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Cardiology > Integrating Pathophysiology, Diagnosis and Management > Flashcards

Integrating Pathophysiology, Diagnosis and Management Flashcards

1
Q

Heart Failure

  • Definition
  • The limitation in heart function can be…
A
  • Definition
    • Syndrome of fluid overload &/or inadequate tissue perfusion related to the heart’s inability to meet demand
    • Not fluid overload unrelated to the heart (ex. cirrhosis, nephrotic syndrome)
  • The limitation in heart function can be…
    • Related to systolic or diastolic dysfunction
    • Ischemic or non-ischemic
    • Acute, chronic, or “acute on chronic”
    • Right or left sided
    • Mild or severe (most severe = cardiogenic shock)
    • Valvular, hypertensive, or other etiology
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2
Q

Questions to Ask when Presented with a Case

A
  • Is this heart failure?
    • Volume overload?
    • Inadequate tissue perfusion?
    • Cardiac cause?
  • What type?
    • Acute, chronic, or “acute on chronic”?
    • Left or right?
    • Systolic or non-systolic?
    • Specific etiology (ischemic vs. nonischemic)?
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3
Q

Tools to Diagnose Heart Failure

A
  • History & physical
  • ECG
  • Chest x-ray
  • Blood work (including biomarkers)
  • Echo
  • Stress / perfusion imaging
  • Non-invasive imaging (CT, MR, PET)
  • Cardiac catheterization
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4
Q

Historical Clues

  • Age, sex, co-morbidities
  • Symptoms
    • Cough, dyspnea on exertion (DOE), & edema
    • Cough
    • Paroxysmal nocturnal dyspnea (PND) & orthopnea
    • PND, orthopnea, ascites, weight gain, (poly)nocturia
    • Fatigue, anorexia, low urine output, depression
A
  • Age, sex, co-morbidities
    • CAD?
      • 64yo male w/ smoking, dyslipidemia, & HTN: high risk for CAD
      • If HF, it could be w/ either preserved or reduced ejection fraction
    • Systolic vs. non-systolic?
  • Symptoms
    • Cough, dyspnea on exertion (DOE), & edema
      • Volume overload?
      • Cough is common in patients w/ HF
      • Dyspnea on exertion is almost universal
    • Paroxysmal nocturnal dyspnea (PND) & orthopnea are specific for HF
    • PND, orthopnea, ascites, weight gain, (poly)nocturia
      • –> volume overload
    • Fatigue, anorexia, low urine output, depression
      • –> low cardiac output & poor tissue perfusion
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5
Q

Exam Clues

  • Tachypnea, edema
  • Jugular venous distention, pulmonary rales, & ascites
  • Hypotension, tachycardia, & diaphoresis
  • Cool, mottled extremities & poor mentation
  • S3
  • S4
  • Cardiac murmurs
A
  • Tachypnea, edema
    • –> volume overload
  • Jugular venous distention, pulmonary rales, & ascites
    • –> volume overload, left vs. right
  • Hypotension, tachycardia, & diaphoresis
    • –> poor perfusion (compatible but not specific)
  • Cool, mottled extremities & poor mentation
    • –> poor perfusion (strongly suggestive)
  • S3
    • –> systolic LV failure
  • S4
    • –> non-systolic HF
  • Cardiac murmurs
    • –> specific etiology of HF (ex. aortic stenosis) or secondary to the HF (ex. mitral regurgitation in stystolic HF w/ LV dilation)
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6
Q

Peripheral Edema w/ Bulla

A
  • Common feature of RHF w/ volume overload
  • Also seen in other volume overload states & in patients w/ venous insufficiency
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7
Q
  • Rhythm
  • BBB
A
  • Rhythm
    • Tachycardic sinus rhythm
  • LBBB
    • Seenn in ischemic or non-ischemic cardiomyopathy
    • May mask evidence of prior infarction
    • Usually indicates more advanced ventricular dilation & dysfunction
    • Represents a possible target for therapy w/ a biventricular pacer (“cardiac resynchronization therapy (CRT)”)
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8
Q
A
  • Pulmonary edema
  • Cardiac enlargement
  • Compatible w/ dilated cardiomyopathy
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9
Q

