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Medical > Heart Failure and Cardiomyopathies > Flashcards

Heart Failure and Cardiomyopathies Flashcards

1
Q

What is the diagnosis:

  • Heart failure with reasonably preserved EF ~ 50%
  • Normal coronaries
  • LV hypertrophy
  • Renal dysfunction
  • FH: brother and maternal grandfather also affected by HF
A

Fabry’s disease

  • X-linked disorder
  • Alpha-galactosidase A deficiency
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2
Q

Describe the findings

A

Restrictive Cardiomyopathy (Doppler)

  • classic findings
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3
Q

What is recommended treatment course for LVNC?

A
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4
Q

What maneuvers would increase HCM murmur?

A
  • Valsalva (decreased preload)
  • Squat-to-stand (decreased preload)
  • Exercise (decreased preload + increase afterload)

*****Dramatically different with maneuvers

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5
Q

What is the diagnosis?

A

RCM - ARVD

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6
Q

What are the main treatment options for HOCM?

A
  • Decrease contractility + Preserve DFP and preload
    • BB
    • Verapamil
    • Diltiazem
    • Disopyramide
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7
Q

What is the best measure of treatment success with HOCM?

A

symptomatic improvement

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8
Q

What is the differential diagnosis of thickened LV?

A
  • LVH
  • HCM
  • Renal failure
  • Cardiac Amyloid
  • Glycogen storage disease
  • Anderson-Fabry’s disease
  • Freidreich’s ataxia
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9
Q

When can genetic testing be utilized to screen family members in HCM?

A

Positive genetic testing in a family member

  • specific genetic mutation identified
  • can be utilized to screen family members for this mutation
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10
Q

Define stroke work of the ventricle

What influences stroke work?

A
  • Represented by the area enclosed by the pressure-volume loop
  • Changes in stroke work are influenced by:
    • Preload
    • Afterload
    • Intrinsic contractility
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11
Q

Describe the classic hemodynamic findings of RCM:

A
  • LVEDP > 5 mmHg + RVEDP
  • Elevated filling pressures
  • Ventricular concordance
  • RVEDP < ⅓ of RVSP
  • RVSP > 50 mmHg
  • Dip and plateau morphology
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12
Q

Describe details of HCM:

  • Prevalence
  • Overall prognosis
  • SCD rate
  • Family screening
  • Exercise
  • Medication
A
  • Prevalence –> 1:500
  • Overall prognosis –> Good
  • SCD rate –> 1% year
  • Family screening –> Needs screening
  • Exercise –> Healthy lifestyle
  • Medication –> Treat symptoms
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13
Q

What is the diagnosis?

A

RCM - Cardiac Amyloidosis

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14
Q

What is the most common symptom associated with LV noncompaction?

A

Dyspnea

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15
Q

When are patiets considered to have obstructive HCM?

A

PG > 30 mmHg (at rest)

  • PG > 50 mmHg –> sufficient to result in symptoms
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16
Q

What patient’s with LVNC would benefit from ICD placement?

A
  • FH SCD
  • NSVT
  • Reduced EF
  • Syncope (unexplained) / Symptoms
  • LGE on cMRI

*****Class IIb recommendations

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17
Q

What are the indications for surgical myectomy or ETOH septal ablation in HOCM?

A
  • LVOT obstruction
  • Angina, dyspnea, and/or syncope resulting in significant impairment in quality of life
  • Symptoms persist despite appropriate medical therapy
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18
Q

Describe key findings of ARVD

A
  • fatty replacement of RV free wall
  • EKG
    • Repolarization abnormality
    • Conduction delay
  • Arrhythmia
    • VT with LBBB morphology
  • 30% with FH
  • No competitive athletics
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19
Q

What is the most likely intervention? (A –> B)

A

Dobutamine (primarily B1-adrenergic agonist)

  • Shift in the end-systolic pressure-volume relationship (ESPVR) –>
    • consistent with an increase in contractility
  • Increase in stroke volume
    • difference between EDV and ESV
      • EDV is reduced, because the increased contractility of the LV has resulted in a lower ESV before onset of diastolic filling
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20
Q

What is the diagnosis?

A

RCM - Hypereosinophilic syndrome (Loeffler’s syndrome)

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21
Q

Describe the diagram

A
  • The end-systolic and end-diastolic pressure-volume relationships (ESPVR, EDPVR) are the boundaries of the PV loop
  • End-systolic elastance (Ees): surrogate for cardiac contractility and is represented by the slope of the ESPVR
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22
Q

Define the pressure-volume loop

A
  • depict instantaneous recordings of ventricular pressure against ventricular volume during a single cardiac cycle
  • Loop area, which represents stroke work, changes based on varying:
    • preload
    • afterload
    • intrinsic properties of the myocardium
      • ESPVR and EDPVR define these properties - remain constant in spite of changing loading conditions of the heart
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23
Q

How can you estimate stroke work?

A

SV x mean LV or aortic pressure (during ejection) = stroke work

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24
Q

Define ESPVR

A

End-systolic PV relationship

  • linear relationship
  • represents the contractile properties of the chamber
  • when the myocardium is maximally contracted
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25
Q

What is the preferred screening methodology in HCM family members?

A
  • Positive genetic mutation (in family member)
    • genetic testing
  • Negative genetic testing (in family member)
    • imaging
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26
Q

What is the inheritance pattern of HCM?

A

Autosomal dominant

  • each offspring will have 50% chance of inheriting
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27
Q

What is the monitoring frequency for HCM family members?

A
  • < 18 years of age –> every 12-18 months
  • Adults –> every 5 years
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28
Q

When should family members be screened for HCM?

