Week 2 Flashcards
How can you determine dominance of coronary vessels? What is more common?
85% right dominant- meaning the RCA gives rise to PDA perfusing posterior 1/3 of septum
Dominant= perfuses the posterior third of septum
What are causes of decreased oxygen supply?
Coronary artery occlusion
Anemia
Pulmonary disease/hypoxemia
Tachycardia
What are reasons for increased oxygen demand
Tachycardia LVH HTN Increase in cardiac work/wall tension- afterload Physical exertion, emotional excitement
What are the four ischemic heart diseases, which three are associated with ACS?
IHD- MI, angina, chronic ischemic heart disease with HF, sudden cardiac death
ACS- disruption of a plaque= MI, unstable angina, sudden cardiac death
How much coronary obstruction do you need to get exertion at rest? With exertion?
75% decrease in cross section of coronary artery= symptoms occur with exertion
90% occlusion= sx at rest
What are the key features of each ACS
Angina stable- fixed stenosis-75% no plaque disruption, pain with exertion
UA- fixed stenosis, plaque disruption, partial thrombus,
Variant /prinzmetal angina- episodic chest pain at rest, not coronary stenosis, secondary to vasospasm, STE on ECG
sudden death- most common cause is ischemia, severe CAD
MI- complete thrombus, subendocardial to transmural infarct
What are the sequence of events in ischemia?
ATP depletion begins in seconds, depleted by 40-50 minutes
Loss of contractility- 2 minutes
**Irreversible injury- 20-40 minutes, endocardial>epicardial
Microvascular injury- hours
Ischemia occurs distal to an infarct or thrombus
By 24 hours the infarct is transmural
Describe how an infarct of each coronary would result in myocardial damage seen and how often seen
LAD- 40-50%, apex, Anterior wall LV transmural and anterior 1/3 of septum
Left circumflex- left lateral LV wall transmural except apex
PDA of RCA 30%- left ventricle inferior/ posterior wall and posterior 1/2 of septum, inf/posterior RV
Describe the gross changes seen with MI
Grossly
No change for first 24 hours
1-3 days- pallor of infected tissue
3-7 days- red granulation tissue surrounds the area of infarction, hyperremic MI
7 days= yellow
7-10 days- sharply defined necrotic area yellow tan soft region with hyperemic border- highly vascular granulation tissue
Weeks- month= scar
When is a rupture mostly likely to occur in s/p MI?
Days 7-8 after an MI becuasing necrosis is making the ventricle weak
What changes can be seen under microscope s/p MI?
4-12 hours= wavy fibers followed by coagulation necrosis, mycotolysis is starting up to one day
2-3 days- acute inflammation most prominent, neutrophils prominent, muscles beginning to break up
5-10 days- macrophages removing myocytes= yellow
2-4 weeks- granulation tissue that will be replaced by fibrosis= red, yellow
6-8 weeks= fully fibrotic- white scar
What is goal and approaches to repurfusion s/p MI?
Attempts to restore perfusion to salvage ischemic myocardium
If done within 20 mins can salvage everything, more time= more death
Use fibrinolytics, balloon ang, PTCA
What changes persist despite repurfusion s/p MI
Infarct will have hemorrhagic appearence d/t leakage from injured vasculature- contraction band necrosis (lose nuclei, striations or bands in muscle, gaps in muscle) hypercontracted sarcromeres
Some new damage from free radicals
Stunned myocardium: functional changes that persist despite repurfusion
What complications can arise s/p MI and when do they present?
Contractile or pump failure= CHF of some type, disycn pumping, early or later, common late months to year complication
Arrtymias- an early complication of MI within day to week
Myocardial rupture- 7-10 days after MI, septal rupture with L to R shunt, pap muscle rupture with severe mitral regurg, free wall rupture associated with hemopericardium and tamponade
Pericarditis- 2-3 days, secondary to incoming inflammation, weeks later can develop dressler’s syndrome
What is chronic ischemic heart disease?
