
free wall rupture
usually within the first 1-4 days
what are the usual immediate complications of free wall rupture
hemopericardium and cardiac tamponade
what is the immediate treatment for free wall rupture
hemodynamic stabilization
pericardiocentesis
surgical repair
T/F interventricular septal rupture following MI is typically worse in prognosis than frree wall rupture
F (better prognostically)
what is the indication for interventricular septal rupture following MI
emergent surgery
time table for interventricular septal rupture following MI
within 10 days
new onset MR folloiwng MI cause
papillary muscle rupture
what is the immediate indication for new onset MR following MI
echo
what is the treatment for papillary muscle rupture
surgical (mitral valve replacement typically)
why are ventricular pseudoaneurysms considered surgical emergencies
tend to become free wall ruptures if left alone
acute pericarditis secondary to MI typically treated with
aspirin
what medications are contraindicated in the case of acute pericarditis following MI
NSAIDs
Immunologically based syndrome consisting of fever malaise pericarditis leukocytosis and pleuritis occuring weeks to months after an MI
dressler syndrome
what is the most effective therapy for dressler syndrome
aspirin
Ibuprofen is a good secondary choice
6 main causes/systems leading to chest pain
Cardiac Pulmonary GI Chest wall psychiatric cocaine
Heart pericardium vascular causes for chest pain
stable angina
USA
variant angina
MI
Pericarditis
Aortic dissection
Pulmonary causes for chest pain (3)
pulmonary embolism
PNA
status asthmaticus
GI causes for chest pain (4)
GERD
diffuse esophageal spasm
peptic ulcer disease
esophageal rupture
Chest wall causes for chest pain (5)
costochondritis muscle strain rib fracture herpes zoster thoracic outlet syndrome
3 main psych causes for chest pain
anxiety panic attacks somatization
3 tests that are obtained for practically all patients presenting with chest pain
ECG
troponins
chest xray
clinical syndrome resulting from the hearts inability to meet the body’s circulatory demands under normal physiologic conditions
CHF
what are the two most common causes for systolic CHF dysfunction
HTN and ischemia (MI)(
echocardiogram showing impaired relaxation of the left ventricle
diastolic dysfunction
which form of CHF is most common
systolic (HTN AND ISCHEMIA MUCH MORE COMMON PATHOLOGIES)
most common cause of diastolic CHF
HTN leading to hypertrophy of myocardium
aoritc stenosis mitral stenosis and aortic regurg cause what form of CHF
diastolic
dyspnea orthopnea paroxysmal nocturnal dyspnea nocturnal cough confusion and memory impairment in advanced forms diaphoresis and cool extremities at rest
CHF
difficulty breathing in the recumbent position relieved by elecation of the head with pillows
orthopnea
rapid filling phase into a noncompliant left ventricular chamber leads to what pathologic heart sound
S3
S3 heard best in what position
apex with the bell of the stethoscope
S3 occurs at what phase in the cardiac cycle
following S2
how to remember S3 S4 and their place in the cardiac cycle
4 is more than 3
tennessee has more letters than kentucky TEN-nes-see relates S4 prior to S1
ken-tuck-Y relates S3 following S2
crackles and rales at the bases of the lungs in CHF indicates what pathologic process
pulmonary edema 2/2 fluid spilling into the alveoli
dullness to percussion and decreased tactile fremitus of the lower lung fields is a sign of
pleural effusion
peripheral pitting edema nocturia JVD hepatomegaly ascites right ventricular heave
all signs of what sidded HF
rightr
T/F given enough time left sided HF will always lead to right sided HF
T
short horizontal lines near periphery of the lung near the costophrenic angles and indicate pulmonary congestion secondary to dilation of pulmonary lymphatic vessels
kerley B lines
prominent interstitial markings and pleural effusion a sign of what on CXR
CHF
what is the initial test of choice in suspected CHF
transthoracic echo
what is the importance of obtaining a TTE in the diagnosis of CHF
gives us the EF
cutoff for preserved left ventricular function in patients treated for CHF
> 40%
T/F ECG is often very helpful in CHF diagnosis
F (not particularly unless there is a component of MI or USA)
consider this test to rule out CAD as an underlying cause for CHF
coronary angiography
test used to assess dynamic response of HR heart rhythm and BP in the setting of CHF
stress testing
conservative management of systolic dysfunction of CHF
sodium restriction water restriction smoking cessation weight loss etoh decrease
most effective means of providing symptomatic relief to patients with moderate to severe CHF
recommended for patients with systolic failure and volume overload
diuretic
T/F diuretics improve mortality in patients with CHF
F (not been shown)
most potent diuretic that is usually used
lasix
lasix is what type of diuretic
loop
HCTZ is what type of diuretic
thiazide
T/F spironolactone has been shown to have survival benefits in patients with CHRF
T
spironolactone used in what types of CHF
advanced forms
which aldosterone antagonist does not cause gynecomastia
eplerenone
usual initial treatment for symptomatic CHF patients
ACE inhibitor and diuretic