A

No later than onset of puberty

or

At any consideration of competitive athletics

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29
Q

What condition would “Bifid impulse” be heard?

A

HOCM or mixed aortic disease with severe AR

  • apex - palpable S4
  • single central pulse wave with two peaks separated by a distinct mid-systolic dip.
    • early component percussion wave results from rapid left ventricular ejection
    • late component tidal wave represents a reflected wave from the periphery due to an artery’s recoil effect.
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30
Q

Define EDPVR

A

End-diastolic PV relationship

  • nonlinear relationship
  • represents the stiffness properties of the ventricular chamber
  • when the myocardium is maximally relaxed and undergoing filling
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31
Q

Define end-systolic elastance

A
  • slope of the ESPVR
  • surrogate for cardiac contractility
  • leftward shift (increased steepness of the slope) of ESPVR
    • positively inotropic drugs
    • increased HR (pacing, physiologic stimuli)
      • “force-frequency relationship”
  • rightward shift (decreased steepness of the slope) of ESPVR
    • negatively inotropic drugs
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32
Q

How is the EDPVR affected in regards to volume?

A

Nonlinear

  • Low chamber volumes –> increases in volume are associated with minimal changes in pressure
    • high LV chamber compliance at low volumes
  • High chamber volumes –> increases in volume are associated steep changes in pressure
    • chamber compliance has decreased as a result of stretch of elastic elements
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33
Q

Describe the findings

A

Positive inotropy - Increased HR (pacing, physiologic stimuli)

  • ESPVR is shifted to the left without change in preload or afterload
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34
Q

Describe the findings

A

Positive Inotropy and Positive Lusitropy

  • ESPVR is shifted to the left
  • EDPVR is displaced down and to the right
  • Inotropes: Epinephrine, Isoproterenol
  • Lusitropy: rate of myocardial relaxation
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35
Q

Describe the findings

A

Increased afterload - Phenylephrine

  • Afterload is elevated without change in contractility or stiffness –> reduce stroke volume
  • Phenylephrine
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36
Q

Describe the findings

A

Decreased afterload

  • Afterload is reduced without change in contractility or stiffness, –> increased SV
  • Sodium nitroprusside, Hydralazine, ACE
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37
Q

Describe the findings

A

Increased preload - IV fluids

  • Preload is elevated without a change in contractility or stiffness –> increased SV
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38
Q

Describe the findings

A

Negative inotropy - BB’s or CCB’s

  • ESPVR is shifted to the right without change in afterload or preload
  • BB’s or CCB’s
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39
Q

Describe the findings

A

Frank-Starling Relationship

  • “Length-Tension” Relationship
  • increases in EDV –> stretch of ventricular myocytes –> increased tension generation –> stronger contraction
    • allows the heart to increase SV when there is increased venous return
  • Increasing chamber volume beyond a certain point –> decreases tension generation
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40
Q

What are the Class I recommendations for ICD implantation in patients with Hypertrophic Cardiomyopathy?

A
  • SCD
  • VF
  • VT (hemodynamically significant)
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41
Q

What are the Class IIa recommendations for ICD implantation in patients with Hypertrophic Cardiomyopathy?

A

Primary Prevention

  • Family History HCM - SCD
    • > 1 first degree relative
  • Unexplained syncope (non-neurocardiogenic)
  • Massive LVH > 30 mm

Class IIb - (Require additional risk factors)

  • Multiple-repetitive NSVT (on Holter)
  • Abnormal exercise BP response

*****Require additional risk factors

  • End-stage (LVEF < 50%)
  • LV apical aneurysm
  • LGE > 15% LV mass**
  • Marked LVOTO ( > 30mm Hg) at rest
  • Modifiable (intense competitive sports, CAD)
  • Age > 60 years
    • SCD uncommon in this age group
  • Alcohol septal ablation (?)
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42
Q

Describe the risk stratification groups in Hypertrophic cardiomyopathy

A
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43
Q

What causes changes to EDPVR?

A

Changes in intrinsic properties or composition of the myocardium

  • ischemia
  • fibrosis
  • hypertrophy
  • infiltrative disease
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44
Q

Describe the features of GCM

  • Pathophysiology
  • Histologically
A
  • Pathophysiology:
    • believed to be mediated by T lymphocytes
    • can be transferred by T lymphocytes in animal models
  • Histologically
    • characterized by a diffuse, nongranulomatous infiltrate of T lymphocytes, histiocytes, and eosinophils with myocyte necrosis and little fibrosis
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45
Q

What are the discharge criteria for HF patients?

A
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46
Q

What are the discharge criteria for HF patients?

Should be considered for patients with advanced or refractory HF?

A
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47
Q

What is one way to confirm HFpEF in patients with normal resting hemodynamics?

A

PASP > 45 mmHg with exercise

  • high sensitivity
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48
Q

Describe excitation-contraction coupling

A
  • Mechanism by which small amounts of extracellular calcium enter the myocyte (first step**) during the plateau phase of the action potential
  • lead to larger intracellular calcium release from the SR to initiate myocardial contraction
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49
Q

What is the diagnosis?

  • commonly seen in younger individuals
  • rapildly progressive (decline in cardiac function - EF 23%)
  • often associated with ventricular arrhythmias
  • high frequency of autoimmune disorders
A

Giant cell myocarditis

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50
Q

Describe the features of Giant Cell Myocarditis

A
  • fulminant, rapidly progressive disease that is usually fatal and affects young, otherwise healthy individuals
  • associated with autoimmune conditions (but specific cause not known)
  • Presentation: (63 GCM patients diagnosed with biopsy)
    • fulminant disease that presents within days to weeks
      • new heart failure symptoms (75%)
      • ventricular arrhythmias (14%)
      • heart block (5%)
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51
Q

Describe the finding

A

Severe TR

  • monophasic “CV” wave
    • CV wave lifted completely off the baseline
    • monophasic event in systole, occurring within the RA
  • ventricularization of RA waveform
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52
Q

What constitutes a pathologic or abnormal “v” wave in PCWP tracings?