Progressive heart failure sp ischemic MI when compensatory mechanisms are exhausted, up to half patients need cardiac transplant
What, where, how does myxoma cause damage, what is it associated with?
90% in atria, usually Left
Usually immoble and planted but if able to move through AV valve can cause obstruction and damage
Can have constitutional symptoms bc of elaboraton of cytokines
10% ass. With Carney syndome= multiple myxomas, spotty skin pigmentation, endocrine over reactivity
LOOKS LIKE STRAWBERRY JAM IN HEART
What are the other cardiac tumors he talked about
Rhabdomyoma- associated with tuberous sclerosis, spider cells
Metastatic tumors from lung breast melanoma, hematologic
Hamartoma- most common tumor in heart of kids, associtated with tuberosus sclerosis
What leads are good for detecting inferior STEMI? what artery is occluded?
II III avF are inferior leads. STE in those leads
RCA = inferior
If II >III circumflex
if III> II RCA
What are goals for reperfussion in STEMI?
Door to fibrinolytic (needle) =30 minutes
Door to balloon (PCI)= 90 minutes
What are the four Killip classes of MI? Define and explain mortality approximately?
Can grade outcomes after MI Class I- no CHF, least mortality 6% II- S3 sound and or basilar rales- 17% III- pulmonary edema= 30-40% mortality IV- Cardiogenic shock- 60-80% mortality
more signs of cardiogenic shock= worse they do
What are some mechanical complications post MI and when do they occur?
Free wall rupture- 2-3 days post MI, tamponade or PEA arrest
VSR- septum rupture less than 5 days after MI, usually with murmur/thrill
Papillary muscle rupture- less than 5 days post MI, 50% have murmur
What are other complications of MI?
A fib
VT/V fib
heart block- anterior less likely to recover
LV aneursym- persistent ST elevation, risk for thrombus
Pericarditis- 1-4 days sp MI, Dresslers syndrome is 2-10 weeks sp MI
Where do narrow complex tachycardias come from
they are supra ventricular, above the AV node
SA node- SA node reentry tachy
Atrium- atrial tachy, a flutter
AV node- AVNRT, ORT
What is inappropriate sinus tachy and who does it affect mostly?
Accelerated baseline sinus rate without physiological stressor
Most common in young women without structural heart disease
What is premature atrial contractions?
early beats in atria from advanced automaticity
2 or more Ps without a QRS everytime, long PR interval
if happens in a long run= atrial tachy
What is atrial tachy and what are common causes?
HR in 120-200bpm from supra ventricular
Can be see with prior sx or ablation
COMMONLY SEEN with digitalis toxicity- dig binds Na/K aptase and competes with K to pump, with hypokalemia little K to compete with digitalis= risk for digitalis toxicity
**likely on exam
What is multifocal atrial tachy and what is it commonly seen with?
Mutliple (3 or more) competing loci in atrium, irreg irreg
P waves with different morphologies, different PP PR intervals
OFTEN SEEN IN CHRONIC LUNG CONDITIONS
What is the most common cardiac arrythmia and describe it
Atrial fibrillation is most common
Rapid and disorganized atrial pulses
Irreg irreg= irregular conduction through AV node leads to RR intervals with no pattern
How do you treat a fib?
control the HR, prevent strokes with anti-coagulation
may need to get aggressive to control arrythmia
What is junctional ectopic tachycardia? what is the cause and what is seen
A supra ventricular NCT. Caused by sudden rapid pacing of an automatic focus in the AV junction right below the AV node
Automaticity from junction up to atrium (may see retrograde P waves) and down to ventricle
Describe re-entry circuits
Electrical impulse travels in a tight circle within the heart leads to fast heart rates
Requires two areas with different conduction speeds and different refractory periods
premature beat typically initiates the cycle
What causes atrial flutter and what does it look like on ECG?
