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
What is the treatment for SA nodes diseases?
if symptoms then need atrial pacemaker
If no symptoms then no tx needed bc atrial kick is only about 20% of filling
What is the characteristics of 1st degree AV block
All P waves are conducted to ventricles but conducted in a delayed fashion, this makes the PR interval longer than 0.2s (1 big box)
Consistent PP interval, every P is followed by a Q (1:1)
Intranodal block- conduction slows in the AV node
What is characteristic of 2nd degree AV blocks
Some P waves are conducted
3rd degree AV blocks are called what and why
complete heart block because no P waves are conducted to ventricles. Independent atrial and ventricular rhythms
PP constant, RR constant (from escape beats)
What is Mobitz Type I AV block
A 2nd degree block with consistent PP interval
PR interval gets progressively longer until one P wave is dropped, PR after the dropped beat is short and right before the dropped beat is long
Intranodal block- decremental conduction through AV node
Explain how decremental conduction through AV node is effected by changes to SNS or PSNS. What about infra nodal?
If AV node (intranodal) problem and exercise or catecholamines or atropine (decrease PSNS and increase conduction) is applied the block gets better less blocked beats, infranodal you drop more beats (you have more beats to drop)
If perform vagal maneuver (increase PSNS and slow conduction) and intranodal more beats are blocked. Or go to bathroom and pass out from increased vagal tone and more dropped beats. Infra nodal- slow sinus rate and fewer beats are dropped
Infranodal conduction is unaffected by autonomic modulation
What is AV block Mobitz type II?
Second degree AV block, Infra nodal block likely in bundle of His
Consistent PP interval (like type I) but PR interval remains the same (unlike Type I) with intermittent dropped beats
More clinically unstable than Type I mobitz
What is 2:1 AV block
A second degree AV block where every other P wave is not conducted to ventricles
Cannot determine level of block (type I or type II)
If affected by autonomic stimulus then it is in AV node, if not then outside or below the node
In third degree AV block what is the relationship btn P and QRS complexes? what is faster?
No relationship btn P waves and QRS complexes
Regular PP intervals and regular RR intervals
Atrial rate must be faster than ventricular rate (coming from higher up and the A and V are not connected. Each beats regularly but with no relation to each other)
What is common causes of AV block? What would you look for first in someone with AV block?
Common causes: high vagal tone (in shape, go to bathroom)
medications: BB, CCB, amiodarone, digitalis
MI- not enough blood and can lose conduction
metabolic/electrolyte derangements
LOOK first for causes that are easy to reverse like electrolytes or thyroid panel
When does someone with AV block get a pacemaker?
If they have symptoms- pacemaker
If they have no symptoms- and infranodal- pacemaker
- and intranodal- typically stable escape rhythm- expectant management (observe)
What leads do you look at to determine BBB? what is normal
V1 and V6
V1- should be no Q, small R up, larger S down, back to isoelectric and then up T wave
V6- small down Q, large up R, S back to isoelectric, up T wave
What is the ECG pattern of RBBB?
Wide QRS > 0.12s Intial QRS is normal Terminal forces reflect slow myocte to myocyte RV depol- R prime + in V1 and V2 wide slurred S in I V5 V6 T may change in V1 and V2
V1- no Q and R is up and smaller than S (normal) but then S shoots up past isoelectric to make R prime then INVERTED T wave
V6- small Q with large R (normal) but S shoots back down past isoelectric then back to iso, T is upright and normal
What are important RBBB causes?
Normal varient in 1 in 500
Ischemic heart disease- new RBBB with symptoms can indicate LAD ischemia
Hypertensive disease- change shape of conduction tissue
Cor pulmonale- lung disease gives RH problems
acute=pulmonary embolism
chronic= COPD
What is the management of RBBB?
Evaluate for underlying cause- cardiomyopathy, IHD, RV overload, check LAD
No therapy needed for isolated RBBB, unless d/t ACS then tx ACS, unclog LAD
What does LBBB look like on ECG
In V1- see a down going QS that is forked, then straight to isoelectric
V6- broad slurred R with fork, no Q , inverted T
What are important causes of LBBB
IHD, HTN heart disease, LVH- walls of pump has to change and remodel to match and exceed pressure in aorta
How do yo treat LBBB?