What are causes?

A
  • “v” wave more than 10 mmHg than PCWP
  • PCWP “v” waves
    • MR
    • VSD
    • Noncompliant LA
      • previous A-fib ablation procedures
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53
Q

Describe the findings

A

Pericardial Tamponade

  • Rapid x only
  • Blunted ‘y’ descent (no early diastolic RV filling)
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54
Q

Describe the findings

A

Pericardial constriction

  • Rapid x and y descents
    • y = early rapid diastolic RV filling
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55
Q

Describe when step-up O2 saturations are significant?

What does this imply?

A

Intra or Extra cardiac shunt may be present

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56
Q

What is the differential diagnosis in a patient with rapidly progressive heart failure and high-grade heart block?

A
  • GCM
  • Sarcoidosis
  • Lyme disease
  • Chagas disease
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57
Q

Diagnose GCM

A

EMB (RV)

  • sensitivity (85%)
    • due to diffuse endocardial pattern of inflammation
  • If results inconclusive or discordant –>
    • re-biopsy of RV or LV EMB should be considered
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58
Q

Describe the findings

A
  • a = atrial systole
  • x = atrial relaxation, decrease of pressure
  • c = closure of the TV
  • v = ventricular systole, atrial diastole
  • y = passive filling of the RV
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59
Q

What is the treatment for GCM?

A
  • GDMT for heart failure
    • avoidance of Digoxin (risk of heart block and proarrhythmia)
  • Mechanical support (IABP, VADs) –> bridge to recovery or transplant
    • 78% of patients on GCM registry with VADs had successful bridging to transplantation
  • Immunosuppression
    • can see histopathologic improvement, but replacement with fibrosis is common
    • cessation –> recurrence (as far as 8 years after diagnosis)
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60
Q

What are the most important predictors of hospital morbidity and mortality in ADHF patients?

A
  • Elevated BUN ( ►43 mg/dL)
  • SBP ( < 100-115 mmHg)
  • Elevated Cr. ( ► 2.0-2.75 mg/dL)

******ADHERE and OPTIMIZE-HF Trials

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61
Q

What is the recommendation for anticoagulation in PPCM?

A

Therapeutic consideration

  • due to high incidence of thrombembolism
  • especially during pregnancy and in the first 6-8 weeks postpartum due to hypercoaguability during these time peiords
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62
Q

What are the indications for invasive hemodynamic monitoring / RHC in heart failure patients?

A

Decompensated HF who:

  • not responding as expected when decision making based on non-invasive methods
    • persistent symptoms
    • hypotension
    • renal failure despite apparent volume overload
  • therapies with significant risks are being considered
    • Inotropes
    • LVADs
    • Transplant
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63
Q

In addition to guideline-directed medical therapy, what intervention for HF patients has also been proven to help reduce rehospitalizations?

A

Standardized disease education

  • 1-hour nurse educator-delivered teaching session at the time of discharge resulted in:
    • improved clinical outcomes
    • increased self-care and treatment adherence
    • reduced cost of care
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64
Q

What is the 5-year mortality rate among individuals newly diagnosed with Heart Failure?

A

50%

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65
Q

What conditions represent the highest population attributable risk for developing HF?

A

Hypertension

and

CAD

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66
Q

What is the treatment for lymphocytic myocarditis?

A

GDMT for heart failure

  • BB, ACE, diuretics
  • No role for immunosuppresive therapies
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67
Q

Describe the findings

A
  • A-fib
  • LVH
  • ST and/or T wave abnormalities secondary to hypertrophy
    • I, V5 and V6
      • downsloping ST-segement depression and TWI in leads
    • V1-V2
      • subtle ST-segment elevation ( < 1 mm)
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68
Q

What is the main reason to initiate chronic inotropic infusion therapy?

A

Palliation

  • mortality is very high in this patient cohort
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69
Q

What is the diagnosis and next best step?

  • 54 year old male with HFpEF presents with volume overload
  • PE: JVP, clear lungs, S4 gallop and pitting edema
  • EKG: low voltage and nonspecific ST-T wave changes
  • Echo: LVEF 50%, severe biatrial enlargement, PASP 50 mmHg
  • RHC: equalization of diastolic pressures, prominent Y descent, “square-root” sign
A
  • Restrictive CMP vs. Constrictive pericarditis
    • ​suspected Cardiac Amyloidosis
  • Endomyocardial biopsy
    • ​gold standard
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70
Q

What are the absolute contraindications to these mechanical support devices?

  • Impella
  • IABP
  • TandemHeart
  • VA-ECMO
A
  • Impella –> LV thrombus
  • IABP –> moderate-severe AR
  • TandemHeart –> LA thrombus
  • VA-ECMO –> severe PAD
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71
Q

What is the screening/monitorig for cardiotoxicity in patients undergoing chemotherapy treatment?

