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

Heart Failure, Hemodynamics, Nuclear, Channelopathies Flashcards

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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
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
**Giant cell myocarditis**
26
Describe the features of Giant Cell Myocarditis
* 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%)**
27
Describe the features of GCM * Pathophysiology * Histologically
* 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
28
What is the differential diagnosis in a patient with rapidly progressive heart failure and high-grade heart block?
* GCM * Sarcoidosis * Lyme disease * Chagas disease
29
Diagnose GCM
**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
30
What is the treatment for GCM?
* 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)
31
In addition to guideline-directed medical therapy, what intervention for HF patients has also been proven to help reduce rehospitalizations?
**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
32
What are the discharge criteria for HF patients?
33
What are the discharge criteria for HF patients? Should be considered for patients with advanced or refractory HF?
34
What is the formula for Fick CO?
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
What is the formula for cardiac index (CI)?
CI = CO (L/min) / BSA (m2)
36
When is Fick (CO) most accurate?
* low output states (valvular heart disease) * TR * multivalvular heart disease * steady state
37
What is the problem with Fick (CO)?
estimate of O2 consumption
38
What PA sat correlates with low CO (on Fick)?
**\< 65%**
39
What are quick estimates of Fick (CO) utilizing PA sats?
* 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
Describe the findings
* 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
When is TD (CO) more accurate? Least accurate?
* Most accurate --\> High Output States * Inaccurate --\> TR or AF
42
What is the formula for PVR (pulmonary vascular resistance, Woods units)?
PVR = mPAP - mPCWP / CO ## Footnote \*\*Normal range = 80-130 dynes \*\*\*Woods units x 80 = dynes \*\*\*\* TPR = mPAP / CO
43
Describe when step-up O2 saturations are significant? What does this imply?
Intra or Extra cardiac shunt may be present
44
Describe locations for mixed venous O2 sats in shunt calculations: * No L-R shunt * L-R shunt present * ASD * No R-L shunt
* 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
What is a normal BP response to exercise?
25-70 mmHg
46
What is the formula for SVR (systemic vascular resistance)? What is normal range?
SVR = mean systemic arterial pressure - mRAP / CO * Normal range = 700-1600 dynes-sec/cm5
47
Describe the finding
**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
What constitutes a pathologic or abnormal "v" wave in PCWP tracings? What are causes?
* "v" wave more than 10 mmHg than PCWP * PCWP "v" waves * MR * VSD * Noncompliant LA * previous A-fib ablation procedures
49
Describe the findings
**Pericardial Tamponade** * Rapid x only * Blunted 'y' descent (no early diastolic RV filling)
50
Describe the findings
**Pericardial constriction** * Rapid x and y descents * y = early rapid diastolic RV filling
51
What is the Gorlin formula?
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
What is the simplified Gorlin or Hakki formula? When does this formula differ?
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
When is the Gorlin formula inaccurate?
* Regurgitation (concomitant) * Low output states * Tachy/Brady cardia \*\*\*Assumes steady state and fixed orifice
54
Describe the findings
**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
How can you differentiate AS and HOCM on intracardiac pressure tracings?
**Post-PVC** * **Pulse Pressure** * HOCM --\> decrease * AS --\> increase **Valsalva** * **Gradient** * **​**HOCM --\> increase * AS --\> decrease
56
Describe the findings
AS
57
Describe the findings
HOCM: L heart pullback
58
Describe the findings
Provocable Gradient: Valsalva Maneuver
59
What are factors that can increase the gradient in HOCM?
* increased contractility * decreased preload * volume depletion * decreased afterload
60
What are factors that can decrease the gradient in HOCM?
* decreased contractility * increased preload * increased afterload * phenylephrine
61
Describe the findings
**ASD**
62
Describe the findings
**AR** * Corrigan's pulse * absence of dicrotic notch
63
When should advanced HF therapies be considered?
* Symptoms become refractory to: * medical (GDMT) therapy * surgical therapy * device therapy * End organ dysfunction becomes apparent
64
What are the most common diagnoses for adult heart transplantation?
* Myopathy (55%) * CAD (36%) * Valvular disease (3%) * Congenital disease (3%) * Retransplantation (3%) * Other Cardiomyopathies (1%)
65
What are the two components of the comprehensive evaluation when evaluating patients for heart transplantation?
* 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
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?
**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
What are the important measures in cardiopulmonary stress testing (CPX)?
* **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
What is an indication to use the HFSS after CPX?
Peak VO2 \> 12 mL/kg/min and ≤ 14 mL/kg/min
69
What are the features of the HFSS?
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
What are the cutoffs for the HFSS?
* High risk \< 7.20 * Intermediate risk 7.20 - 8.09 * Low risk ≥ 8.09
71
Describe the mortality difference between HFrEF and HFpEF?
no difference
72
Describe the findings
73
# Define Brugada Syndrome * Type I
* 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
# Define Brugada Syndrome * Type II * Type III
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
Describe the findings
Brugada Syndrome (Type I)
76
When should diagnostic provocative testing be performed in Brugada Syndrome? What agents are used?
* Type 2 and Type 3 patterns * Sodium channel blockers - Class Ic agents * Flecainide * Ajmaline * Procainamide
77
What are the Class I recommendations for lifestyle changes in Brugada Syndrome?
* 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
What are the Class I recommendations for ICD implantation in Brugada Syndrome?
* Survivors of cardiac arrest * Spontaneous VT (documented) with or without syncope
79
What are Class IIa recommendations in regards to ICD in Brugada Syndrome?
* Spontaneous diagnostic type I ECG * History of syncope judged to be likely caused by ventricular arrhythmias
80
What are Class IIa recommendations in regards to medical therapy in Brugada Syndrome?
* 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
Describe the genes associated with this syndome: * BrS1 * Protein encoded * Functional defect * Percent of BrS
* **SCN5A** * Cardiac **Sodium** channel - alpha sub-unit * Loss of function - reduced Na current * 20-30%
82
Describe the genes associated with this syndome: * BrS2 * Protein encoded * Functional defect
* **GPD1-L** * Glycerol-6-phosphate-dehydrogenase * Loss of function - reduced Na current
83
Describe the genes associated with this syndome: * BrS1 * Protein encoded * Functional defect * Percent of BrS
* **CACNA1c** * **L-type calcium channel -** alpha sub-unit * Loss of function - reduced Ca2+ current * 5-10%
84
Describe the findings
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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