Evaluate for AMI not because of blood supply to LBBB (gets dual supply) bc the ST segments are hard to interpret with LBBB
Consider resynch therapy if LV EF is less than 35%
What are indications for pacemaking?
Both symptoms and documented evidence of arhythmia
Also sick sinus syndrome is Class I indication if symptoms attributable to SSS
- bradycardia
- chronotropic incompentence- heart needs to speed up but can’t
- symptomatic bradycardia from necessary drug therapy
Also in 3rd degree AB block or 2nd degree with symptoms, HR less than 40, post surgery, d/t necessary drug tx, or a fib with pauses of 5 seconds or greater
Also Carotid hypersensativity- carotid massage causes bradycardia, indication for pacing if carotid sinus massage causes recurrent syncope
What are the three mechanisms of arrhythmia?
Enhanced automaticity, triggered rhythms- impulse intiate
Re-entry- impulse propogation
where does automaticity come from?
Spontaneous action potentials from diastolic depolarizatin caused by a net inward current during phase 4 of action potential (Ca) to bring to threshold
Describe the SA node action potential
Phase 0- occurs by increased Ca conductance through L type Ca channels, slow movement so rate of depolarization is slower than in other cardiac cells like purkinje fibers
Phase 3- repolarization, K channels open and K out which hyper polarize cells
Phase 4- funny current (lf) are activated during hyper polarization and inactive during depolarization, they depolarize the sarcolemmal membrane, is a mixed Na-K inward current modualted by ANS through cAMP
What are the paces of the different heart tissues
SA node= 60-100bpm
AV= 45-50 bpm
Ventricular muscle= 30-40bpm
How do drugs that cause QT elongation work?
they affect Ikr, block to make depolarization longer
What determines the RMP (phase 4) of myocardium?
SA node it is funny Na currents
But in myocardium automaticity results from moving to RMP (-90mV) to threshold at -30 to -70mV
RMP in myocardium is mainly determined by IK1 activity-pumps K out at rest
things that reduce IK1 enhance automaticity: increased extracellular K, reduced IK1 channels, long QT syndrome
What are triggered arrhythmias?
Abnormal depolarizations of cardiac myocytes that interrupt depolarization
Typically caused by Ca overload- gene defect of digoxin toxicity
Can lead to arrhythmias by causing depolarization before the myocardium is fully repolarized
Afterpolarizations can lead to spontaneous AP= triggered response
What is an example of triggered arrhythmias
Torsade de pointes, digoxin toxicity, some ventricular tachycardias
How can 2:1 block lead to VT
2:1 block is long diastolic filling, high Ca intracellularly leads to triggered arrhythmias that are Polymorphic VT
Tx with fixing bradycardia
How does RVOT VT happen?
It is caused by intracellular Ca overload that enhances the Na/Ca exchanger- leads to increasing inward current and after depolarization
Afterdepolartizations can lead to another AP and initiate tachycardia
cAMP has a substantial role in regulating intracellular Ca
when concentration of cAMP is increased after depolarizations are more likely
What is the tx for RVOT VT
adenosine is the tx for RVOT VT because its ability to lower cAMP- less afterdepolarzations
BB are effective bc inhibit adenylyl cyclase that makes cAMP
Verapamil works by inhibiting L type Ca channels and decreasing Ca intracellular that can decrease cAMP
or ablate
How can you test for exercise induced VT
could give isuprel- alpha beta agonist that acts like you get on treadmill- reproduces the triggered VT
Re-entrant rhythms are caused by what
caused by a circus motion around a functional or fixed obstacle
Cells take turns in recovering from excitation so that they are ready to be excited again when next wavefront arrives
Need unidirectional block and long enough circuit to allow each site to recover before depol wavefront returns
How can MI lead to VT
VT can be reentrant around prior infarct scar
What are the class Ia AAD. What is their action
quinidine, procainamide, disopyramide
They block NA mostly and little K- prominent AP prolong
What are class Ib AAD. what is their action
Lidocaine, mixlitine
What are the class Ic AAD. what is their action
flecainide, propafenone
block Na channels
What are the varying potencies of class I AAD
CAB- potentcy
BAC= fast to slowest kinetics
if bind strong then potent but slow
What are the effects of the different class I AAD
class Ia- block Na and K a little Decrease the slope of phase 0, increase QRS= decrease the conduction, prolongs the QT= longer to depol and repolarize
Class Ib- unique that they shorten the AP, shorten the QT- useful in long QT syndrome
Class Ic- most effect on decreasing slope of phase 0= increase QRS
It says all of them increase PR and QRS, slow conduction and reduce excitability _not sure if true
What is the Class III AAD? what is their effect
Ikr blocking, prolongs refractory period (increase AP duration), QT prolonging
amiodarone, sotalol, dofetilide, ibutilibe- all block different portioins of channel, have different side effects
What is mutated in long QT syndrome
Ikr channels- block repolarization - prolongs refractory period to increase AP duration
QT prolonging drugs usually block Ikr
What are the class IV AAD? What is their effect?