T/F ACE inhibitors have reduced mortality benefit
T
CONSENSUS and SOLVD trials proved what point
ACE inhibitors reduce mortality in patients with CHF
T/F all patients with CHF should be on a ACE inhibitor regardless of symptomatology
T
ACE inhibitors should be started at a low dose to avoid
hypotension
patients that experience dry cough with ACE inhibitors can be switched to what type of medication
ARBs (-sartans)
beta blockers are shown to decrease mortality in CHF for what specific patient demographic
post MI CHF
stable patients with mild to moderate CHF should be given
beta blockers
what are the three beta blockers known to be safe in CHF
metoprolol
bisoprolol
carvedilol
useful agent in patients with EF <40%, severe CHF or severe Afib
digitalis
typically employed for patients with refractory symptoms despite being on diuretic ACE inhibitor and aldosterone antagonist
digitalis
two medications commonly employed in patients who cannot tolerate ACE inhibitors
hydralazine and isosorbide dinitrates
4 medication types that are contraindicated in CHF
metformin (can cause lethal lactic acidosis)
thiazolidinediones (fluid retention)
NSAIDs increase risk of CHF exacerbation
negative inotropic antiarrhythmics
what are the medications that reduce mortality in diastolic heart failure
none
what are the two devices that shown to reduce mortality in select patients
ICD prevents SCD
indicated for patients at least 40 days poist MI EF,35% and class II or III symptoms despite optimal medicla treatment
ICD
biventricular pacemaker in patients with QRS >120 ms
CRT
T/F most patients that meet criteria for CRT are also candidates for ICD and receive combined devices
T
last alternative if all else fails in CHF management
heart transplant
acute dyspnea associated with elevated left sided filling pressures with or without pulmonary edema
acute decompensated HF
what are the two most common causes for acute decomp HF
LH systolic or diastolic dysfunction
severe form of HF with rapid accumulation of fluid in the lungs
flash pulmonary edema
DIFFERENTIAL FOR RAPID RESPIRATORY DISTRESS
PULMONARY EMBOLISM ASTHMA pna AND FLASH PULMONARY EDEMA
diagnostic tests for an individual with flash pulmonary edema
chest xray ecg ABG BNP echo coronary angio (possibly)
what is the management of a patient with acute pulmonary (flash) edema
oxygenation and ventilation assistance
diuretics
dietary sodium restriction
nitrates
present in 50% of adults who undergo holter monitoring and mean nothing in a healthy heart
PACs
what is the treatment for asymptomatic PACs
usually just observation
what is the treatment for symptomatic PACs (palpitations)
beta blockers
causes for PVCs
hypoxia electrolyte abnormalities stimulants caffeine medications structural heart disease
why is the QRS wider in PVCs than with regular electrical activity of the heart
through the ventricular muscle and not the conduction pathways, therefore takes a longer time
patients with frequent repetitive PVCs and underlying heart disease are at increased risk for
sudden death (Vfib etc)
what test should be ordered in patients with PVCs and underlying structural or physiologic heart disease
electrophysiology test (may benefit from ICD)
multiple foci in the atria firing continuously in a chaotic pattern causing a totally irregular rapid ventricular rate
atrial fib
atrial rate in afib is usually over ______bpm but are blocked at the AV node so ventricular rate ranges between ___ and ____
400
75
175
T/F PVCs in patients with normal hearts is associated with increased mortality
T
what are the causes for afib (9) (double H triple S triple P E)
- Heart disease: CAD, MI, HTN, mitral valve disease
- Pericarditis and pericardial trauma (e.g., surgery)
- Pulmonary disease, including PE
- Hyperthyroidism or hypothyroidism
- Systemic illness (e.g., sepsis, malignancy
- Stress (e.g., postoperative)
- Excessive alcohol intake (“holiday heart syndrome”)
- Sick sinus syndrome
- Pheochromocytoma
acute hemodynamically unstable afib treatment
immediate cardioversion
acute afib in a hemodynamically stable patient
rate control (60-100bpm)
beta blockers
CCBs (alternatively)
delivery of a shock that is in synchrony with the QRS
cardioversion
delivery of shock that is NOT in conjunction with the QRS complex
defibrillation
if left ventricular dysfunction is present in the setting of afib
what two medications can be considered
amio or dig
three cases of cardioversion being appropriate in afib
hemodynamically unstable
those with worsening symptoms
those having their first ever case of AFib
what is the use of ibutilide procainamide flecainide sotalol or amiodarone in afib
pharmacologic conversion if electrical cardioversion is unfeasible or doesnt work
when should anticoagulation be employed in the setting of atrial fibrillation
present greater than 48 hours
what are the timing parameters for anticoagulation surrounding cardioversion
3 weeks before and 4 weeks afterwards
what is the INR goal in anticoagulation in patients with afib prior to and following cardioversion
2-3
what can be done (in theory) to avoid 3 weeks of anticoagulation prior to cardioversion in the case of afib)
TEE to image the left atrium for thrombus, if none, start IV heparin and perform cardioversion within 24 hours
