midterm 2 Flashcards
what are we looking for with atrial hypertrophy
what would we see normally
look at V1
and II
normally you have a little cute P wave in II and a biphasic in V1
With RAH you have a peaked P in II and a peaked by in V1
with LAH you have a notched P wave in II and a negative biphasic wave in V1
what causes RAH (4)
pulmonary HTN
COPD
Tricuspid stenosis
congenital
what causes LAH
mitral stenosis
combined with LVH
Causes of LVH
aortic stenosis
mitral incompetence
HCM
HTN
criteria for LAH
Less than 1 box
notched P in I and II
criteria for RAH
greater than 1 small bok in V1 and
>2.5mm P in II
other than lead II where else would you expect to see a peaked p in a pt suspected of RAH
II AVF (all inferior)
lateral precordial and coronal leads
I
V5 and V6
RVH
V1–>V4
very large R wave
RAD in the is usually seen
usually you have a very small R with negative S in these leads
when attempting resuscitation of cardiac arrest what is not shockable
PEA asystole
only vtach and vfibb are shockable
how do you distinguish wandering pacemaker from MAT
MAT is wandering pacemaker over 100
remember we are seeing a P prime wave in all of these because it is not sinus paced
why do we see MAT
COPD or digitalis toxicity
no single impulse is depolarizing the atrium in this tachy that is seen with occasional impulse escape causing ventricle depolarization
A fibb
what is the increase in stroke associated with a fibb
fivefold
what is the increase in dementia associated with a fibb
twofold
what is the increase in heart failure associated with a fibb
threefold
what is the increase in deatg associated with a fibb for men/women
men 50%
women 100%
risk of developing a fibb in adults 40 and older
1/4 lifetime risk
supraventricular tachy associated with depolarization of 300-600 bpm
a fibb
why does a fibb occur
foci and frequency of ectopy increase with remodeling as fo electrical reentry
RF for Afibb
obesity OSA hyperthyroidism diabetes cardiomyopathy heart failure LAE excessive alcohol and genetic predisposition
10!
sxs of a fibb (5)
palpitations dyspnea fatigue exercise intolerance lightheadedness
MC physical exam finding for afibb
irregular and rapid pulse
other than irregular pulse what are some signs of a fibb
signs associated with heart failure
ischemic heart dz
and valvular heart dz
murmur, gallop, JVD, atrial bruits, crackles, hepatomegaly, peripheral edema,
how do we evaluate cardiac function and structure in a pt with afibb
TTE
transthoracic echocardiogram
what should we do for a pt that has had a fibb
ecg
tte
blood work (metabolic and thyroid panels)
how can you dx transient a fibb
ambulatory rhythm monitoring and mobile telemetry
can use trans esophageal echocardiograph (before cardioversion as this could cause embolus)
categories of a fibb
paroxysmal
persistent
longstanding persistent
permanent
what is paroxysmal A fibb
AF that terminated spontaneously or with intervention within 7 days and may reoccur with variable frequency
what is persistent A fibb
continuous AF (more than 7 days)
what is longstanding persistent a fibb
12 months
permanent a fibb
joint decision to stop trying
therapeutic attitude
two types of therapy for a fibb
rate control- sxs
rhythm control- for pts with sxs despite rate control
goal for rate control
and how do we achieve it
under 80 bpm
BB
non- dihydropyrodine CCB
(not in pts with HF)
digoxin adjunct to both of these
electrical cardioversion success for a fib
success 75-90%
returns 40-60% of the times
60-80% of pts in 12 months
success of antiarrythmic drugs for pts with a fibb
50%
what is the most frequent site of AF electrical triggers and what kind of therapy targets them
MC cite is the pulmonary veins
can be targeted with transvenous catheter ablation
reoccurrence
primary goal of AF managment
stroke prevention
what is thought to be the reason for increased stroke risk
decreased blood flow velocity in the left atrial appendage
this allows for thrombus formation
sxs of pericardial effusion
CP
SOB
DOE
feels better when you lean forward
what is the most common EKG finding with pericardial effusion
low voltage QRS
electrical alternans points to
cardiac tamponade
what is electrical alternans
positively deflected QRS followed by low voltage amplitude
regularly irregular
low voltage is defined as a peak to peak QRS amplitude of
<5mm in the limb and or <10 mm in precordial
what causes low voltage EKG other than tompanade
obesity COPD severe hypothyroidism subcutaneous emphysema massive MI infiltrative/restrictive diseases such as amyloid cardiomyopathy
what is beck’s triad
hypotension
JVD
muffled heart sounds
for cardiac tamponade and pericardiocentiusis
beck is eating a muffin with JVD and hypo
ecg triad for cardiac tamponade
sinus tachy
low voltage
electrical alternans
POCUS triad
point of care ultrasound
pericardial fluid
RV diastolic collapse
dilated IVC
how to determine tahcy junctional rhythm
When assessing a rhythm strip for junctional tachycardia, look for a rate of 100 to 200 beats/min. The P wave is inverted in leads II, III, and aVF and can occur before, during (hidden P wave), or after the QRS complex.