Ca Channel blockers, block automaticity in SA node, slow AV node conduction
Negative inotropes, increase threshold for phase 4 depolarization in SA/AV nodes
What is Class I AAD use dependence? why?
Class I are Na channel blockers that bind and work when channels are open in phase 0 or inactive in phases 2,3.
Faster HR= more drug binding= use dependence (forward dependence)
What is Class III AAD use dependence? Why?
Class III iKr blockers have reverse use dependence. They have more affinity for resting channels, more active in slower HR
On the page with the charts, what are the Class I AAD drug effects that are important?
Class Ia- Increase QRS, Increase QT, decrease slope 0
(also decrease slope and slows conduction= wide QRS)
Class Ib- Decrease the QT
(unique in that they shorten AP, useful in long QT)
Class Ic- Biggest effect on decreasing slope phase 0
(no effect on QRS widening, QRS prolongation is main effect)
They slow conduction and decrease excitability
Ia=prolong QT
Ib=shorter QT
Ic= decrease slope phase 0
what is the MOA of quinidine? What is effect? what is it used for?
MOA: blocks Na current mostly, some effect on K channels
Effect: prolongs PR, QRS, QT
Tx: effective in atrial and ventricular arrhythmias, bogoda
What is quinidine side effects?
GI is most common- nausea, anorexia, diarrhea
Cinchonism- combo of neuro effects- tinnitus, hearing loss, visual loss, confusion
Thrombocytopenia, hemolytic anemia
Hypotension from vasodilation
Increase QT and torsade de pointes- start them in the hospital
What is the MOA of procainamide? What is it used for?
Blocks Na channels mostly and some K
Drug of choice for atrial fibrillation in WPW (aka preexcited a fib- don’t give adenosine, give procainamide)
Works by blocking accessory pathway muscle conduction and his-purkinje system
Can be used to unmask Brugada
test for Infranodal block
How is procainamide excreted and why important
60% renal excreted, careful in renal insufficiency
NAPA is a metabolite of procainamide and 100% renal excreted and a pure III AAD agent
What is Brugada syndrome? What mutation? Who gets it and what effect?
It is a loss of Na channel function, hertiable syndrome predisposing to sudden death at night or rest
SCN5A loss of function
Genetric predisposition becomes phenotypically apparent with fever, BB, Na CB (don’t give)
More common in SE Asian men
How do you test for Brugada?
Normally don’t give Na CB bc they have a Na channel defect but give procainamide and look at ECG
See ST elevation- Saddleback deformities in V1-3 at high levels
What are the important side effects of procainamide?
DRUG INDUCED LUPUS- in about 30%, 80% have +ANA but don’t need to check unless suspicous
Agranulocytosis
QT prolongaion
Torsade de pointes- idiosyncratic
vasculitis raynauds GI hypotension bradycardia
What is lidocaine MOA? Where does it have effects? What is it used for? Where is it metabolized? What side effects?