T/F if the TEE route is carried out to expedite cardioversion, patients still need to be anticoagulated 4 weeks following cardioversion
T
what are the two agents typically used in the setting of chronic afib for rate control
beta blockers
CCBs
patients with lone afib or afib in the absence of any underlying heart disease or cardiovascular risk can take what medication
aspirin
patients with afib and underlying CVD or risk factors need what type of anticoagulation
warfarin
what is the most common cause for aflutter
heart failure
ECG exhibiting a saw tooth baseling with a QRS complex appearing after every second or third tooth
aflutter
flutter waves seen best in which lead
II III AvF (inferior leads)
how many different P wave morphologies are required to make the diagnosis of MAT
3
MAT is identical to this separate diagnosis except that the heart rate in this other entity is between 60-100
wandering atrial pacemaker
MAT is strongly associated with what type of disease
lung disease
if LV function is not preserved in MAT what medication can be given
digoxin
T/F electrical cardioversion is often effective in MAT
F (not effective do not use)
what is the most common cause of PSVT
nodal re-entry tachycardia`
ECG will show what characteristic in PSVT
narrow complexes with no discernible P waves (P waves buried in the QRS)
what is the underlying process in orthodromic AV reentrant tachycardia
accessory pathway between the atria and ventricles that conducts retrogradely
what would be seen on ECG in orthodromic reentry AV tachy
narrow QRS complexes with P waves may or may not be discernible depending on the rate (could bne buried, re-entrant circuit takes longer the self contained AV reentry, therefore P waves have a higher chance to be revealed)
Six (6) causes of SVT
a. Ischemic heart disease
b. Digoxin toxicity—paroxysmal atrial tachycardia with 2:1 block is the most
common arrhythmia associated with digoxin toxicity
c. AV node reentry
d. Atrial flutter with rapid ventricular response
e. AV reciprocating tachycardia (accessory pathway)
f. Excessive caffeine or alcohol consumption
paroxysmal atrial tachycardia with 2:1 block is the most
common arrhythmia associated with ___________ toxicity
digoxin
what is the agent of choice for correcting SVT
IV adenosine
what is the reason that IV adenosine is the agent of choice in SVT
short duration of action and effectiveness in terminating SCTs
works by decreasing sinoatrial and AVE nodal activity
what agents can be used in patients with SVT if left vent function is preserved as an alternative to IV adenosine
Iv verapamil and IV esmolol (less commonly digoxin)
treatment preferred if episodes of SVT are recurrent and symptomatic
radiofrequency cardiac ablation
narrow complex tachycardia and short PR interval with upward deflection seen before thje QRS complex
WPW syndrome
what is the typical treatment used for WPW syndrome
radiofrequency cardiac ablation
WHAT DRUGS should be avoided in WPW syndrome
drugs that act through blocking AV conduction (beta blockers CCBs digoxin) as they can facilitate conduction through the accessory pathway
rapid repetitive firind of three or more PVCs in a row at a rate between 100 and 250
ventricular Tachy
ventricular tachy typically originates where in the conduction structure
below the bundle of his
what is the most common cause for ventricular tachy
prior MI with CAD
causes for V tach
a. CAD with prior MI is the most common cause
b. Active ischemia, hypotension
c. Cardiomyopathies
d. Congenital defects
e. Prolonged QT syndrome
f. Drug toxicity
Vtach progresses to what arrhythmia if left untreated
Vfib
T/F Vtach lasts longer than 30 seconds and is almost always symptomatic
T
brief limited runs of VT is an indipendent risk factor for SCD in what cases
with concurrent CAD and LV dysfunction
connan A waves in the neck secondary toi AV dissociation and variable S1 intensity commonly associated with
Vtachy
what are the more serious presentations of Vtachy
sudden death
cardiac shock
ecg showing wide and bizarre QRS complexes with tachycardia
Vtachy
all QRS complexes are identical in this form of Vtach
monomorphic
QRS complexes are different in this form of Vtach
polymorphic
T/F VT also responds to vagal maneuvers as with PSVT
F (does not)
what should be given to patients with hemodynamically stable patients with mild symptoms and systolic BP >90
IV amio
IV procainamide
IV sotalol
(one of these)
hemodynamically unstable patients with Vtachy or with severe symptoms treatment
immediate synchronous DC cardioversion
what mnedication is given following DC cardioversion
amiodarone (sustains rhythm)
nonsustained VT with no underlying heart disease a recent MI or evidence of left ventricular dysfunction or symptomatology
order electrophysiologic study
electrophysiology study shows inducible rhythm in the case of nonsustained VT, what should be done
placement of ICD
second line treatment for unsustained Vtach
amiodarone
most episodes of Vfib happen following
Vtach
T/F if Vfib is not associated with MI we shouldnt expect it to recur
F (Vfib not associated with MI has a higher rate of recurrence)
what two treatments can be utilized in the treatment of patients with Vfib not associated with MI
