ACCSAP Flashcards
Clinical & lab features of mycocarditis?
History of fever, cough, myalgia (URI sx)
Hypotension (low output), congestion (pulmonary edema), cool extremities, low urinary output, lactic acidosis, elevated LFTS >> cardiogenic shock
Labs might show: Elevated troponin, high BNP, leukocytosis, AKI, transaminitis
EKG: NSVT, VT, PVCs, ST changes
Viral pathogens implicated in myocarditis?
Parvovirus (B19) and HHV-6. Previously most common pathogens were adenovirus and coxasakie viruses
Diagnosis of myocarditis?
Usually made with endomyocardial biopsy which shows lymphocytic infiltration and myocyte necrosis. It can also help exlcude other causes like giant cell arteritis, sarcoidosis and eosinophillic myocarditis
CMR findings in myocarditis?
Edema in T2 weighted image
Presence of early gladolinum enhancement
Abnormal late gladolinum enhacement with rim-like uptake in septum or subepicardial patchy distribution in lateral walls
Treatment of fulminant myocarditis?
These patients are in low output failure with decreased forward flow and pulmonary congestion. Decreased forward flow can lead to multi-organ failure (liver, kidneys, brain etc).
Initially treat with dobutamine/milrinone plus diuretic such as furosemide. If still hypotensive could consider adding levophed. However, if no impovement these patients would require mechanical support either with ECMO or percutaneous LV assist device.
Note: High dose steroids can be used in checkpoint induced myocarditis, eosinophillic myocarditis, sarcoidosis, giant cell myocarditis seen on biopsy. However, acute stabilization is important.
Indications for right heart catheterization?
Consider when patient has following:
- Concern for acute decompensated heart failure but there is ambiguity whether its lung or heart disease
- When effective therapy has not improved clinical outcomes, for example worsening AKI in light of optimal treatment
- When physical examination is not accurate or difficult to assess volume status
Indications for CRT in HFreF?
LVEF less than or equal to 35% with
Sinus rhythm and LBBB with QRS >150 and NYHA class II-IV
CRT improves mortality, decreases hospitalizations in these patients.
Treatment of secondary MR in HFrEF patients?
In HFrEF we should first optimize GDMT and if indicated do CRT (In MIRACLE trial, CRT improved LV dimensions and caused reduction in MR)
If there is still severe MR present from HFrEF, we should consider transcatheter edge to edge mitral valve repair (TMVR) (COAPT trial showed TVMR reduced mortality and hospitalizations; 29.1% vs 46.1% and 35.8% vs 67.9% respectively in patients with moderate to severe secondary MR and LVEF 20-50% with NYHA Class II-IV symptoms despite GDMT and/or CRT)
Surgical treatment has limited evidence and is not usually recommended.
Features and treatment of low output heart failure?
Hypotension
Cool extremities
AMS
Low urine output
Congestive symptoms (dyspnea)
Treatment involves ionotropic support with milrinone or dobutamine. Note: Initiation of vasoactive agents like phenylephrine or vasopressin can increase SVR in cardiogenic shock and would be contraindicated
EKG findings of amyloidosis?
Low voltage QRS complexes out or proportion to LV wall thickness.
Criteria for limb leads include
Criteria for precordial leads include
Pseudoinfarct patterns: Mostly in anterior leads (q waves, poor R wave progression) or inferior leads (q waves)
Echocardiographic findings of amyloidosis?
Biatrial enlargement
Biventricular increased wall thickness
Apical sparing pattern with a 2:1 ratio on strain assessment “classic cherry on top with severely diminished basal strain”
Diagnosis of cardiac amyloidosis?
If pre-test probability is high based on EKG and echo findings we should obtain:
PYP scan and urine and srum assessment of serum kappa/lambda free light chain ratio for plasma cell dyscrasias
Note: PYP scans can be falsely positive in patients with light chain amyloidosis and thus a diagnosis of transtherytin amyloidosis cannot be made without assessment of plasma cell dyscrasias.
Theophyllline & Heart failure?
Theophylline relaxes bronchial smooth muscle and decreases airway resistence but increases heart rate and causes atrial tachyarrythmias. This can lead to acute decompensation of chronic heart failure.
NSAIDs and heart failure?
NSAIDs decrease prostaglandins and therefore, decrease blood flow to the kidneys which leads to ADH and RAAS activation. This leads to water and sodium retention and edema. It also causes diuretic resistence and increased systemic vascular resistence.
NSAIDs such as ibuprofen should be avoided in heart failure
Amlodipine and heart failure?
PRAISE-2 trial showed no benefit of amlodipine with regards to CV death and hospitalization. It’s use lead to increased peripheral edema and pulmonary edema. It’s use should be avoided in HF patients with reduced ejection fraction.
How is PCWP measured?
The pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP] or pulmonary artery wedge pressure [PAWP]) estimates the left atrial pressure.
The PAOP tracing is obtained by inflating the balloon at the distal tip of the catheter. The balloon obstructs blood flow through a branch of the pulmonary artery. This creates a static column of blood between the catheter tip and the left atrium. Pressure at both ends of the column equilibrates, after which the pressure at the distal end of the catheter is equal to the pressure of the left atrium]. Thus, PAOP is a reflection of left atrial pressure.
PCWP and LVEDP?
PCWP usually estimates the left ventricular end-diastolic pressure (ie, left ventricular preload) if there is no obstruction to flow between the left atrium and left ventricle and the compliance of the left ventricle is normal. Importantly, it does not directly measure the left ventricular end-diastolic volume, capillary hydrostatic pressure, or transmural pressures. Thus, the PCWP may not reliably indicate left ventricular preload when compliance of the left ventricle is abnormal (eg, large myocardial infarction or in cardiac tamponade).
Normal PCWP?
Normal wedge pressures vary from 6 to 15 mmHg, with a mean of 9 mmHg
PCWP tracing segments?
Physiologically, the PCWP tracing has similar components to the right atrial waveform with three positive and two negative deflections:
●The a wave reflects contraction in atrial systole, while the x descent reflects the fall in left atrial pressure that follows.
●The c wave, reflecting the closure of the mitral valve, is often not seen.
●The v wave represents both ventricular systole and passive atrial filling in atrial diastole.
●The y descent reflects the fall in left atrial pressure following opening of the mitral valve and the initiation of passive filling of the left ventricle.