A
  • Detailed CV history and exam
  • Medical management of CV risk factors
  • Imaging Assessment of cardiac function
    • prior to and during therapy
  • Consideration of Biomarker assessment
    • Troponin, NT-proBNP
    • prior to and during therapy
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72
Q

Describe the findings

A

HOCM - Brockenbrough sign

  • PVC –> ventricular contraction will be more forceful, and the pressure generated in the LV will be higher
    • Pressure gradient –> increased
    • Pulse pressure –> decreased
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73
Q

Describe the findings

A
  • NSR
  • 1st degree AV block
  • 2:1 AV block
  • LAD
  • LVH
  • RBBB, complete
  • ST and/or T wave abnormalities secondary to hypertrophy
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74
Q

What medications can caused myocardial dysfunction in cancer treatment (chemotherapy)?

A
  • Anthracyclines (doxorubicin)
  • Trastuzuamab (Herceptin)
  • Sunitinib (Sutent)
    • tyrosine-kinase inhibitor
    • used for renal cell and gastric stromal tumors
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75
Q

Which functions in the heart is tropinin necessary for?

A

Cardiomyocyte contraction and relaxation

  • myosin, actin, tropomyosin and troponins are sarcomeric proteins that interact with calcium and ATP to produce myocardial contraction and relaxation
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76
Q

Which patient populations are aldosterone antagonists indicated for mortality benefit in HF patients?

A

post-MI patients

and

chronic HF (LVEF < 35%) + NYHA II-IV functional class

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77
Q

What are typical echocardiographic findings of HFpEF?

A
  • concentric LV remodeling
  • diastolic dysfunction
  • LA dilatation
  • PH
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78
Q

What is the recommended Echo surveillence (after baseline achieved) for patients undergoing chemotherapy?

  • Anthracyclines
  • Trastuzumab (Herceptin)
A
  • Anthracyclines –> annually
  • Trastuzumab (Herceptin) –> every 3 months
79
Q

What are the most frequently identified viral patogens in myocarditis?

A

Parvovirus B19

and

HHV-6

80
Q

What medication is frequently utilized to protect against anthracycline cardiotoxicity in chemotherapy treatment?

A

Dexrazoxane

  • free radical scavenging
81
Q

Describe the findings

A
  • SB
  • ST and/or T wave abnormalities suggesting electrolyte disturbances
  • Hyperkalemia
82
Q

Describe the findings

A
  • NSR
  • PVC’s
  • RAD
  • LA enlargement
  • RBBB, complete
83
Q

Describe the findings

A
  • Sinus arrhythmia
  • AV junctional escape complexes
  • AV block, 3rd degree
  • RBBB, complete
  • LAFB
84
Q

What is the differetial for dual-pacing in RBBB morphology?

A
  • Bi-V pacing
  • septal or free wall perforation of the lead into the LV
  • LV pacing trhough intracardiac defects such as a PFO/septal defect
85
Q

What is the diagnosis and next best step?

  • 68 year old with decompensated heart failure (new diagnosis) –> controlled over 48 hours with medical therapy
  • PMH: HTN, OA, DM
  • EKG: A-fib with RVR
  • BP 190/100
  • Echo with normal LVEF
A
  • Hypertensive heart failure
    • AF + HFpEF
  • TEE + DCCV
86
Q

What is the next most appropriate step?

  • 62 year old woman with chronic HFrEF, started on Milrinone gtt 3 days ago, awaiting transplant
  • PA/RHC
    • RAP 20
    • PCWP 30
    • PAP 60/30/40
    • CI 1.5
    • BP 80/50
A

LVAD placement

87
Q

What factors contribute to cardiorenal syndrome?

A
  • venous congestion
  • low renal perfusion
  • dysfunctional autoregulation of the kidney
88
Q

What is the benefit of Torsemide over Furosemide?

When should this be utilized?

A
  • Greater oral bioavailability (approaching its IV action)
    • furosemide has variable absorption
  • Recurrent HF as outpatient on high doses of Furosemide and medication/dietary compliance + on high doses of PO Furosemide already
89
Q

Describe the findings

A
  • A-fib
  • Ventricular demand pacemaker (VVI), normally functioning
90
Q

Describe the findings

A
  • PVC’s
  • Dual-chamber PPM (DDD), normal functioning
    • Paced beats are in a RBBB –> typically raises suspicion for
      • Bi-V device or
      • septal or free wall perforation of the lead into the LV or
      • LV pacing through intracardiac defects such as a PFO/septal defect
    • However, uncomplicated RV pacing can sometimes produce this RBBB finding
91
Q

Describe the findings:

  • RA pressure tracing
A

Pericardial tamponade

  • RA pressure is high = 15 mmHg (normal = 6 mmHg)
  • Normal: A waves, X descents, V waves
  • Abnormal:
    • Y descent is blunted
92
Q

Differentiate the two on RA pressure tracing:

  • Constrictive pericarditis
  • Pericardial tamponade
A
  • Constrictive pericarditis (or RCMP)
    • prominent “X” and “Y” descents
  • Pericardial tamponade
    • Loss or blunted “Y” descent
93
Q

How can you differentiate AS and HOCM on intracardiac pressure tracings?

A

Post-PVC

  • Pulse Pressure
    • HOCM –> decrease
    • AS –> increase
  • Gradient
    • ​Both –> INCREASE

Valsalva

  • Gradient
    • ​HOCM –> increase
    • AS –> decrease
  • Pulse Pressure
    • Both –> DECREASE
94
Q

What is the most common cause of death in the first month after heart transplantation?

A

Primary graft failure

  • defined as dysfunction of the transplanted organ within the first 24 hours
  • Risk factors:
    • older donor age
    • longer ischemic times
95
Q

What are complications following transplantation?