prophylactic amiodarone or placement of ICD
T/F if Vfib follows MI by <48hours then the outcome is bleak and recurrence rate is high
F (prognosis is good and recurrence is low)
T/F chronic therapy is needed for patients with Vfib secondary to MI
F (not necessary)
most common cause for vfib
ischemic heart disease
cannot measure BP
unconscious patient
absent heart sounds and pulse
vfib
ECG no strial P waves can be identified
no QRS complexes can be identified
VFIB
what is the immediate treatment for vfib
(MEDICAL EMERGENCY)
IMMEDIATE cardiac defibrillation and CPR
immediate initiation of unsynchronized DC cardioversion immediately, if equipment not on hand, begin CPR immediately
up to three sequential shocks to establish another rhythm
treatment for persistent vfib following sequential shocks
continue CPR
consider intubation
epi (1mg bolus initially and then every 3-5minutes)
attempt to defibrillate again 30s-1min following first epi dose
if vfib persists past administration of epi, intubation and reshock
IV amiodarone followed by shock
lidocaine, magnesium procainamide alternatives
If cardioversion is successful in vfib, what next
maintain continuous IV infusion of the effective antiarrhythmic agent
ICD mainstay of chronic therapy in these patients (those at risk for VF)
bradycardia clinically significant when persistent below what threshold
45bpm
pathologic causes for bradycardia (3)
cardiac ischemia
increased vagal tone
antiarrhythmic drugs
what medication can be used to raise BP in the case of persistent bradycardia
atropine
prolonged PR interval with a QRS following each P wave
1st degree heart block
progressive prolongation of PR interval until a P wave fails to conduct
Mobitz type I
T/F type I heart block is a benign condition that does not require treatment
T
Pwaves fail to conduct sudndenly without a preceding PR interval prolongation
often progresses
Mobitz II
where is the conduction defect in a Mobits II
His-Purkinje system of conduction
what is the necessary treatment for MObitz II
placement of PCI
absence of conduction of atrial impulses to the ventricles; no correspondence between P waves and QRS complexes
complete HB
what is the treatment of choice for complete heart block
cardiac pacemaker
Most common type of cardiomyopathy
dilated cardiomyopathy
ischemia infection alcohol casuing dysfunction of left ventricular contractility leads to what type of cardiomyopathy
dilated
what is the prognosis for dilated cardiomyopathy
poor
most die within 5 years of diagnosis
what is the most common cause for dilated cardiomyopathy
idiopathic
toxins that lead to dilated cardiomyopathy
alcohol
doxorubicin
adriamycin
ALL CAUSES FOR dilated cardiomyopathy (>;))
a. CAD (with prior MI) is a common cause
b. Toxic: Alcohol, doxorubicin, Adriamycin
c. Metabolic: Thiamine or selenium deficiency, hypophosphatemia, uremia
d. Infectious: Viral, Chagas disease, Lyme disease, HIV
e. Thyroid disease: Hyperthyroidism or hypothyroidism
f. Peripartum cardiomyopathy
g. Collagen vascular disease: SLE, scleroderma
h. Prolonged, uncontrolled tachycardia
i. Catecholamine induced: Pheochromocytoma, cocaine
j. Familial/genetic
what heart sounds are typically associated with dilated cardiomyopathy
S3 S4 and mitral regurg or tricuspid insufficiency
what is the common pathology associated with the enlarged ventricles of dilated cardiomyopathyt
cardiac arrhythmia
this type of testing might be warranted in a patient with DCM with no cause and fam hx of disease
genetic testing
what is the treatment for DCM
(similar to treatment for CHF)
beta blockers
diuretics
dig
should be considered because DCM patients have risk of embolization
anticoagulation
Hypertrophic cardiomyopathy mode of inheritance
autosomal dominance
diastolic dysfunction due to a stiff hypertrophied ventriclewith elevated diastolic filling pressures
HTCM
what kind of obstruction can occur in patients with assymmetric hypertrophy of the ventricular septum
dynamic outflow obstruction
dyspnea on exertion chest pain syncope after exertion or the valsalva palpitations arrhythmias cardiac failure sudden death years without symptomatology
HTCM
sustained PMI
loud S4
systolic ejection murmur
decreases with squatting lying down or straight leg raise
intensity increased with valsalve and standing (decreases LV size and increases obstruction)
HTCM
effect of the murmur with HTCM with sustained handgrip
decrease due to increased systemic resistance leading to decreased gradient across aortic valve
rapidly increasing carotic pulse with two upstrokes indicative of
HTCM
what is the test that establishes the diagnosis of HTCM
cardiac echo
T/F asymptomatic patients with HTCM do not need treatment
T
what is the initial drug used in symptomatic patients with HTCM
beta blockers
used in HTCM if patient nonresponsive to beta blockers
CCBs
surgery for HTCM
myomectomy
opening snap followed by a low pitched diastolic rumble and presystolic accentuation
mitral stenosis
S2 followed by opening snap
mitral stensosi
the distance between S2 and the opening snap of mitral stenosis tells us
severity of the valvular disease
long standing disease of mitral stenosis can lead to what clinical findings
(right heart failure) right ventricular heave JVD pulmonary congestion hepatomegaly ascites