Bloodwork

  • Elevated BUN & creatinine
  • Hyponatremia
  • Non-cardiac processes like anemia or infection
  • B-type natriuretic peptide (BNP)
  • Other biomarkers for HF
A
  • Elevated BUN & creatinine
    • –> intrinsic renal disease, volume depletion, or renal hypoperfusion related to low cardiac output
  • Hyponatremia
    • Correlates w/ HF severity & prognosis
  • Non-cardiac processes like anemia or infection
    • Can exacerbate HF
    • Can be detected by blood testing
  • B-type natriuretic peptide (BNP)
    • Biomarker for presence & severity of HF (right vs. left, systolic vs. non-systolic)
    • Addition of routine BNP monitoring to standard care can improve outcomes (ex. re-admission for HF)
    • NT-proBNP: related biomarker
  • Other biomarkers for HF
    • Troponin I
    • Uric acid
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10
Q

Echo

  • Pros & cons of echo
  • Critical information obtained by echo
  • This echo
A
  • Pros & cons of echo
    • Pros
      • Widely available
      • Non-invasive & risk-free
      • Provides a lot of structural & functional information about the CV system
    • Cons
      • Occasional poor image quality
  • Critical information obtained by echo
    • Left & right atrial & ventricular size
    • Wall thickness
    • Indices of systolic & diastolic function
    • Regional LV wall motion
    • Hypokinetic or akinetic areas
      • –> prior infarction
    • Aortic & inferior vena cava size
    • Structure & function of the mitral, aortic, tricuspid, & pulmonic valves
    • Estimates of RA & RV pressures
    • Direct & indrect markers of pericardial disease
  • This echo
    • LV dilation
    • Severe systolic dysfunction
    • Regional wall motion abnormalities
    • –> ischemic cardiomyopathy
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11
Q

Echo

  • Ejection fraction
  • Diminished LV EF on echo
  • Regional wall motion abnormalities
  • Global hypokinesis
  • Increased LV wall thickness & enlarged LA
  • RV hypertrophy, dilation, & high velocity tricuspid insufficiency jet
A
  • Ejection fraction
    • Most common load-dependent index of LV systolic function
    • Value can be visually estimated or calculated
    • Affected by changes in preload (LV filling) & afterload (systemic vascular resistance or BP)
    • Easy to obtain & validate
    • Not a pure marker of ventricular contractile ability
  • Diminished LV EF on echo
    • –> systolic HF
    • Degree of ventricular dilation
      • Directly related to duration of disease
      • Indirectly related to chance of recovery of ventricular function
  • Regional wall motion abnormalities
    • –> ischemic disease
  • Global hypokinesis
    • –> non-ischemic cardiomyopathy
  • Increased LV wall thickness & enlarged LA
    • –> non-systolic (diastolic) HF
  • RV hypertrophy, dilation, & high velocity tricuspid insufficiency jet
    • –> pulmonary HTN & RHF
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12
Q

Catheterization

  • Cardiac catheterization
  • Left heart catheterization involves…
  • Right heart catheterization involves…
A
  • Cardiac catheterization
    • Critical diagnostic modality for patients w/ suspected HF
  • Left heart catheterization involves…
    • Arterial access (usually femoral or radial)
    • Coronary angiography
    • Left ventriculography
    • Measurement of LV pressures
    • Aortography (occasionally)
  • Right heart catheterization involves…
    • Venous access (usualy internal jugular or femoral)
    • Measurement of pressures & cardiac output of right heart, pulmonary artery, & pulmonary capillary wedge
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13
Q

Coronary Angiography

  • Coronary angiography
  • Endomyocardial biopsy
  • This coronary angiography
A
  • Coronary angiography
    • Yields concrete evidence of presence, extent & severity of atherosclerosis
    • Advantages in patients w/ cardiomyopathy b/c perfusion imaging has suboptimal sensitivity & specificity
  • Endomyocardial biopsy
    • Rarely performed in patients w/ newly diagnosed cardiomyopathy if a specific, infiltrative process is suspected
  • This coronary angiography
    • High grade multivessel coronary disease compatible w/ ischemic cardiomyopathy
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14
Q

Right Heart Catheterization

  • Critical in evaluating patients with…
  • Information gained
  • Aid in the determination of…
A
  • Critical in evaluating patients with…
    • Hypotension
    • Unexplained dyspnea
    • HF
  • Information gained
    • Left & right heart filling pressures
    • Pulmonary pressures
    • Cardiac output
    • Mixed venous oxygen saturation
  • Aid in the determination of…
    • Overall volume status
    • Contractile state of the heart
    • Pulmonary & systemic vascular tone
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15
Q