A
  • cardiac allograft vasculopathy
  • renal insufficiency
  • rejection
  • infection
  • malignancy
96
Q

Describe the findings

A
  • NSR
  • 1st degree AV block
  • LAD
  • LBBB, complete
  • Pacemaker malfunction, failure to sense
    • pacer spikes that are not conducting QRS complexes
    • intrinsic QRS begins about 0.4 ms prior to the pacer spikes in the V1 rhythm strip
    • PPM is under-sensing the intrinsic ventricular depolarizations and firing inappropriately
97
Q

What is the gold standard for diagnosis of cardiac transplant rejection?

A

endomyocardial biopsy

98
Q

What is the recommended surveillence for transplant recipients?

A

Endomyocardial biopsy

  • periodically over the first 6-12 months postoperatively for surveillence rejection
  • > 1 year for those at high risk for acute rejection
99
Q

What is the most common form of rejection in heart transplant patients?

What is the treatment?

A

Cellular rejection

  • occurs at least once in 35% of heart transplant recipients

IV corticosteroids

  • Hemodynamic compromise –> cytolytic therapy with anithymocyte antibodies is added
100
Q

What are common causes of RCM?

101
Q

Describe EKG findings:

  • Posterior MI age indeterminant, or probably old
A
  • V1 and/or V2
    • dominant R waves - R/S > 1
    • without significant ST depression
  • Must be distinguished from other causes of tall R waves in V1, V2:
    • RVH
    • WPW
    • RBBB
  • Evidence of inferior wall ischemia/infarction is often present
102
Q

Describe key differentiating features on Echo:

  • Constrictive pericarditis
  • Restrictive cardiomyopathy
A
  • RCM:
    • thickened
      • walls
      • interatrial septum
      • valves
    • granular sparkling texture
  • CP:
    • Normal wall thickness
    • pericardial thickening
    • prominent early diastolic filling with abrupt displacement of the interventricular septum
103
Q

What are causes of dominant R wave in V1 (R/S > 1)?

A
  • RBBB
  • WPW
  • Posterior MI
    • usually with associated inferior Q wave MI
  • RVH
  • Counterclockwise rotation of the heart along its longitudinal axis
    • Normal Variant
104
Q

Describe key differentiating features on Cardiac cath:

  • Constrictive pericarditis
  • Restrictive cardiomyopathy
A
  • Restrictive cardiomyopathy
    • LVEDP often > 5 mmHg greater than RVEDP
    • may be identical
    • Concordant respirophasic ventricular pressure changes
  • Constrictive pericarditis
    • RVEDP and LVEDP usually equal
    • RVSP < 50 mmHg
    • RVEDP > 1/3 of RVSP
    • Discordant respirophasic ventricular pressure changes
105
Q

Describe key differentiating features on Doppler studies:

  • Constrictive pericarditis
  • Restrictive cardiomyopathy
A
  • Restrictive cardiomyopathy
    • Inspiration:
      • decreased RV and LV velocities
      • augmentation of hepatic-vein diastolic flow reversal
    • MR and TR common
  • Constrictive pericarditis
    • Inspiration:
      • increased RV systolic velocity and
      • decreased LV systolic velocity
    • Expiration:
      • augmentation of hepatic-vein diastolic flow reversal
106
Q

What is the likelihood of survival at 5 years after transplantation?

A

70%

  • 1 year –> 90%
  • 5 year –> 70%
  • 10 year –> 50%
107
Q

Describe typical arrhythmias of digoxin toxicity on EKG?

A
  • Paroxysmal AT with block
  • A-fib with CHB
  • 2nd or 3rd degree AV block
  • CHB with accelerated idioventricular or junctional rhythm
  • SVT with alternating BBB
  • VT with alternating bidirectional BBB
108
Q

What are common findings of sinus pause or arrest on EKG?

A
  • PP interval > 2.0 s
  • Resumption of SR at a PP interval that is not a multiple of the basic sinus PP interval
    • If SR resumes at a mulitple of the basic PP –> SA exit block
109
Q

Describe the findings

A

HOCM

  • postextrasystolic beat (Brockenbrough sign) –>
    • increase in pressure gradient
    • greater apposition of the interventricular septum to the anterior leaflet of the MV –> increased obstruction
    • effect overwhelms any benefit obtained from the higher EDV
    • SV and aortic pulse pressure falls
110
Q

What testing is recommended for HCM evaluation when Echo is inconclusive?

111
Q

What constitutes a diagnosis of chemotherapy related cardiotoxicity?

A
  • Asymptomatic changes in LVEF:
    • > 10% from baseline to < 50%
    • > 20% decrease from baseline
    • > 10% reduction from baseline to < 53% (ASE recommendations)
  • Diastolic dysfunction (worsening)
  • Symptomatic HFrEF or HFpEF
112
Q

What are required findings of Digoxin toxicity on EKG?

A
  • sagging ST depression with upward concavity
  • T waves:
    • flattened, inverted or biphasic
  • shortened QT interval
  • cardiac arrhythmia
    • Paroxysmal AT with block
    • Afib with CHB
    • CHB with Accelerated junctional or ventricular rhythm
    • SVT with alternating bidirectional BBB
    • VT with alternating bidirectional BBB
113
Q

What are the next steps in treatment if chemotherapy-induced cardiotoxicity is diagnosed?

A
  • Discontinuation of chemotherapy
  • Initation of ACE and BB’s
114
Q

Describe EKG findings of Hypercalcemia

A
  • QT shortening
    • ​primarily due to shorening of the ST segment
  • Little effect on the QRS complex
  • Severe hypercalcemia –> Osborne waves
115
Q

41 year old woman with a diagnosis of recurrent triple negative breast cancer who has received a cumulative dose of anthracyclines of 450 mg/m2 undergoes an Echocardiogram with strain.