A flutter is caused by re entrant rhythm typically in the RA around cavo tricuspid isthmus, not dependent on nodes
See F waves or sawtooth pattern on ECG
Tx: like a fib, control HR and anti-coagulate and maybe get aggressive on anti rhymics
Describe AV nodal reentrant tachycardia
most common reentrant SVT, more common in women
Requires “dual AV nodal physiology”- if fast pathway has long refractory period and slow has short refractory period then hit with next stim and it must go down the slow pathway- by the time it gets down the slow pathway the fast has repolarized accepts the impulses
Can be fast or slow, anterograde or retrograde
What is AVNRT ecg look like?
P waves are in QRS or shortly after QRS as pseudo Rprime in V1
impulse travels up fast pathway due to nearly simultaneous activation of atria and ventricles
What is atypical AVNRT?
Reentrant circuit with AV node anterograde conduction in fast pathway and retrograde conduction in slow pathway
P waves usually visible bc of delay traveling up slow pathway
Describe ORT vs ART
More common in men. Requires an accessory pathway that connect atrium and ventricle allowing bypass of AV node.
Orthodromic- down the AV to ventricle and up the ventricle to the atrium through an accessory pathway. Anterograde through AV and retro through pathway= reentry circuit- retrograde P wave after QRS
Seen narrow QRS, and delta wave bc got to muscle early, short PR, retrograde P after QRS in inferior leads
Antidromic is down the accessory pathway up through the node retrograde, look like Vtachy but will respond to adenosine and VT won’t, wide complex tachy
Describe WPW
An accessory pathway that starts in SA node down both the AV node and an accessory pathway leading to delta wave from pre excitation, QRS >100ms, short PR interval
If atrial rhythm is regular how do you dx NCT?
can try to slow conduction through the AV node to help with dx to better visualize atrial activity and terminate re entry circuits depending on AV node
Vagal maneuvers: carotid sinus massage, valsalva- decrease preload to heart (as side not hand grip increases after load)
or give adenosine and see if it stops, AV node block, terminates AVNRT or AVRT
does not terminate a fib or MAT
What is most sensative cardiac biomarker?
Myoglobin is most sensative for MI, not specific at all
what is myoglobin used for as biomarker?
it is a good early detector of MI and for reinfarct analysis
how often should blood be drawn after ACS onset?
at presentation and every 6-9 hours
What is the difference in CK and CKMB
CK is the activity of kinase, CKMB is the amount or weight
What is the timeline for CK increases and peak and resolved after AMI?
rises 3-8 hours, peaks 10-24 hours, normal by 48 hours
Is CKMB cardiac specific? What is its timeline? how is it measured
not cardiac specific but concentration greater in cardiac muscle, after MI there is 10 fold increase in CKMB
abnormal by 4 hours
Measured as index: concentration/activity CK
is myoglobin cardiac specific? timeline?
no its in cardiac and skeletal muscle, not specific but most sensitive
abnormal within 2 hours, normal within 24 hours after AMI
What is the best biomarker for MI
troponin
what are the troponin subunits used for testing in AMI and why?
CTI subunits exist. C is genetically same in cardiac and skeletal muscle so not good biomarker
T and I are used as biomarkers
Compare and contrast troponin T and I in uses for biomarkers, length after MI, cytosolic compensate and prognostic value
troponin T= coexpressed in skeletal and cardiac muscle during fetal develop and in muscle trauma/kidney disease
cytolosic compostion= 6% more sensative than I
longer presence after AMI bc continued release as result of repeated cardiac injury, used as indicatior of UA
0.1-0.2 is cutoff
troponin I is not expressed in skeletal muscle- 3 additional amino acids in cardiac form= more specfic than troponin T, cytosolic fraction is about 3% so less sensitive than T, cut off is 0.3 but can vary
Describe the rise and fall of troponin in AMI dx
It is required now for dx of AMI
blood samples every 6-9 hours to increase sensativity to rule in AMI, look at absolute changes
now suggestion to draw blood every 2-3 hours but not done here yet
rises by 4 hours and is abnormal for about 1 week
do all MI have pain and symptoms
no especially in DM or obese
might not see EKG changes either
What percent of US population is affected by HF
2-3%, only lung cancer is worse prognosis
how do you dx HF
based on clinical signs and symptoms rather than stand alone test results, unlike MI biomarkers are not required for dx but NP are helpful
What are goals for HF biomarkers
to identify underlying and reversible causes of HF, help confirm dx of HF, assess severity of HF and risk of progression
What is the mechanism of release and function of naturietic peptides?