It is a class Ib agent, blocks vg Na channels with most effect in ischemic tissue, little effect on atrial tissue or AV conduction
Useful in ischemic myocardium
Metabolism is dependent on hepatic blood flow, be careful with CHF and liver cirrohirosis= dec dose
Side effects: neuro- delirium and serizures
What is Class Ic agents MOA and contradicitions?
Potent Na channel blockers, minimal effect on refractoriness
Marked negative inotropic effects- do not give in CAD, HR, structural heart disease, or to suppress post myocardial PVCs
What is propafenone MOA? Who is a slow metabolizer of it? Side effects? and toxicities?
Propafenone- is a potent Na CB with some weak beta blocking
Whites are slow metabolizers- could increase BB and worsen HF or bradycardia
Side effects: dizziness, blurred vision, no effects on pacing or defib thresholds
Increase digoxin level (renal) and warfarin (CYP)
What is digitalis MOA? Effects and how are they increased?
Na-K ATPase blocker, increases Na influx and active Na-Ca exchange, so increases Na that leads to increase intracellular Ca too
Effect is greater in hypokalemia
PSNS effects in atrium and AVN- shorter cycle lengths in atria bombard AVN- decrease conduction (concealed conduction)
Intracellular Ca (DADs) and and SNS and arrythmias (AV block, a or v tachy) in toxic doses
What is adenosine MOA? Effects? Uses?
MOA is A1 receptor inhibiting of adenylyl cyclase, reduces cAMP, downstream reduction in CA
Hyper polarizes cells by increasing outward K efflux- also causes endothelial dependent relaxation of smooth muscle, decrease lf in SA node, makes phase 3 more negative
Useful in termination of SVT that depends on AV node
Don’t worry about but what BB are lipophilic vs hydrophilic
lipo- metropolol, propanolol, labetalol, acebutolol, liver short half life
hydo- atenolol, nadolol, pindolol, sotolol, kidney long half life
What are the Class III AAD? what are they effects? and use dependence?
Ibutilide, dofetilide, sotalol, amiodarone (has a little of every class)
They block Ikr, prolong repolarization, increase refractoriness, increase AP duration (QT)
reverse use dependence
can cause Ventricular arrtymias
What is Long QT syndrome type II? Tx?
mutation in Ikr, repolarize slow when does not work, prelonged QT longer than .48s predisposes to sudden death from polymorphic VT or VF
triggered arrhythmia by emotion or scarred, alarm clock, exercise
75% penetrance
Nadolol is treatment
What is important about amiodarone? Side effects?
Has more Na CB properties than class III but call it class III
most commonly used AAD- used for atrial and ventricular arrhythmias, a fib or VT
large volume of distribution and long half life
Significant side effects: hypothyroidism and prevent T4 to T3 (increased TSH and low T4), supplement with T4
Possible hyperthyroid too, need to stop amio
Pulmonary: CHF appearance on CXR, lung fibrosis, eye problems, liver must be watched
skin blue discoloration or photosensativity
eye- photosensative
What is endocarditis?
inflammation (not necessarily infection) of endocardial surface of heart (including valve)
what are risk factors for endocarditis?
Structurally abnormal valve
IV drug use- staph or strep
indwelling foreign material - can lead to infection
persistent bacteremia and inflammed valve- leads to vegetation
What is vegetation and what is it made up of?
A visible often mobile mass on valve
Made up of fibrin, platelets, blood component
secondary infection with collection of organisms
How do you form vegetations on valve from infective endocarditis?
