Cardiology Flashcards
Sinus arrhythmia (normal sinus pattern but with varying rate) is a sign of increased _____________.
vagal tone
Sinus arrhythmia is normal in ______________.
teenagers; no workup needs to be done unless there is concern that it is potentially symptomatic
PR interval is the distance from _________________.
the start of P to the start of R (or Q if there is a Q wave)
The QT interval is the distance from ________________.
the start of Q to the end of T
The QRS interval is the interval from ________________.
the start of Q to the end of S
How do you calculate the QTc?
QT / (square root of preceding RR)
What does the standardization box mean if the right half is shorter than the left half?
That the precordial leads are 1/2 height and the rest of the leads are normal.
Which type of graft lasts longer, saphenous vein or LIMA?
LIMA
LIMA lasts 10-15 years, SVG only 6-7.
________ makes it hard to estimate ejection fraction.
Atrial fibrillation
The beat-to-beat variation leads to different filling amounts which can make it hard to assess what the true EF is.
Studies have shown that treatment with prednisone increases the recurrence rate of what cardiac condition?
Pericarditis
As such, prednisone is typically reserved for refractory cases of pericarditis (i.e., those that don’t respond to therapy with colchicine and ASA).
ST elevations in leads II, III, and aVF are indicative of ischemia in the ____________.
right coronary descending branch
This pattern suggests posterior ischemia which affects the RV. Do not give NO.
The medical management of NSTEMI includes aspirin, heparin, and _____________.
P2Y-12 inhibitor such as ticagrelor or clopidogrel
The accessory pathway in WPW is the bundle of _______.
Kent
If possible, you should avoid cardioverting someone in atrial fibrillation if the onset might have been longer than ________ hours.
48
Of course, if someone is unstable and not responding to medications then cardiovert regardless of the time.
The initial management of flash pulmonary edema due to hypertension includes which antihypertensive?
Nitroglycerin boluses (up to 2 mg)
Flash pulmonary edema results from increased afterload, increased preload, and pulmonary congestion. Nitroglycerin decreases afterload, decreases preload, and relaxes the pulmonary vasculature.
ST elevation in I, aVL, V5, and V6 is most commonly from occlusion of the _____________.
the circumflex branch of the left coronary
ST elevation in V1 and V2 is commonly from occlusion of which branch of the LAD?
Septal branch
The LAD diagonal branch will cause ST elevations in which leads?
V2-V4
What are the indications of emergent PCI in an NSTEMI?
- Any ventricular arrhythmia
- Any arrhythmia that causes hemodynamic compromise
- Hypotension
- New heart failure
- Ischemic pain with maximal medical therapy
Review the criteria for diagnosing submassive PE.
- RV strain on echo
- Elevated BNP
- Elevated troponin
____________ occurs from a reentrant circuit around the tricuspid annulus.
Atrial flutter
What do the five letters of the AICD pacemakers mean?
1st: chambers paced
2nd: chambers sensed
3rd: inhibition function
4th: programmability
5th: anti-tachycardia functions (aka cardioverter/defibrillator)
What defines cardiogenic shock?
There is not a single discrete set of criteria that are agreed upon, but generally it is at least two markers of shock (decreased UOP, increased Cr, AMS, elevated lactate) in the setting of a known cardiac diagnosis with worsening or an acute cardiac event.
There are RHC criteria that can also define cardiogenic shock.
Normal SvO2 of mixed venous blood (in the R heart) is ______%.
75-80
Central line SvO2 may be a little lower, like 75%.
Normal SaO2 is ______%.
97
Cardiogenic shock generally happens at cardiac indices less than ________.
2.2 L/min/m2
A patient presents post-PCI with SOB and chest pain. Other than ACS, what could be happening?
Post-PCI tamponade from a perforated coronary
Review the etiologies of cardiogenic shock.
Myopathies:
- Decompensated CHF
- Infiltrative disease (like amyloidosis)
- Myocarditis
Ischemia
- MI
Valvular:
- Acute mitral regurgitation
- Acute aortic insufficiency
- Severe aortic stenosis
Pericardial:
- Tamponade
- Constrictive pericarditis
Review the etiologies of cardiogenic shock.
Myopathies:
- Decompensated CHF
- Infiltrative disease (like amyloidosis, sarcoidosis, hemochromatosis)
- Myocarditis
Ischemia
- MI
Valvular:
- Acute mitral regurgitation
- Acute aortic insufficiency
- Severe aortic stenosis
Pericardial:
- Tamponade
- Constrictive pericarditis
You’re worried about cardiogenic shock in the ED. What workup should you do to help differentiate this?
- EKG
- CMP, CBC, trop, lactate, ABG, BNP
- Central line SvO2
- POCUS, CXR
Rule out other causes of shock PRN.