Swan-Ganz Catheter

  • Swan-Ganz catheter
  • Procedure
A
  • Swan-Ganz catheter
    • Placed in vena cava, through right heart, into pulmonary artery
    • Measures right & left heart filling pressures & cardiac output
  • Procedure
    • Catheter is balloon-tipped & flow-guided
      • Allows for easier navigation throught the right heart & into the pulmonary artery
    • When advanced distally, the balloon occludes a tertiary or quaternary PA branch
      • Creates a closed connection w/ the LV
    • Resulting “pulmonary capillary wedge pressure” is a reliable measure of left heart filling pressure
      • Should be identical to the LA & LV EDPs
      • Due to technical challenges or unusual physiological circumstances, this pressure may not accurately reflect LV filling pressure
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16
Q

Hemodynamic Assessment of Right Heart Catheterization

  • Elevated pulmonary artery (PA) & pulmonary capillary wedge (PCW) pressures
  • Depressed cardiac output (CO) & cardiac index (CI)
  • Normal transpulmonary gradient (TPG) & pulmonary vascular resistance (PVR)
A
  • Consistent with…
    • Decompensated HF
    • Volume overload
    • Inadequate tissue perfusion
  • Absence of pulmonary arterial disease
17
Q

Acute Decompensated Heart Failure: Hemodynamic Subsets

  • Conditions
    • Warm
    • Cold
    • Wet
    • Dry
  • Subsets
    • Warm & dry
    • Warm & wet
    • Cold & dry
    • Cold & wet
  • Majority of patients w/ HF
  • Vasodilatory drugs
  • IV inotropic therapy
  • IV vadodilator therapy
A
  • Conditions
    • Warm = high output + high cardiac index
    • Cold = low output + low cardiac index
    • Wet = congestion + high pulmonary capillary wedge
    • Dry = no congestion + low pulmonary capillary wedge
  • Subsets
    • Warm & dry
    • Warm & wet
    • Cold & dry
    • Cold & wet
  • Majority of patients w/ HF
    • Volume overload (“wet”)
    • Unchanged or decreased cardiac index
    • Most have elevated systemic vascular resistance
      • Few have unchanged or decreased systemic vascular resistance
  • Vasodilatory drugs
    • Therapeutically benefit “wet & warm” & most “wet & cold” patients
  • IV inotropic therapy
    • Reduce filling pressures & improve cardiac output
    • Therapeutically benefit “dry” patients w/ systemic hypoperfusion
  • IV vadodilator therapy
    • Similar to IV inotropic therapy w/o aggravating ischemia or arrhythmias & w/ easier transition to oral vasodilator regimens
18
Q

Pharmacotherapy of Systolic HF

  • Fluid removal
  • Vasodilator therapy
  • Inotropic therapy
  • Once stabilized
A
  • Fluid removal
    • Diuretics
    • Ultra-filtration
    • Nesirtide
  • Vasodilator therapy
    • Trinitroglycerine
    • Sodium nitroprusside
    • ACE-Is
    • Hydralazine
  • Inotropic therapy
    • Dobutamine
    • Milrinone
    • Dopamine
  • Once stabilized
    • Re-instutition of chronic therapy (ACE-Is, beta blockers, diuretics, digoxin, spironolactone, etc.)
    • Patient education
19
Q

Intra-Aortic Balloon Pump (IABP)

  • General
  • use
  • Timing to the cardiac cycle
  • Aortic pressure tracings
  • Limitations
A
  • General
    • Most readily available short-term mechanical circulatory support device
    • Placed percutaneously via the femoral artery & advanced retrograde to just below the aortic knob
  • Use
    • When a patient w/ decompensated systolic HF can’t be stablized w/ pharmacotherapy alone
  • Timing to the cardiac cycle
    • Systole –> balloon deflates abruptly –> decrease afterload –> beneficial hemodynamic effects
    • Diastole –> balloon re-inflates rapidly –> increase arterial pressure & coronary blood flow
  • Aortic pressure tracings
    • No IABP
      • Dicrotic notch = aortic valve closure
    • IABP
      • Balloon inflation after aortic valve closure –> increase systolic pressure
      • Balloon deflation –> decrease diastolic pressure –> decrease afterload
  • Limitations
    • Vascular complications
    • Infection
    • Tachyarrhythmias –> interfere w/ proper timing of balloon inflation & deflation –> detrimental hemodynamic effects
    • Bedrest
20
Q

