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Medical > Heart Failure, Hemodynamics, Nuclear, Channelopathies > Flashcards

Heart Failure, Hemodynamics, Nuclear, Channelopathies 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

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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3
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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4
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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5
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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6
Q

How can you estimate stroke work?

A

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

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7
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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8
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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9
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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10
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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11
Q

Define chamber stiffness (in PV loops)

A
  • ratio of change in pressure to change in volume
  • increases as EDV and pressure increase
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12
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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13
Q

What are the components of chamber stiffness?

Examples?

A
  • LV wall volume and Chamber volume
  • Hypertrophic Cardiomyopathy –> abnormally increased chamber stiffness
  • Normal growth or Athletic hypertrophy –> chamber stiffness not affected
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14
Q

Describe the findings

A

Positive inotropy

  • ESPVR is shifted to the left without change in preload or afterload
  • Increased HR as a result of pacing
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15
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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16
Q

Describe the findings

A

Increased afterload

  • Afterload is elevated without change in contractility or stiffness –> reduce stroke volume
  • Phenylephrine
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17
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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18
Q

Describe the findings

A

Increased preload

  • Preload is elevated without a change in contractility or stiffness –> increased SV
  • IV fluids
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19
Q

Describe the findings

A

Negative inotropy

  • ESPVR is shifted to the right without change in afterload or preload
  • BB’s or CCB’s
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20
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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21
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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22
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

Require additional risk factors

  • Multiple-repetitive NSVT (on Holter)
  • Abnormal exercise BP response
  • LGE > 15% of LV mass

*****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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23
Q

Describe the risk stratification groups in Hypertrophic cardiomyopathy

A
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24
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 and lead to larger intracellular calcium release from the SR to initiate myocardial contraction

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25
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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26
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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27
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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28
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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29
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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30
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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31
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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32
Q

What are the discharge criteria for HF patients?

A
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33
Q

What are the discharge criteria for HF patients?

Should be considered for patients with advanced or refractory HF?

A
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34
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

35
Q

What is the formula for cardiac index (CI)?

A

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

36
Q

When is Fick (CO) most accurate?

A
  • low output states (valvular heart disease)
    • TR
    • multivalvular heart disease
  • steady state
37
Q

What is the problem with Fick (CO)?

A

estimate of O2 consumption

38
Q

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

39
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
40
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
41
Q

When is TD (CO) more accurate?

Least accurate?

A
  • Most accurate –> High Output States
  • Inaccurate –> TR or AF
42
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

43
Q

Describe when step-up O2 saturations are significant?

What does this imply?

A

Intra or Extra cardiac shunt may be present

44
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
45
Q

What is a normal BP response to exercise?

A

25-70 mmHg

46
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
47
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
48
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
49
Q

Describe the findings

A

Pericardial Tamponade

  • Rapid x only
  • Blunted ‘y’ descent (no early diastolic RV filling)
50
Q

Describe the findings

A

Pericardial constriction

  • Rapid x and y descents
    • y = early rapid diastolic RV filling
51
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

52
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
53
Q

When is the Gorlin formula inaccurate?

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

***Assumes steady state and fixed orifice

54
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
    • reduction in pulse pressure in a post-PVC beat
      *
55
Q

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

A

Post-PVC

  • Pulse Pressure
    • HOCM –> decrease
    • AS –> increase

Valsalva

  • Gradient
    • ​HOCM –> increase
    • AS –> decrease
56
Q

Describe the findings

57
Q

Describe the findings

A

HOCM: L heart pullback

58
Q

Describe the findings

A

Provocable Gradient: Valsalva Maneuver

59
Q

What are factors that can increase the gradient in HOCM?

A
  • increased contractility
  • decreased preload
    • volume depletion
  • decreased afterload
60
Q

What are factors that can decrease the gradient in HOCM?