Which pressor should not be used in cardiogenic shock?
Vasopressin
What is Impella?
It is a mechanical circulatory support (MCS) device that is inserted into a peripheral artery and passed into the LV. It sucks blood into itself from the LV and dumps it into the aorta.
It can provide more improvement to cardiac output than IABPs.
The two afterload agents that you should start in cardiogenic shock are ___________.
nitroprusside and hydralazine
Other than widened mediastinum, what are some other radiographic findings of aortic dissection?
Rightward displacement of the trache
Downward displacement of the left mainstem bronchus
Review the four classes of aortic transection.
I: intimal tear
II: transmural hematoma
III: pseudoaneurysm
IV: rupture
In aortic dissections, keep HR _____________.
60-80
What will CT show in cardiac contusion?
Nothing usually.
POCUS can sometimes show WMAs, but those are non-specific for contusion.
Cardiac contusion is a clinical diagnosis based on mechanism of injury combined with elevated troponin, chest pain, and/or unexplained tachycardia.
What is pulsus paradoxus?
Decreased BP with inspiration
The decreased intrathoracic pressure pulls more blood/fluid into the pericardial space and thus decreases RV preload further.
The mediastinal should not be wider than _______ cm.
8
What things should you assess in an LVAD patient with a decompensation?
- Is the LVAD on and working? Listen to the hum of the device in the chest and check the box.
- Is there evidence of clot? Look at the device and see if there is increased resistance.
- Is there evidence of infection? Check for redness/erythema and cultures.
Review the causes of sinus tachycardia.
Decreased oxygen-carrying:
- Anemia
- Hypoxia (PE, PNA, CHF)
Decreased volume
Cardiac dysfunction:
- ACS
- Tamponade
- Valvular disease
Increased demand:
- Fever
- Sepsis
- Acidosis
Medication:
- EtOH or drug withdrawal
- Sympathomimetic drugs
- Anticholinergic drugs
Psych:
- Anxiety
- Pain
Misc:
- Hyperthyroidism
Review the management of stable and unstable SVT.
Stable:
- First line: vagal maneuvers
- Second line: adenosine 6 mg IV or IO
Unstable:
- Synchronized cardioversion (120 - 200 J)
Review the causes of AF.
PIRATES
- PE
- Ischemia
- Respiratory distress
- Anemia
- Thyroid dysfunction
- EtOH
- Sepsis
When would you cardiovert a stable AF patient?
If the onset is known and is less than 48 hours or if you confirm that they don’t have a clot on TEE.
Low voltage cardioversion is often successful in which arrhythmia?
A flutter
Often as low as 25 J can work.
True or false: defibrillate stable torsades de pointes refractory to magnesium.
False
Perform synchronized cardioversion.
Review the etiologies of ventricular tachycardia.
Ischemia
CHF
Trauma
Hypothermia
Electrolyte disturbances
QT-prolonging drugs
True or false: synchronized cardiovert pulseless V tach.
False
Defibrillate pulseless VT. Cardiovert unstable VT.
What is the dose of procainamide for stable VT?
100 mg IV over 2 minutes
What infections can cause AV node blockade?
Myocarditis
Lyme disease
If the rhythm is regular, then you know the type of heart block must be _______________.
either 1st or 3rd degree block
What is Levine’s sign?
Clenched fist over sternum — an old sign for MI
What is the mortality from STEMI at 45 minutes vs 200 minutes?
3% vs 9%
“Chest pain plus” should make you think of…
Aortic pathology
Ask about pain elsewhere in the body (neck, throat, arms, back, abdomen, legs), paresthesias, numbness, and weakness elsewhere.
How should you treat SVT in a pregnant woman?
Same as in non-pregnant women
The data on adenosine affecting fetuses is just case report level but suggests that it does not hurt them. Shocking by is unclear but if the mother is unstable then the baby is unstable and you should not wait.
What are the two life-saving interventions in flash pulmonary edema?
- BiPAP
- Nitrates
Why do nitrates help flash pulmonary edema?
Flash pulmonary edema happens because of a positive feedback cycle in the adrenergic system. When cardiac output decreases in someone with CHF, the adrenergic system ramps up to try to increase CO. With a failing heart, sometimes the adrenergic system has more affect on the systemic vascular resistance and not the heart. This increases afterload without increasing contractility. Increased afterload also increases preload which overflows the heart and leads to worse pulmonary congestion. Fluid then begins to accumulate in the lungs and that stimulates more adrenaline which perpetuates the problem further.
Nitroglycerin decreases afterload quickly reduces both afterload and preload, correcting both problems.
What dose of NO is given in flash pulmonary edema?
You can give 0.4 mg every 5 minutes orally. You can also give a drip at a rate of 40-400 mcg/minute
The three most common causes of CHF in the US are what?