Already damaged valve exposes endocardium for activated platelets to bind to, fibrin sticks
then bacteria flowing through blood can stick on top of that
What is difference in subacute vs acute infective endocarditis
Acute- normal valve becomes inflamed, highly virulent organism sticks, more damage, higher mortality, days to weeks
Subacute- previously abnormal valve, low virulence organism, most recover with antibiotics, weeks to months
what is most common organism causing infective endocarditis and who gets it
IE from IV drug user, staph aureus is most common
strep viridans, HACEK, enterococci, coag neg staph
What valves are most effected in infective endocarditis
AV and MV most comply affected
TV in IV drug users
will see blood products build up in bacterial endocarditilis
How does IE present
2 phenomenon:
Vascular- emboli in left or right, mycotic aneurysm, Janeway lesions, intracranial hemorrhage, conjuctival hemorrhage
Immune complex mediated- glomerlonephritis, osler nodes (digit pad), fluffy exuadate on retina, rheumatoid factor
What are the three levels of infective endocarditis and how do you dx
Definite endocarditis- 2 major, 1 major 3 minor, 5 minor
possible- 1 major 1 minor, 3 minor
rejected- not meeting that or sx not up to it
Major: bacteremia of usual organisms on 2 cultures
evidence of endocardial involvement- vegetation or regurg
Minor:
predisposing factor, fever, new murmur, vascular phenomonon, immune phenomonon, blood culture
What is treatment for IE
IV antibiotics- more for left
Remove indwelling pacemaker or catheter
Surgery if: vegetation is about 1.5 cm, ongoing embolic phenomon, HF d/t valve dysfunction, can’t clear bactermiena, paravalvular extension- abscess or heart block
What is Libman sacks endocarditis? what valves affected? what seen?
Non infective endocarditis from SLE!!!
MV and TV affected
See small sterile granule vegetations on both sides of valve
What is myocarditis?
Inflammation of muscle of myocardium lead to damage and dysfunction
what is major cause of myocarditis in the US
Viral, coxaskie A and B (enterovirus)
Coxaskie B if flu like illness before myocarditis
Adenovirus if subclinical myocarditis
what is most common cause of myocarditis in south america? how get it and prognosis? histo?
Trypanosme cruzi- chagas disease
from kissing bug, life long infection, few people get symptoms but most deaths chronically are from arrhythmia or CHF from chronic inflammatory cardiomyopathy
Histo see parasite balls in cardiomyocytes
how does myocarditis present? what can it cause
very variable- asymptomatic to sudden death
arrythmia- esp in giant cell
Heart failure- elevated troponin, elevated pressures in ventricle= ischemia
idiopathic dilated cardiomyopathy can be caused by asymptomatic myocarditis presenting later as LV systolic dysfunction
what do you see histo for myocarditis
not much, maybe some lymphocytic infiltration and some damage to myocardium
How can you get non infective myocarditis?
Giant cell is most important
Transplant rejection or hypersensativity reaction
what is giant cell myocarditis? what causes it
Giant cell myocarditis is aggressive inflammatory process target at cardiac myocytes, infilitration of lymphocytes (CD8) eosinophils plasma cells PMN and mulinucleated giant cells (macrophages with many nuclei)
thought to be T lymphocyte mediated inflammation (CD8), prominent myocyte necrosis seen
some assocation in some people with abs and autoimmune disorders
How does giant cell myocarditis present and how is it treated/dx
It presents with preceding flu like symptoms
progresses to heart failure and shock and ventricular arrhythmias in days to weeks from inflamed myocardium
Rapid progression and can be fatal, ARRHYTHMIA- lots of destruction and inflammation in myocardium- myocyte necrosis seen with giant cells
Treat with immunosupreesion with steroids, if suspicious get a biopsy to dx
Heart transplant and mechanical support often needed
What is pericardial effusion? what causes it
excess fluid in pericardial sac, more than the normal 50mL
not tamponade or pericarditis
Caused by: 1) **malignancy
autoimmune, hemodyalsis, idopathic, sp radiation
If hemorrhagic consdier: TB malignancy, trauma, aortic dissection
What is acute pericarditis? presentation? exam? EKG?