Mechanism of release: cardiac volume and pressure overload and cardiac stretch
Function: naturesis (Na excretion), vasodilation, renin inhibition
Can actually give BNP to reduce pressures as a drug
What are the biomarkers for HF
BNP and proBNP correlated to HF
Compare the sythesis of NT proBNP and half life- what is the effect?
Pro BNP is cleaved by corin in response to stretch or ischemia to create 1 BNP and 1 NT pro BNP
BNP half life is shorter, NT pro BNP is longer and can accumulate in renal patients
What is the site of action for BNP?
NPR-A is receptor for BNP after release
could determine dyspnea from HF from COPD potentially
When is BNP elevated and why?
BNP and NT pro BNP levels occur in setting of elevated filling pressures in patients with cardiac dysfunction and can provide relatively reliable diagnostic and prognostic values
what are the cutoff levels for BNP vs proBNP in dx HF
BNP is 100 and proBNP is 300 bc half life is longer
BNP less than 50 effectively rules out HF
BNP higher than 500 with clinical sx is almost always secondary to HF
BNP btn 100-300 is not effective in distinguishing HF from other diseases
have negative predictive power in ruling out HF with patients presenting with dyspnea
What are normal intervals on ECG
PR= 0.12-.2 QRS= 0.06-0.10 QT= 0.35-.43
What halves of the P wave does each represent
first half is RA depol
second half is LA depol
What leads are best to see P waves
II and V1
How can you determine a LA abnormality
delayed terminal portion of P wave
Notched P wave in II, biphasic with dip in V1
How can you determine RA abnormality
Tall upright P waves in II > V1
What is a likely cause of global PR depression
pericarditis
What does high voltage on ECG mean
possible LVH or RVH,
specific, not sensitive
What changes on ECG are seen in LVH
in lateral leads I AVL V5 V6 see downsloping ST depression with T wave inversions and asymmetry
What changes on ECG seen in RVH
R wave in V1 is upright (positive) more than usual and is bigger than S which is abnormal for V1
What do flattened T waves mean
coronary ischemia
What are tall T waves from
hyperkalemia
What are U waves from
hypokalemia, repol of purkinje fibers
How do you treat LEF monomorphic VT? Normal EF monomorphic VT?
Low EF: amiodarone, lidocaine
normal EF: procainamide, amiodarone, lidocaine
What should be avoided in monomorphic VT
Adenosine or AV node blockers
How do you treat polymorphic VT?
If unstable= defib
If long QT= IV magnesium, increase HR with isoproterenol
if suspect ischemia= amiodarone, lidocaine to improve coronary flow
What is treatment for VF
need high energy cardioversion
How can a ICD control VT
by giving short bursts of anti tachy ventricular pacing in low energy can prevent VT most times
what is difference in single and double chambered ICDs
Single chamber pacemaker- no need for A V sync, not for bradycardia pacing, good for chronic a fib and primary prevention of sudden cardiac death
Dual chambered: sinus rhythm with so AV block or SA node dysfunction, bradycardia control
cardiac resync- 3 lead system in RA RV LV, LBBB patients
What is characteristics of sick sinus rhythm
Also called tachy-brady syndrome
Dysfunctional SA node that sometimes fires too quick sometimes too slow
Rate varies but sinus rhythm (narrow QRS from above AV node)
What is sinus arrest? how is it different from sick sinus
Sinus arrest is failure of impulse formation of SA node, in sick sinus the SA is just dysfunctional and fires too fast or slow
In sinus arrest must look for escape rhythm from either the ventricles or the junction, SA node is not pacemaking something lower is