Describe the image and recommendations

A
  • Radial strain, usuing a short-axis image at the level of the papillary muscles
  • Discontinue anthracycline, finish treatment with a nonanthracycline containing regimen, and initiate beta-blockers
    • ​radial strain is abnormal at 11% (normal is 40%-60%) –> suggestive of subclinical LV dysfunction
116
Q

What cumulative dose of Doxorubicin should prompt further evaluation?

What evaluation?

A
  • 500 mg/m2
  • Repeat evaluation after every additional 50 mg/m2
117
Q

What are cardioprotective strategies for anthracycline-induced cardiotoxicity?

A
  • Prolonged infusions (rather than IV bolus)
  • Liposomal doxorubicin
  • Early initiation of medical therapy: ACE and BB’s
  • Aggressive CV risk factor modification
  • Dexrazoxane
118
Q

What can amplify chemotherapy-induced cardiotoxicity even further?

A

Chest radiation ► 30 Gy

119
Q

What are risk factors for anthracycline-cardiotoxicity?

A
  • Cumulative dose
    • ​400 mg/m2 –> 3-5%
    • ​550 mg/m2 –> 7-26%
    • ​700 mg/m2 –> 18-48%
  • Higher single doses / IV bolus administration
  • h/o prior mediastinal radiation
  • Increased length of time since anthracycline completion
  • Concomitant agents with cardiotoxic effects
    • cyclophosphamide, trastuzumab, paclitaxel
  • CV disease (underlying)
  • Extremes of age
  • Female sex
120
Q

How is a diagnosis of familial cardiomyopathy made?

A
  • Clinical diagnosis
  • Requires 3 generations to be affected
    • usually autosomal dominant
121
Q

Describe the findings

A
  • Atrial flutter
  • AV block 2:1
  • Inferior MI, age indeterminant or probably old
122
Q

Describe the findings

A
  • ST
  • LAD
  • RBBB, complete
  • Inferior MI, age recent or probably acute

*****ST-segment elevation in the inferior leads with reciprocal depression in leads I and aVL.

******don’t let presence of a RBBB obscure your intepretation of ST-segment elevation

123
Q

Describe the findings

124
Q

Describe the findings

A

HOCM: L heart pullback

125
Q

What findings are indicative of subsequent cardiotoxity in chemotherapy patients?

A

GLS < 19%

or

Troponin I > 30 pg/mL

126
Q

Describe the findings

A

Provocable Gradient: Valsalva Maneuver

127
Q

What is the formula for Fick CO?

A

CO = O2 consumption (mL/min) / VO2 difference (mL/100mL blood) x10

  • O2 consumption estimated using 3 mL O2/kg or 125 mL/min/m2
  • VO2 difference = difference (0.95 - 0.65) x 1.36 x Hgb x 10

**** Larger difference between A and V O2 content –> lower CO

128
Q

Describe the findings

129
Q

Describe the findings

A

AR

  • Corrigan’s pulse
  • absence of dicrotic notch
130
Q

Digitalis toxicity can cause almost any type of cardiac dysrhythmia or conduction disturbance except?

A

Bundle branch block

131
Q

Based on the Expert consensus for the multimodality imaging of the adult patient during and after cancer therapy, subclinical LV dysfunction is defined as:

A

15% reduction in GLS when compared to baseline value

132
Q

What is the formula for cardiac index (CI)?

A

CI = CO (L/min) / BSA (m2)

133
Q

Describe the findings

A
  • ST
  • AV junctional rhythm/tachycardia
  • 3rd degree AV block
  • RBBB, complete
  • Inferior MI, age indeterminant or probably old
134
Q

When is Fick (CO) most accurate?

A
  • low output states (valvular heart disease)
    • TR
    • multivalvular heart disease
  • steady state
135
Q

What are typical Echo features of Athletic heart?

A
  • Doppler E’ TDI - Normal tissue Doppler E’ (may be slightly decreased)
  • Mitral inflow pattern - Normal, pseudorestrictive (Grade II)
  • Strain normal (higher than HCM)
  • LA size - larger range smaller-larger in diameter
  • LV - normal/slightly increased:
    • wall thickness
    • LV dimension
  • EF - normal-slightly decreased
    • normal-increased LVEDV
  • RV
    • FAC - larger range smaller-larger
    • EF - normal-slightly decreased
136
Q

What helps to differentiate:

  • anteroseptal infarction
  • anterior infarction
A

V1 - Q waves –> anteroseptal MI

137
Q

What is the problem with Fick (CO)?

A

estimate of O2 consumption

138
Q

What PA sat correlates with low CO (on Fick)?

139
Q

When does peripartum cardiomyopathy typically occur?

A

within 5 months of delivery

140
Q

What is the first step after a significant change in GLS is noted?

A

repeat Echo with GLS to ensure findings are accurate

141
Q

What are quick estimates of Fick (CO) utilizing PA sats?

A
  • PA sat 70-80% –> Normal CO
  • PA sat < 65% –> Low CO
  • PA sat > 85% –> High CO (or L-R shunt)
    • AV graft for HD
142
Q

When is TD (CO) more accurate?

Least accurate?

A
  • Most accurate –> High Output States
  • Inaccurate –> TR or AF
143
Q

What is the formula for PVR (pulmonary vascular resistance, Woods units)?

A

PVR = mPAP - mPCWP / CO

**Normal range = 80-130 dynes

***Woods units x 80 = dynes

**** TPR = mPAP / CO

144
Q

What is the formula for SVR (systemic vascular resistance)?

What is normal range?

A

SVR = mean systemic arterial pressure - mRAP / CO

  • Normal range = 700-1600 dynes-sec/cm5
145
Q

What is considered a significant change in GLS?