Inflammation of pericardial sac
Presentation: chest pain THAT IS IMPROVED WHEN SITTING FORWARD, SOB, tachycardia
Exam: may hear friction rub
EKG: PR depressions diffuse in II* and STE
What is cause of acute pericarditis?
usually viral or idiopathic
post MI= dressler’s
post cardiac surgery
Infectious- TB fungal bacteria
What is most common cardiac tumor
metastatic tumor, came from somewhere else
what is most common primary cardiac tumor
atrial myxoma (L more than Right), not malignant, mesenchymal, surgery if embolic but usually benign symptoms from obstruciton= sweat fever weight loss
What are 2 ways to get CHF
Forward failure- low CO
Backward failure- accumulate blood in venous system
What are common causes of LHFailure
Ischemic heart disease
HTN
Aortic/mitral valve disease
Nonischmic heart disease`
What is seen with LHFailure
LV hypertrophy and dilation with secondary elnargement of LA
Congestion and edema of lungs, heart failure cells in lung- leads to dyspnea, orthopnea, PND
Reduced renal perfusiion- increase RAA- salt water retention- edema
In advanced cases get hypoxic encephalopathy of brain
What is seen histo in LHF
See yellow brown histiocytes in HF, HF cells- hemosiderin iron laden macrophage
fluid in lung alveoli
What is most common cause of RHF besides LHF
Then associated with pulmonary HTN= COR pulmonale, or lung diseases like COPD
What are findings of RHF
minimal pulmonary congestion, engorged systemic and portal venous systems
Liver- congestive hepatomegaly from passive congetion- nutmeg liver
if with L heart hypoxia- centrilobular necrosis
with central fibrosis- cardiac cirrhosis
Also: increased portal vein pressure, congestive splenomegaly, ascites
pleural and pericaridal effusions
peripheral edema of SUBCUT tissue
Renal congestion
brain hypoxia
What is cardiomyopathy?
Heart disease resulting from a primary abnormality of myocardium, may be ischemic related or nonischemic
not including cardiac infections
What are the three categories of cardiomyopathy
Dilated- most common, usually d/t alcohol, LV dilates to MV to LA. Increase cardiac mass, poor wall motion, all chambers dilate
Hypertrophic= thickening of LV esp the septal side, interfere with blood flowing into aorta
Restrictive= wall is normal to thick, things inside the heart make it harder to beat efficiently
What are consequences of dilated cardiomyopathy and prognosis
mural thrombi can form from poor blood motion
Valvular regard from pulling the valves apart
Genetic in 35%
Remainder of people acquire it from 20-50 yo
it is a slow progression of signs and symptoms of CHF with acute decompensation
Death secondary to CHF or arrhythmia
transplant recommneded
What is the etiology and causes of dilated cardiomyopathy?
Most common cardiomyopathy in young people
Causes: Previous myocarditis is most common known causes, then alcohol (or thiamine deficiency) is most direct toxic effect leading to it in 15-45% of cases. then other drugs or metals
Genetics in 25-35%- AD, abnormalities in cytoskeleton
Others: idiopahtic, drugs: coke, doxirubicin, sniffing flue, post partum,
thyroid or K level problems, nutritional or thiamine deficiency , iron overload
what is pathophysiology of dilated cardiomyopathy
generalized decrease in contractility leading to global enlargement of the heart
See RHF LHF narrow pulse pressure d/t decreased SV and arrythmias
What are the CO and EF in hypertrophic cardiomyopathy
CO is low- less diastolic filling bc ventricle is so big
EF is high- i guess bc what volume you do have is pumped out
What are finding of hypertrophic cardiomyopathy
exertional dyspnea Limited CO from bad filling and increased pulmonary venous pressure harsh systolic ejection murmur angina sudden death d/t arrthymias in athletes
sporadic myocytes histo and banna shaped LV grossly
What is etiology and prognosis and genetics of hypertrophic cardiomyopahty
most common cause of death in young athletes
1:500 affected
60-70% genetic linked- AD with complete penetrance
affects young people
genes mapped to chromosomes 11 and 14q missense mutation- LEADS TO BETA MYOSIN HEAVY CHAIN GENE MUTATION, affects myosin binding protein C and troponin T
sporadic form in old peole
What causes some of the problems in hypertrophic cardiomyopathy
most people have no obstruction but it is possible for anterior leaflet of MV to be drawn against the septum in systole- regurg?