Large a waves in PCWP?
Increased amplitude of the a wave can be seen with increased resistance to left ventricular filling of any cause. Potential causes include:
Mitral stenosis
Left ventricular systolic dysfunction
Left ventricular diastolic dysfunction
Left ventricular volume overload
Myocardial ischemia or infarction with decreased left ventricular compliance
Large v waves of PCWP tracing?
Large v waves - Increased amplitude of the v wave in the PAOP tracing may represent mitral regurgitation (MR)

LV non compaction is characterized by?
Left ventricular noncompaction (LVNC) is a distinct phenotype characterized by prominent LV trabeculae and deep intertrabecular recesses
LV non compaction morphological features?
An altered myocardial wall with prominent trabeculae and deep intertrabecular recesses, resulting in thickened myocardium with two layers consisting of noncompacted myocardium and a thin compacted layer of myocardium
Continuity between the LV cavity and the deep intertrabecular recesses, which are filled with blood from the ventricular cavity without evidence of communication to the epicardial coronary artery system.

Genetic of LV non compaction?
LVNC can be either sporadic or familial.
Autosomal dominant inheritance is more common than X-linked inheritance or autosomal recessive inheritance.
In patients with LVNC, mutations have been reported primarily in genes coding for sarcomeric, cytoskeletal, Z-line, and mitochondrial proteins.
Sarcomere (TTN and MYH7)
Alpha-dystrobrevin (DTNA)
Tafazzin gene