Ischemia
HTN
Valvular disorders
When a person presents in a CHF exacerbation, what dose of Lasix should you start in the ED?
If they are on Lasix already, then do IV at the same dose they take orally (so effectively twice the dose). If they are not on Lasix and have no renal dysfunction then you can start low, at 20 mg IV.
What is the EMRAP approach to ECGs?
1) Is it too fast or too slow? If so then go to tachycardia and bradycardia algorithms.
2) If it’s a normal rate, are there any emergency features?
- ST elevation or depression
- QRS widening
- T wave rising or flipping
The formal name for benign ST elevation is ___________.
benign early repolarization
When you see peaked T waves, you next should look for ____________.
bradycardia and widening of QRS
One feature of peaked T waves that is worrisome is that they are ______________.
pointy, symmetric, and big relative to the QRS complex
STEMI is usually _________ at the top of the wave.
rounded (whereas hyperkalemia is very pointy and benign early repolarization is mildly pointy)
What is the de Winter T wave?
It is a tall, peaked T wave that looks like hyperkalemia but is actually from a developing STEMI. The telltale findings are slight ST segment depression and that the waves will quickly change to more rounded, tombstone-like waves on subsequent ECGs.
What are ECG signs that ST segment elevation is benign?
- Notching between the R wave and the ST complex
- J waves
- Concave upward sloping of the ST complex
- Slurring of the wave between the R wave and the T wave
- Lack of reciprocal depression
- Nonvascular territory
- Absence of Q waves and T-wave inversion
Review the EMRAP approach to ECGs in the setting of syncope.
Active things:
- Arrhythmia
- Ischemia
- PE
Latent things:
- Structural: LVH, ARVD
- Electrical: WPW, Brugada, QT prolongation
- Just don’t forget that aortic stenosis can also cause syncope, it just won’t appear on an ECG.
What are signs of ARVD (say, in the ECG of a person who came in with syncope)?
RBBB
Epsilon wave (an extra notch after the J wave)
T wave inversions in V1-V3
What is the pathophysiology of Brugada syndrome?
It is a sodium channelopathy.
Describe the Brugada morphology.
It is an RSR’ complex with J point elevation and a gently downsloping R wave into an inverted T wave (called “sharkfin”),
The classic strain pattern is ____________.
asymmetric T wave inversion (sloping down gently, rising quickly)
Needle-like Q waves is a sign of what disorder?
HOCM
There are four ECG signs of PE: ____________.
RAD, S1Q3T3, deep symmetric T waves in the precordial leads, and tachycardia
Particularly if any of the above are acute (i.e., you have an old ECG)
True or false: The QT interval goes to the beginning of T.
False
It is from the beginning of Q to the end of T.
What is overdrive pacing?
Pacing someone at a faster rate to make the heart always be refractory and unable to develop arrhythmia (used in TDP).
Athlete’s heart presents with what two things on ecg?
Bradycardia and PR prolongation
A “mid-diastolic rumble” is typical of which cardiac pathology?
Mitral stenosis
Patients who develop atrial fibrillation after ______________ are likely to convert to sinus in a couple days.
cardiac surgery
That being said, if someone develops post-operative atrial fibrillation then they are more likely to have other underlying disease and are at high risk of recurrence.
True or false: chest pain that radiates to the right side is less worrisome than non-radiating chest pain.
False
Any kind of radiating pain is more worrisome than non-radiating pain. It doesn’t matter where the pain radiates to.
Rhythmol is what drug?
Propafenone
What is a suction event in a person with an LVAD?
The LVAD sucks blood out of the LV. If the person is dehydrated then the pump can suck the LV wall. This presents often with pump failure (so cardiogenic shock) and tachyarrhythmias.
Why is echo helpful in an LVAD patient with crisis?
You need to know if they are hypovolemic, have RV failure, or if the pump has signs of failure:
- Hypovolemic: small LV and RV
- Possible pump failure: big LV and RV
- RV failure: small LV, big RV
Which gene is most commonly mutated in HOCM?
Beta myosin heavy chain
What are the doses of cardioversion for pediatric SVT?
0.5-1.0 J/kg
Remember “2, 4, 6, 8, that’s how we defebrillate” and then just like in adults, the dose for cardioversion is 1/2 that of defibrillation.
In addition to rib notching, you can also see __________ on CXRs of those with aortic coarctation.
the “3 sign”
This is when you notice a notch in the aorta that make the arch look like a 3.
Review the ECG and significance of the de Winter pattern.
The de Winter pattern happens in occlusions of the proximal LAD. It presents with ST elevations in aVR and tall T waves with or without ST depression in V2-V4.
It is a STEMI equivalent.