paroxysmal tachy rate range
150-250
flutter rate range
25-350
a fibb range
350-450
3 pathophysiologies of a fibb
- dilation in intra atrial pressure leads to activation of RAAS and atrial remodeling and fibrosis
- disorganized electrical impulses develop usually originating from pulmonary veins
- left atrial squeeze is diminished LA appendage is stunned
pathophysiology behind a fibb
larger number of ectopic sites can lead to fault atria and low CO or more commonly
atria do not empty completely into ventricles because
sxs of A fibb
palpitations tachycardia DOE fatigue lightheadedness
but symptoms are absent in 1/3
RVR
the heart rate is on average 150
permanent af s also known as
longstanding persistent
RF for AF
OSA Obesity long standing HTN or CHF /heart dz valvular heart disease cardiac surgery hyperthryoidism genetic predisposition dehydrating factors: viral colonoscopy, cancer, alcohol
what type of valvular disease are we likely to see leading to A fibb
left sided (mitral regurgitation and mitral stenosis)
other than their pathophys origin how do AF stokes differ
more likely to reoccur and are often more fatal
where do AF stroke occur
thrombus formation in the left atrial appendage
what are the three treatment goals of Afibb
- prevent embolic stroke through anticoagulation
- prevent cardiac damage through heart rate control
- back to normal when necessary
what is the stroke assessment?
CHADS2VASC score
also want to assess LV function and LA size and function?
CHADVASC
CHF Hypertension Age over 75 Dm Stroke Vascular disease Age between 64-75 Sex: female
what medication should you be using based on a pts CHAD score
greater than 2 should be on . OACa
if 1 should be on OAC or ASA
1 point stands for
clinically relevant non major
2 point chad score stands for
clinically relevant risk factor major
HASBLED stands for
Hypertension abnormal liver/renal stroke bleeding labile INR elderly >65 Drugs or alcohol
which HASBLED criteria are worth 2 points
abnormal liver or renal
and drugs or alcohol
because they are two categories
goal of anticoagulation therapy
to prevent embolic stoke by reducing thrombus burden in the heart LAA
what is the go to anticoagulant for pts with AF
warfarin titrated to an INR 2-3
normal INR IS 1
what do we use HAS-BLED for
Estimates risk of major bleeding for patients on anticoagulation to assess risk-benefit in atrial fibrillation care.
with a score of 3+ the pt is at increase risk of bleeding
need individualized approach
Types of NOACs
Xa inhibitors
IIa inhibitors
IIa inhibitors -name
dabigatran
Xa inhibitors names
rovaroxaban
apixaban
edoxaban
benefits of NOACs
what are the CI
no blood testing
no food interactions
less drug interactions
safer bleeding profile
contraindicated in mechanical heart valves/ severe mitral stenosis/ESRD
how does Warfarin work
2,5,7,9
binds Ca and prevents the factors from forming a fibrin clot
(from fibrinogen to fibrin)
which Xa inhibitor has low risk of bleeding and mortality benefit
eliquis (apixaban)
need to dose twice
dabigatran pros and cons
direct thrombin IIa inhibitor
superior for ischemic CVA prevention
high risk for GI bleed and dyspepsia
meds for rate control in AF
BB bis met carve neb
Non dihydropyrodine CCB (verapamil and dilitizem)
Digoxin for synergistic
last resort pacemaker
when do we have to attempt rhythm conversion
in an unstable pt in emergent setting
when comorbidities have destabilized a pt (HF CAD pt with unstable angina)
thing of the algorithm unstable with a pulse
when should you consider rhythm control (5)
symtomatic AF despite rate control difficult rate control pts who have tachycardia mediated cardiomyopathy younger active pts small left atrial size
target HR in afibb
<110 is lenient
<80 is strict
need to titrate meds to lower rate based on symptoms with target being
70-90 is the range you want people to be in
three types of rhythm control
electrical w/ TEE- echocardiogram of heart with a probe placed in the esophagus
Chemical cardioversion with amioderone
any medication has a toxic potential though
- transvenous catheter ablation- radio-frequency and cryotherapy on pulmonary veins (reoccurrence rate is 70-80%)
what are we looking at with TEE
Atrial appendage
what is the rules around stable rhythm conversion for a pt with a fibb as far as onset and treatment go
THERE IS A QUESTION ABOUT THIS
with onset unknown pt must be anti-coagulated fro 4 weeks prior
with onset known must occur within 48 hours and no TEE needed
how would amiodarone be used
for rhythm control
high success and safe for all types of pts but can only be used for a short time due to EF
how does a flutter treatment differ from AF
SVT re-entry tachy
use anticoagulation and rate control
rhythm control is considered early but doesn’t respond well to meds
atrial flutter ablation is typically much easier than AF (97%)
what is the AF alogrithm
anticoagulation bassed hon HASBLED and CHADSVASC
rate control less than 110 to prevent heart damage
consider rhythm conversion based on continued symptoms and co morbidities