most important test in confirming mitral stenosis
echocardiogram
what are the two medications commonly used in mitral stenosis
diuretics (if signs of RHF) beta blockers (decrease HR and CO)
what are t he two options surgically for mitral stenosis
perc balloon valvuloplasty
open commissurotomy and mitral valve replacement
when the aortic valve falls below what threshold is the cardiac output not able to increase with exertion, resulting in angina
0.7
what is the cause for mitral regurg with long standing aortic stenosis
LV dilation pulls the leaflets of the mitral valve apart resulting in MR
what are the three main causes for aortic stenosis
calcification of a bicuspid valve
calcification in the elderly
rheumatic fever
development of what symptoms would be a sign that aortic stenosis is worsening
syncope
angina
CHF
which of angina syncope and CHF in the setting of aortic stenosis carries the worse prognosis
CHF
harsh crescendo-decreascendo systolic murmur heard in second right intercostal space radiating to carotid arteries soft S2 S4 parvus et tardus sustained PMI precordial thrill
aortic stenosis
what is parvus et tardus
delayed and diminished carotid upstrokes
which test is diagnostic in aortic stenosis
echocardiography
what is the definitive diagnostic test in aortic stenosis
cardiac angiography
what test can measure valve gradient and calculate valve area in aortic stenosis
cardiac catheterization
what is the treatment for aortic stenosis
valvular replacement in all symptomatic patients
treatment for asymptomatic aortic stenosis
none
inadequate closure of aortic valve leaflets causing blood to flow into left ventricle during diastole
aortic regurg
what occurs in the left ventricle in response to aortic regurgitation
LV dilation and hypertrophy to maintain stroke volume
5 year survival for chronic regurgitation
75%
how long do patients typically survive following onset of angina with aortic regurg
4 years
how long do patients typically survive following onset of CHF with aortic regurg
2 years
4 main causes for acute aortic regurgitation
infective endocarditis
trauma
aortic dissection
iatrogenic
causes for primary valvular aortic regurgitation (6)
rheumatic biscupid aortic valve marfans ehlers danlos ankylosing spondylitis SLE
causes for aortic root disease leading to aortic regurg (6)
syphilitic aortitis osteogenesis imperfecta aortic dissection behcet reiter syndrome systemic HTN
widened pulse pressure concerning for what valvular disease
aortic regurgitation
low pitched diastolic rumble due to competing flow anterograde from the LA and retrograde from the aorta
austin flint murmur
aortic regurgitation
rapidly increasing pulse that collapses suddenly as arterial pressure decreases rapidly in late systole and diastole
water hammer pulse, indicates aortic regurg
what happens to aortic regurg with handgrip sustained
increases
what is the utility of echo in aortic regurg
assess chronic patients for surgery over time
what is the treatment for chronic asymptomatic aortic regurg
conservative restrict salt diuretics vasodilators afterload reduction restriction of strenuous activity
what is the definitive treatment for aortic regurgitation
surgical replacement
abrupt elevation of left atrial pressure in the setting of normal LA size and compliance with pulmonary edema
possible hypotension and shock due to decreased CO
acute MR
gradual elevation of left atrial pressure in setting of dilated LA and LV
pulmonary HTN can result from chronic backflow
chronic MR
3 main acute causes for MR
endocarditis
papillary muscle ruption (infarction)
chordae tendinae rupture
4 main chronic causes for MR
rheumatic fever
mitral valve prolapse
marfans
cardiomyopathy
T/F chronic MR has a worse prognosis than acute MR
F (acute is worse prognostically)
holosystolic murmur at the apex radiating to the back or clavicle
MR
what arrhythmia is common seen with MR
afib
what diagnostic tests can show signs of MR
CXR
echo
device used as a bridge to surgery for MR
IABP
what medication outcome should be sought in patients with symptomatic MR
afterload reduction
what is the definitive treatment for MR
valvular replacement
results from a failure of the tricuspoid valve to close completely during systol causing regurgitation of blood into the RA
tricuspid regurg
TR regurg usually 2/2
RV enlargement
what is the most common cause for tricuspid regurg with LV dilation
left ventricular failure
when is tricuspid endocarditis typically seen
IV drug users
congenital malformation of the tricuspid valve in which there is a downward displacement of the valve into the RV
epstein anomaly
TR regurg usually asymptomatic unless what occurs
development of RGF or Pulmonary HTN
what would be expected to be some of the symptoms of tricuspid regurg
ascites hepatomegaly edema JVD pulsatile liver prominent V waves in jugular venous pulse with rapid y descent inspiratory S3 along LLSB blowing holosystolic murmur at LLSB increased with inspiration reduced during expiration or valsalva
how is the diagnosis of tricuspid regurg made
echo
treatment for volume overload and venous congestion/edema of TR regurg
diuretics
what needs to be absent in order for tricuspid valve resplacement surgery to be an available option