A

> 15% from baseline

146
Q

Describe the findings

147
Q

What is the stepwise progression / algorithm for evaluation of suspected CTRCD?

148
Q

Describe locations for mixed venous O2 sats in shunt calculations:

  • No L-R shunt
  • L-R shunt present
  • ASD
  • No R-L shunt
A
  • No L-R shunt
    • Mixed venous = PA sat
  • L-R shunt present
    • Mixed venous = O2 sat in chamber proximal to shunt
  • ASD
    • Mixed venous = Caval O2 sat = (3 x SVC) + (1 x IVC) / 4
  • No R-L shunt
    • Mixed venous = PV O2 sat = FA O2 sat
149
Q

What is a normal BP response to exercise?

A

25-70 mmHg

150
Q

What is the Gorlin formula?

A

Area (cm2) = value flow (mL/s) / K x C x √MVG

  • K = constant = 44.3
  • C = empiric constant
    • AV, TV, PV = 1
    • MV = 0.85

***MV flow = CO / DFP x HR

***AV flow = CO / SEP x HR

151
Q

What is the simplified Gorlin or Hakki formula?

When does this formula differ?

A

AVA = CO / √MG

  • differs by 18% +/- 13% from real formula
    • Bradycardia
    • Tachycardia
    • Low flow states –> overestimate severity of AS
      • CO < 2.5 L / min –> constants should be used
152
Q

When is the Gorlin formula inaccurate?

A
  • Regurgitation (concomitant)
  • Low output states
  • Tachy/Brady cardia

***Assumes steady state and fixed orifice

153
Q

What are factors that can increase the gradient in HOCM?

A
  • increased contractility
  • decreased preload
    • volume depletion
  • decreased afterload
154
Q

What are factors that can decrease the gradient in HOCM?

A
  • decreased contractility
  • increased preload
  • increased afterload
    • phenylephrine
155
Q

When should advanced HF therapies be considered?

A
  • Symptoms become refractory to:
    • medical (GDMT) therapy
    • surgical therapy
    • device therapy
  • End organ dysfunction becomes apparent
156
Q

What are the most common diagnoses for adult heart transplantation?

A
  • Myopathy (55%)
  • CAD (36%)
  • Valvular disease (3%)
  • Congenital disease (3%)
  • Retransplantation (3%)
  • Other Cardiomyopathies (1%)
157
Q

46 year old woman with previous history of breast cancer treated with mastectomy, chemotherapy, and radiation therapy presents for evaluation of symptoms of fatigue. On examination, she has a heart rate (HR) of 100 bpm, BP 85/60 mmHg, elevated JVP, decreased breath sounds at the lung bases, ascites, and 3+ peripheral edema. TEE and TTE Doppler images are shown. What is the most likely diagnosis?

A

Constrictive Pericarditis

158
Q

What are the two components of the comprehensive evaluation when evaluating patients for heart transplantation?

A
  • determine if the prognosis of the patient will benefit from heart transplantation
  • evaluate other determinants that could have an impact on post-transplant outcomes

**primary indication for transplantation is based on objective measures of functional capacity, but is integrated into a comprehensive assessment of patient risk and prognosis

159
Q

What measure on cardiopulmonary exercise testing (CPX) is used to determine prognosis and cardiac transplant eligibility?

What is one situation in which this should be adjusted?

A

VO2 ≤ 14 mL/kg/min

  • 1 year survival rate 70% compared with 94% if > 14 mL/kg/min

Beta Blockers

  • VO2 had a potential survival benefit after heart transplantation
160
Q

What are the important measures in cardiopulmonary stress testing (CPX)?

A
  • Peak VO2 ≤ 14 mL/kg/min
    • 1 year survival rate 70% compared with 94% if > 14 mL/kg/min
  • Peak VO2 ≤ 50% predicted
    • recommended for transplant candidacy
    • based on data from Stelken and colleagues that demonstrated patients in this category had a 1-year survival of 74% and that this parameter was a strong predictor of death
  • RER > 1.05
    • Respiratory Exchange Ratio
    • used to describe maximal effort
  • VE/VCO2 > 35
    • ventilation efficiency
    • slope of ventilation to carbon dioxide
    • used in those who cannot achieve maximal effort (level of exercise)
    • likely elevated from decreased pulmonary perfusion
    • >35 is stronger predictor of cardiovascular death than peak VO2
161
Q

What is an indication to use the HFSS after CPX?

A

Peak VO2 > 12 mL/kg/min and ≤ 14 mL/kg/min

162
Q

What intervention would be responsible for the change?

A

Decreased preload and Decreased afterload

  • X-axis = preload
    • Leftward shift → decrease in preload
  • Y-axis = myocardial performance
    • Upward shift → increase in contractility
163
Q

What are the features of the HFSS?

A

Heart failure survival score

  1. CAD (presence)
  2. HR (resting)
  3. LVEF
  4. Mean arterial BP
  5. Prolonged QRS ≥ 120 ms
  6. Serum Sodium
  7. Peak VO2
164
Q

What are the cutoffs for the HFSS?

A
  • High risk < 7.20
  • Intermediate risk 7.20 - 8.09
  • Low risk ≥ 8.09
165
Q

Describe the findings

A
  • NSR
  • WPW
    • Q-waves seen in the inferior leads are secondary to WPW abnormality (pseudo-infarction) –> should not be confused with a true prior myocardial infarction
    • Pre-excitation of the ventricle from WPW –> affects the overall QRS axis –> true axis abnormality (LAD in this EKG) should not be coded
166
Q

Describe the mortality difference between HFrEF and HFpEF?