Abbrent muscle fibers may cause arrthymias and sudden cardiac death
What is ARVC
arrthymogenic right ventricular cardiomyopathy
Inherited disease of cardiac muscle that causes right ventricular failure and rhythm disturbances leading to death in young people
RV wall is thin and fatty with fibrosis
AD with variable penetrance, defect in cell adhesion proteins in cardiac myoctes
What is restrictive cardiomyopathy. What is it associated with
decrease in ventricular compliance with impaired filling during diastole
associated with amyloidosis - leads to stiff ventricle ad diastolic dysfucntion
what are the types of amyloid discussed
Can get cardiac amyloid from systemic or isolated just to cardiac tissue
If just in cardiac tissue then can be:
Senile Cardiac amyloidosis: transthretin (prealbumin)
or
Isolated atrial amyloidosis- ANP, most common
SCA is better prognosis than systemic amyloid
What is the histo you need to know for restrictive cardiomyopathy
Look for cardiac amyloid btn heart cells keeping it from functioning well
see extracellular eosinophilic protein deposited btn cardiac myocytes
BUT NEED TO KNOW: congo red stain amyloid is bright pink and then under polarized light see APPLE GREEN BIREFRINGENCE
What is carcinoid heart disease
Dense endocardial fibrosis of R heart and valves, intimal thickening
1/2 patients have Right heart involvement= mass in small bowel or liver produce serotonin and 5HA that is goes to R heart before can be broken down = FIBROSIS CAUSING TV REGURG AND PV STENOSIS
patient with mall in small bowel and liver and flushing and sweating and RHF- carcinoid
What is similar to caricnoid heart disease but in left heart
phen-fen and ergots
What is a major causes of sudden death in adults less than 40
myocarditis
What causes myocarditis
viruses- adenovirus most common, cosakie A and B
or Chagas from T cruzi
How do you dx viral myocarditis
by serology or PCR but diffciult
myocardial biopsy may show lymphocytes and dead myocytes
How do you treat viral myocarditis causes by T cruzi
nifurtimox
What is effects of myocarditis on heart
global enlargement and dilation of all chambers and lymphocytic infiltration with focal areas of necrosis
see arrythmia, friction rub, biventricular heart failure with S1 and S2 sounds
Heart murmur from mitral regurg
How do you dx myocarditis and what is seen on lab? Tx
Diagnosis- echo, ecg, cath
Lab- increased troponin, CKMB, antibodies to pathogen
Treat underlying cause- 50% die in 5 years
What causes pericarditis
Usually idiopathic and secondary- drugs, RF, post MI, malignancy
If primary- then usually viral
What is the difference btn serous and fibrinous pericarditis and purulent and hemmorhagic and Caseous
Serous- related to rheumatic fever, clear fluid
Fibrinous- clear fluid with fibrous exudate, seen after MI with Dressler’s syndrome
ASSOCIATED WITH PERICARDIAL FRICTION RUB
Purulent- infectious organism in pericardial space, lympathic or other cause, exudate is pus, red granular surface, leads to constrictive pericarditis
hemmorhagic- malignancy, TB clotting disorder, sx
Caseous- TB
Important pericarditis findings
Tachy fever, chest pain relieved leaning forward, friction rub not disappear with breath hold, remote heart sound, decreased CO, neck vein distention on inspiration, hypotension in pulsus paradoxus- GREATER than 10mm decrease in systemic blood pressure with inspiration, troponin may be elevated
What do you see with chronic pericarditis?
Soldier’s plaque- white benign plaque of epicardium
or
Adhesive medistinalpericarditis
or
Constritictive pericarditis- thick fibrous obliteration of pericardial sac
what is the problem with pericardial effusion
pericardial and intraplueral pressures rise
pericardial= less diastolic filling R>L
Slow and larger from myxedema may be benign and small and fast can be fatal from trauma
what is the most common cause of constrictive pericarditis in the world?
Tuberculous pericarditis
what are forms of pericardial effusion and their causes
chylous- thoracic duct obtructed
cholesteral effusion- myxedema, RA, TB
hemmorhagic- TB tumorr infection bleeding disorder, sx
What is a pericardial tamponade?
hemodynamic compromise resulting from a rapid increase in pericardial pressure, rapidly developing with significant volume, impairs diastolic filling, RA and RV collapse on echo
CO falls- compression from blood in pericardium