pulmonary hypertension
typical mid systolic click and murmuer
mitral valve prolapse
common valvular disease in patients with connective tissue disorders
MVP
most common cause of MR in developed countried
MVP
what do standing and valsalva do in regard to the murmur involved with MVP
increase
what does squatting down have in terms of effect on MVP
decrease
what is the most useful diagnostic tool for MVP
echo
what should be used for the atypical chest pain that can accompany MVP
beta blockers shown to be helpful
T/F MVP often requires surgery
F (often benign, asymptomatic for peoples entire lives)
most common valvular abnormality 2/2 rheumatic heart disease
mitral stenosis
what are the major signs of acute rheumatic fever
migratory arthritis acute myocarditis subcutaneous Nodules erythema marginatum syndenham chorea
what medication should be given to patients with streptococcal pharyngitis to avoid rheumatic fever
penecillin or rythromycin
how is acute rheumatic fever treated
NSAID
what marker is used to track treatment progress
C-RP
infection of the endocardial surface of the heart
endocarditis
acute endocarditis most commonly caused by
staph aureus
acute endocarditis happens on what type of heart valve
normal
if acute endocarditis is left untreated what is the outcome
fatal in 6 weeks
subacute endocarditis caused by
strep viridans and enterococcus
subacute endocarditis occurs on what type of valves
previously injured
what are the more rare forms of native valve endocarditis
HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kindella)
most common organism for prosthetic valve endocarditis
staph epi (and then staph aureus)
Endocarditis in IV drug users
Right sided endocarditis
what valve is typically involved in right sided endocarditis
tricuspid
which bug is most common in right sided endocarditis
staph aureus
what are the four main complications from endocarditis
cardiac failure
myocardial abscess
various solid organ damage from showered emboli
glomerulonephritis
what combination of Duke criteria is necessary for the diagnosis of endocarditis
2 major
1 major 3 minor
5 minor
what are the major DUKE criteria
sustained bacteremia
endocardial involvement diagnosed by echo or by new valvular murmur on clinical exam
what are the minor DUKE criteria for endocarditis
predisposing condition (abnormal valve or abnormal risk)
fever
vascular phenomena (septic arterial or pulmonary emboli mycotic aneurysms intracranial hemorrhage janeway lesions)
Immune phenomena (Glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor)
Positive blood cultures not meeting major crit
Positive echo not meeting major crit
what is the treatment for endocarditis
extended parenteral antibiotics (4-6 weeks)
what are the two factors necessary to warrant endocarditis antibiotic prophylaxis
qualifying cardiac indication: prosthetic heart valve history of infective endocarditis congenital heart disease cardiac transplant with vulvulopathy
Qualifying procedure
Dental procedures
procedures involving biopsy or incision of respiratory mucosa
procedures involving infected skin or musculoskeletal tissue
associated with debilitating illnesses susch as metastatic cancer
sterile deposits of fibrin and platelets forming along the closure line of cardiac valve leaflets
vegetations can embolize to the brain or periphery
marantic endocarditis (nonbacterial thrombotic endocarditis)
typically involving the aortic valves in individuals with SLE
characterized by the formation of small warty vegetations on both sides of valve leaflets and may present with regurgitant murmurs
can be a source of systemic embolization
libmann sacks endocarditis
what is the most common type of atrial septal defect
ostium secundum
what are the three types of ASDs
ostium secundum (central portion opening) ostium primum (low in septum) Sinus venosus (high in the septum)
what is the rare but serious complication that can occur with ASD
pulm HTN
what is the tell tale sign on clinical exam for ASD
fixed split S2
what is the diagnostic test for ASD
TEE with bubble study (bubbles can be seen crossing through the defect often used and can aid in the Dx)
what are the CXR findings c/w ASD
Large pulm arteries
increased pulm markings
pulmonary HTN for ASD typically occurs after what age if at all
40
late complication of ASD in which irreversible pulm HTN leads to reversal of shunt, HF and cyanosis
eisenmenger syndrome
most common of the congenital cardiac malformations
VSD
what happens to the shunt in VSD if PVR becomes larger than SVR
reversal of shunt and potential eisenmenger syndrome
sign symptoms of eisenmenger syndrome
high PVR SOB dyspnea on exertion chest pain syncope cyanosis
harsh blowing holosystolic murmur with thrill at fourth left intercostal space that decreases with valsalva and handgrip
VSD
is a louder or softer VSD more concerning
softer (smaller VSD causes louder murmur)
what is the structure that is responsible for the enlarged cardiac silhouette seen on CXR in VSD
enlargement of the pulmonary artery
what are the complications associated with VSD
endocarditis
progressive aortic regurg
heart failure
pulmonary HTN and shunt reversl (eisenmengers)
when is endocarditis PPX not recommended in VSD