A
  • decreased contractility
  • increased preload
  • increased afterload
    • phenylephrine
61
Q

Describe the findings

62
Q

Describe the findings

A

AR

  • Corrigan’s pulse
  • absence of dicrotic notch
63
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
64
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%)
65
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

66
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 < 12 mL/kg/min had a potential survival benefit after heart transplantation
67
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
68
Q

What is an indication to use the HFSS after CPX?

A

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

69
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
70
Q

What are the cutoffs for the HFSS?

A
  • High risk < 7.20
  • Intermediate risk 7.20 - 8.09
  • Low risk ≥ 8.09
71
Q

Describe the mortality difference between HFrEF and HFpEF?

A

no difference

72
Q

Describe the findings

73
Q

Define Brugada Syndrome

  • Type I
A
  • Type I
    • ST-segment elevation with ≥ 2mm in ≥ 1 lead among the right precoridal leads V1-V2, positioned in the 2nd, 3rd, or 4th intercostal space in the resting ECG
    • occurring either spontaneously or after provocative drug test with IV administration of class I antiarrhythmic drugs
74
Q

Define Brugada Syndrome

  • Type II
  • Type III
A

ST-segment elevation in ≥ 1 lead among the right precoridal leads V1-V2, positioned in the 2nd, 3rd, or 4th intercostal space with a provocative drug test with IV administration of class I antiarrhythmic drugs

  • Type II
    • > 2mm of saddleback shaped ST elevation
  • Type III
    • can be the morphology of either type 1 or type 2
    • < 2mm of ST segment elevation
75
Q

Describe the findings

A

Brugada Syndrome (Type I)

76
Q

When should diagnostic provocative testing be performed in Brugada Syndrome?

What agents are used?

A
  • Type 2 and Type 3 patterns
  • Sodium channel blockers - Class Ic agents
    • Flecainide
    • Ajmaline
    • Procainamide
77
Q

What are the Class I recommendations for lifestyle changes in Brugada Syndrome?

A
  • Avoidance of drugs that may induce or aggravate ST-segment elevation in right precordial leads
    • Class IC, Anesthetics, Psychotropic drugs
  • Avoidance of excess ETOH, Cocaine, Cannabis
  • Immediate treatment of fever with antipyretic drugs
78
Q

What are the Class I recommendations for ICD implantation in Brugada Syndrome?

A
  • Survivors of cardiac arrest
  • Spontaneous VT (documented) with or without syncope
79
Q

What are Class IIa recommendations in regards to ICD in Brugada Syndrome?

A
  • Spontaneous diagnostic type I ECG
  • History of syncope judged to be likely caused by ventricular arrhythmias
80
Q

What are Class IIa recommendations in regards to medical therapy in Brugada Syndrome?

A
  • Quinidine
    • can be useful in patients with a diagnosis of BrS and history of arrhythmic storms (≥ 2 episodes of VT/VF in 24 hours)
    • can be useful in patients with a diagnosis of BrS:
      • qualify for ICD but present a contraindication to the ICD or refuse it
        • and/or
      • have a history of documented SVT requring treatment
  • Isoproternol
    • can be useful in suppressing arrhythmic storms
81
Q

Describe the genes associated with this syndome:

  • BrS1
  • Protein encoded
  • Functional defect
  • Percent of BrS
A
  • SCN5A
  • Cardiac Sodium channel - alpha sub-unit
  • Loss of function - reduced Na current
  • 20-30%
82
Q

Describe the genes associated with this syndome:

  • BrS2
  • Protein encoded
  • Functional defect
A
  • GPD1-L
  • Glycerol-6-phosphate-dehydrogenase
  • Loss of function - reduced Na current
83
Q

Describe the genes associated with this syndome:

  • BrS1
  • Protein encoded
  • Functional defect
  • Percent of BrS
A
  • CACNA1c
  • L-type calcium channel - alpha sub-unit
  • Loss of function - reduced Ca2+ current
  • 5-10%
84
Q

Describe the findings

A
  1. a wave - peak of atrial contraction
  2. LAP during start of ventricular systole
  3. v wave - peak of atrial filling
  4. earliest LAP during ventricular filling
  5. pressure during diastasis
  6. pressure during diastasis

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