A

no difference

167
Q

Describe the findings

A
  • Atrial flutter ( +4 )
  • Low Voltage, limbe leads ( +1 )
  • Nonspecific ST and/or T wave abnormalities ( +1 )
168
Q

What substances may be utilized to prevent maladaptive remodeling in post-MI patients?

A

​​​Natriuretic peptides (ANP and BNP)

  • vasodilators that may directly inhibit myocayte hypertrophy
  • animal models and small human studies have demonstrated reduced remodeling after MI with infusions of both
169
Q

What is required for diagnosis of U-waves on EKG?

A

brief isoelectric baseline following the T wave

  • most often seen in the right precordial leads
170
Q

Describe the findings

A
  • Normal EKG ( +4 )
  • NSR ( +1 )
171
Q

Describe the findings

A
  • A-flutter
    • Flecianide –> slows conduction in myocardial fibres and tissues (more pronounced in atrial tissues)
    • Slow atrial-flutter is a common finding ( < 300 bpm)
    • BB should be added to prevent A-flutter with 1:1 conduction to the ventricles
172
Q

Define Cheyne-Stokes Respiration

A
  • CSR is a form of SDB
  • characterized by a crescendo-decrescendo pattern of breathing with
  • periods of hyperventilaion alternating with central apneas
    • lack of airflow without respiratory effort
  • Patients often awaken during the period of hyperventilation –> contributes to PND
  • 2/3 of CHF patients will have some form of SDB
173
Q

Describe the findings

A
  • NSR
  • RAD
  • RVH
  • Acute cor pulmonale including PE
    • ​S1 Q3 T3 pattern
  • Nonspecific ST and/or T wave abnormalities
174
Q

What is one characteristic that has been linked to worse prognosis in HF patients?

A

lower cholesterol

  • likely related to poor nutritional status (cardiac cachexia) and elevated circulating inflammatory cytokines
175
Q

Describe the prognostic implication in HF patients:

  • Loop diuretics
A

Higher doses –> worse outcomes

176
Q

Describe the findings

A
  • A-fib ( +4 )
  • Nonspecific ST and/or T wave abnormalities ( +1 )
177
Q

Describe the findings

A
  • NSR ( +1)
  • ST and/or T wave abnormalities suggesting myocardial ischemia ( +4)
178
Q

Describe the prognostic implication in HF patients:

  • Obesity
A

Obese patients –> better outcomes

  • “obesity paradox”
    • obese patients have better outcomes compared to thinner counterparts
179
Q

What lab findings can identify patients with HF, who are at risk for poor outcomes?

A
  • Hyponatremia
  • Anemia
  • Renal insufficiency
  • Elevated natriuretic peptides
  • Elevated Troponins
180
Q

What is the cause of a substantial increase in PA saturation over a short period of time?

A

distal migration into wedge position

  • can occur even with the balloon down
  • blood sample will reflect pulmonary venous O2 saturation
181
Q

What diagnoses are associated with myosin heavy chain mutations?

A

Dilated cardiomyopathy

and

HCM

182
Q

What diagnoses are associated with tafazzin mutation?

A

Dilated Cardiomyopathy

and

LV noncompaction

183
Q

What is one major limitation of initation of aldosterone receptor blockers?

A

compliance - follow up

184
Q

What is the lifestime risk at age 40 years, in both men and women, of developing heart failure according to the Framingham Heart Study?

A

1 in 5 (20%)

185
Q

What are laboratory contraindications to initiation of aldosterone receptor antagonist therapy?

A

Cr. ► 2.5 (men) and Cr. ► 2.0 (women)

or

K ► 5

186
Q

What is the Class I recommendation for endomyocardial biopsy?

  • heart failure
  • arrhythmias
A
  • New-onset heart failure of 2 weeks - 3 months with
  • Dilated LV and
  • Arrhythmias:
    • ventricular arrhythmias
    • 2nd or 3rd degree heart block
  • Or Failure to respond to usual care within 1-2 weeks
187
Q

Describe the findings

A
  • A-fib ( +2 )
  • PVC’s ( +1 )
  • LBBB, complete ( +2 )
  • Functional (rate-related) aberrancy ( +1 )
    • Mean QRS duration is > 120 ms in the setting of rapid HR’s
    • returns to normal duration at slower HR’s

*****3 QRS complexes that appear to have a wider width and differet morphology than the other baseline complexes

******6th beat is likely aberrantly conduced, while the first and eighth beats are likely PVC’s

188
Q

What is a common association between:

  • Diuretics
  • BB
A

Volume retention

  • common complication of BB therapy
  • should be treated with an increase in diuretic thearpy to achieve clinical euvolemia
189
Q

What is the risk in PPCM and subsequent pregnancies?

  • recurrence
  • mortality
A
  • Normal EF / Recovered
    • ​recurrence –> 21%
    • mortality –> 1%
      • Reduced EF / persistent LV dysfunction
    • ​recurrence –> 44%
    • mortality –> 19%
190
Q

What is the best method to determine prognosis in advanced heart failur patients?

A

Cardiopulmonary exercise testing

  • prognosis is best determined by functional capacity:
  • Indications for heart transplantation are O2 consumption:
    • < 14 cc/kg/min or
    • < 12 cc /kg/min (on BB)
191
Q

What is the treatment for Cheyne-Stokes Respiration?

A

Optimization of GDMT for CHF

192
Q

Describe the findings:

A
  • Pericardial tamponade
    • parallel shift in myocardial stiffness
193
Q

Describe the findings:

A
  • Large anterior MI
    • decreased compliance/increased stiffness
    • decreased contractility
    • increased preload
      • ***differentiates from Amyloidosis

Medical (69 decks)

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