uncomplicated and no prior history of endocarditis
narrowing/constriction of aorta usually at the origin of left subclavian artery near ligamentum arteriosum
coarctation of the aorta
hypertension in the upper extremities and hypotension in the lower extremitis
coarctation of the aorta
well developed upper body with underdeveloped lower bodyu
coarctation of the aorta
CXR showing notching of the ribs
coarctation of the aorta
prevalence of this cardiac malformation is increased in patients with Turner syndrome
coarctation of the aorta
what are the 4 main complications associated with coarctations of the aorta
severe HTN
rupture of cerebral aneurysms
infective endocarditis
aortic dissections
communication between the aorta and pulmonary artery that persists after birth
patent ductus arteriosus
what are the two factors that maintain patent ductus arteriosus during fetal development
low O2 tension
prostaglandins
when does cyanosis occur in PDA
late
cardiac malformation associated with rubella syndrome
high altitude
premature births
PDA
continuous machine like murmur at the left second intercostal space
RVH
wide pulse pressure and bounding peripheral pulses
PDA
CXR showing increased pulmonary vascular markings
dilated pulmonary artery
enlarged cardiac silhouette
calcifications in tract coming off of the aorta
PDA
If pulmonary vascular disease is absent what is the treatment for PDA
surgical ligation
when is surgery contraindicated in PDA
when there is significant right to left shunting
what is the medication that can be used for closure of PDA
indomethacin
medication used to keep PDA open in cases of transposition
PGE1
Ventricular septal defect
right ventricular hypertrophy
pulmonary artery stenosis
overriding aorta
tetrology of fallot
tetrology of fallot arise secondary to defects in the development of what structure
infundibular septum
most common symptom of tetrology of fallot
cyanosis
degree of symptoms in tetrology of fallot depends on
degree of pulmonary outflow obstruction
three substances that can be used in patient with frequent tet spells that are refractory to mechanical position to correct
oxygen
morphine
beta blockers
what is the diagnostic modality of choice in tet of fallot patient
echo
CXR showing boot shape to the heart
TOF
what is the treatment for TOF
surgery
two most common causes of death following surgery for TOF
sudden cardiac death and CHF
hypertensive emergency defined as
systolic above 220
diastolic above 120
in addition to end organ damage
elevated BP levels of hypertensive emergency without end organ damage
urgency
5 systems that need to be assessed in a patient with blood pressures in the emergency range
eyes : papilledema
CNS: AMS or hemorrhage, confusion
kidneys: failure, hematuria
heart: USA, MI, CHF, aortic dissection
radiographic condition postulated to be caused by autoregulatory failure of cerebral vessels as well as endothelial dysfunction
PRES
insidious onset of headache altered level of consciousness visual changes and seizures with posterior cerebral white matter edema
hypertensive or normotensive
PRES
how should BP be brought down in hypertensive emergencies
reduce MAP by 25% in 1 to 2 hours (get the patient out of danger and then decrease gradually)
rate typically sought for BP decrease in hypertensive urgency
normotensive in 24 hours
long standing HTN cocaine use trauma connective tissue diseases bicuspid aortic valve coarctation third trimester pregnancy
aortic dissection
what are the two classifications of aortic dissection
type A
Ascending
Type B (distal to subclavian)
descending
servere tearing rippin stabbing pain
typically abrupt in onset
anterior or back opf chest interscapular
aortic dissection
anterior chest pain is more common with what type of aortic dissection
A
posterior chest pain more common with what type of aortic dissection
B
CXR finding typical for aortic dissection
widened mediastinum
which is more accurate for aortic dissection MRI or CT
MRI
best test for determining the extent of dissection in aorta for surgery
angiography
what medication should be initiated immediately in aortic dissection
beta blockers IV nitroprusside (BP below 120)
most type A dissections are treated as surgical emergencies to avoid
MI aortic regurg or cardiac tamponade
what is the typical management of type B dissections
lower blood pressure, IV beta blockers
morphine for pain
abnormal localized dilation of aorta typically between the renal arteries and iliac bifurcation
AAA
average ages for diagnosis of AAA
65=70
most cases of AAA what process is occuring in vessel
atherosclerosis
5 things other than atherosclerosis that predispose to AAA
HTN smoking vasculitis truama pos famHx
pulsatile mass on abdominal exam
AAA
sudden onset of severe pain in the back or lower abdomen with ecchymoses on back and flanks and ecchymoses aroiund umbilicus
AAA rupture
Grey turner sign
ecchymoses on flank/back
cullen sign
ecchymoses around umbilicus
triad of abdominal pain
hypotension
palpable pulsatile abdominal mass
AAA rupture
AAA rupture treatment
immediate laparotomy and repair
test of choice to evaluate location and size of AAA
US
test that can be used in hemodynamically stable patients with AAA for preop planning
CT
size at which surgical repair of AAA should be recommended
> 5cm diameter
most common site for peripheral vascular disease
superficial femoral artery
what is the most important risk factor for PVD
smoking
patient with PVD and intermittent claudication prognosis
best
patient with PVD and rest pain / non healing ulcers prognosis
bad
ABI above what value indicates severe PVD
1.3
claudication ABI
<0.7
rest pain ABI in PVD
<0.4
gold standard for diagnosing and locating PVD
arteriography
conservative management for PVD
stop smoking! graduated exercise program foot care atherosclerosis reduction avoid extreme temp aspiring +/- ticlopidine/clopidogral cilostazol
three indications for PVD surgery
rest pain
ischemic ulcerations
severe symptoms refractory to conservative therapy
two main options for surgery in PVD
angioplasty
bypass
most common site of acute arterial occlusion
common femoral artery
most common site and cause for embolus of acute arterial occlusion
heart afib
6 Ps of acute arterial occlusion
pain pallor poikilothermia (cold blooded) paralysis paresthesias pulseless
three tests usually obtained in acute arterial occlusion
arteriogram
ecg (MI, afib)
echo (valves thrombus shunts)
amount of time that skeletal muscle can tolerate ischemia
6 hours
what is the immediate therapy for embolus causing acute arterial occlusion
immediate IV heparin
surgical embolectomy with cutdown and fogarty balloonm)
when is bypass employed for acute arterial occlusion
failure of embolectomy
small discrete areas of tissue ischemia
blue black toes
renal insufficiency
abdominal pain or bleeding
treatment
cholesterol embolization syndrome\
Do not anticoagulate
control BP
surgical only in very extreme circumstances
aneurysm resulting from damage to aortic wall 2/2 infection
mycotic aneurysm
what is a luetic heart
complication of spyphilitic aortitis in which the dilation of the proximal aorta blocks the aortic branches most commonly the coronaries
needs surgical repair
virchows triad
venous stasis
endothelial injury
hypercoaguable
lower extremity swelling/pain
calf pain on ankle dorsiflexion
palpable cord
fever
DVT
initial test for DVT
doppler and duplex US
duplex is good for what location of DVT
proximal
most accurate test for DVT of calf
venography
intermediate to high pretest probability of DVT plus Doppler +
begin anticoagulation
intermediate to high pretest prob of DVT with neg doppler
repeat doppler 2-3days for 2 weeks
low-intermediate pretest prob of DVT and soppler neg
no need for anticoagulation
painful blue swollen leg following DVT
phlegmasia cerulea dolens
indicated treatment for phlegmasia cerulea dolens
venous thrombectomy
how long should warfarin be kept following DVT
3-6 months
indicated for DVT/PE massive with hemodynamic instability
systemic thrombolytics
treatment for patient with DVT and absolute contraindication to anticoagulation
inferior vena cava filter
what is the typical preceding illness that leads to venous stasis
DVT (destroys valvs in the system)
what is the reason for the brawny induration and bron black color of sjkin in chronic venous insufficency
extrav of proteins and RBCs
what is the complication common with chronic venous stasis
venous ulceration
how does elevation of legs differ in chronic venous insufficiency versus acute arterial insufficency
provides relief in venous disease
mildly painful ulcears rapidly recurring
above the medial malleolus
chronic venous stasis
three main treatment s to combat complications of chronic venous insufficiency
leg elevation
avoiding long periods of sitting and standing
compression stockings
superficial thrombophlebitis in lower extremities usually associated with
Varicose veins
superficial thrombophlebitis in upper extremity usually associated with
IV placement
neoplasms of the heart are commonly of what origin
metastatis
benign helatinous growth usually pedunculated and arising from the interatrial septum of the heart in the region of the fossa ovalis
atrial myxoma
fatigue fever syncope palpitations malaise and a low pitched diastolic murmur that changes character with changing body position
atrial myxoma
tachycardia decrease in BP and malfunction of underperfused organ systems
shock
fever and possible site of infection in shock patient
septic
trauma gi bleed vomiting or diarrhea in shock patient
hypovolemic
MI angina or heart disease in shock patient
cardiogenic
JVD present in a shock patient
cardiogenic
spinal cord injury or neurologic deficits are present
neurogenic shock
initial steps in ALL shock patients
establish two large bore venous catheters +/- central line and art line
fluid bolus of 2L
draw CBC lytes renal funcrtion PT/pTT
ECG CXR
pulse ox
vasopressors if still hypotensive following fluids
Changes in the following for cardiogenic shock
CO
SVR
PCWP
-
+
+
Changes in the following for hypovolemic shock
CO
SVR
PCWP
-
+
-
Changes in the following for neurogenic shock
CO
SVR
PCWP
-
Changes in the following for septic shock
CO
SVR
PCWP
-
treatment
start with ABCs!
fluid resuscitation
most common cause for cardiogenic shock
MI
vassopressor usually used in cardiogenic shock
dopamine
what is more important in hypovolemic shock, the rate or amount of loss
rate
% of blood loss in following classes of hypovolemic shock I II III IV
10-15%
20-30
30-40
40>