Left Ventricular Assist Device (LVAD)

  • General
  • Mechanism
  • Use
  • Biventricular assist device (biVAD)
  • Cardiac transplantation
A
  • General
    • Implanted pump restores circulatory support
    • External control system promotes patient discharge & mobility
    • Textured surfaces minimize thromboembolic events & anti-coagulation therapy
    • Able to supply up to 10 liters per minute
  • Mechanism
    • Surgically implanted via a median sternotomy
    • LVAD receives blood from the LV & returns it to the aorta for distribution throughout the circulatory system
    • External, wearable system controller monitors & controls all pump functions
    • Pump receives power through the system controller from batteries or an external AC power supply
  • Use
    • “Bridge” to cardiac transplantation
    • “Destination therapy” for patients who aren’t candidates for transplant
  • Biventricular assist device (biVAD)
    • For patients w/ severe biventricular failure
    • Cumbersome & doesn’t lend itself to long term use
  • Cardiac transplantation
    • Gold standard for patients w/ advanced CHF
21
Q

Case

  • History
    • 74yo female
    • Type II DM, HTN, obesity, & longstanding slowly progressive DOE
    • Acute SOB after trip w/ dietary & medication non-adherence
  • Physical exam
    • Tachypneic
    • HR = 100 + AFib
    • BP = 190/90
A
  • Possible non-systolic HF
  • Volume overload
  • Elevated cardiac filling pressures
  • Preserved LV systolic function
22
Q

Lab Data

  • ECG
  • CXR
  • Echo
A
  • ECG
    • AFib
    • Rapid ventricualr response
    • LVH
  • CXR
    • Pulmonary edema
    • Normal cardiac silhouette
    • Enlarged aortic knob seen in chronic systemic HTN
  • Echo
    • Severe LVH
    • Preserved systolic function
    • Enlarged LA
23
Q

Non-Systolic Heart Failure

  • Non-systolic HF sensitivity to volume changes
  • LVEDV vs. CO
  • LVEDV vs. LVEDP
  • Common important conditions that contribute to decompensation in patients w/ non-systolic HF
A
  • Non-systolic HF sensitivity to volume changes
    • Patients w/ non-systolic HF are very sensitive to volume changes
    • These patients must be maintained in a very narrow volume window
  • LVEDV vs. CO
    • Increases in LV preload –> improved cardiac performance
    • Non-systolic HF: steep curve –> decrease preload –> abrupt fall in CO
  • LVEDV vs. LVEDP
    • Increase LVEDV –> increase LVEDP
      • Pressure is felt back into the pulmonary capillary bed
      • Sufficient increase in pressure –> pulmonary edema
    • Non-systolic HF: steep curve –> little increase in volume –> significant increase in LV pressure
  • Common important conditions that contribute to decompensation in patients w/ non-systolic HF
    • Coronary ischemia
    • Poorly controlled HTN
    • Atrial fibrillation w/ rapid ventricular response
      • –> loss of “atrial kick” contributing to ventricular filling
      • –> rapid heart rate –> loss of diastolic filling time
24
Q

Pharmacotherapy of Non-Systolic HF

  • Fluid removal
  • Contributing conditions
  • Once stabilized
  • Inciting factors
A
  • Fluid removal
    • Often only a modest amount needed
  • Contributing conditions
    • HTN
    • Ischemia
    • Dysrhythmia
  • Once stabilized
    • Re-institution of chronic therapy
    • Patient education
  • Inciting factors
    • Dietary or medication non-adherence
    • Non-cardiac co-morbidities
    • Progression of underlying cardiac disease
25
Q

Case

  • History
    • 46yo female
    • Longstanding pulmonary arterial hypertension, on epoprostenol
    • Abdominal bloating, BLE edema, & syncope after climbing stairs
  • Physical exam
    • Tachypnea
    • HR = 100
    • BP = 90/50 (hypotension)
    • Ascities & edema
    • Loud P2
    • RV lift
A
  • Hisotry
    • Pulmonary HTN + ascites + edema + syncope
    • –> RV failure & decompensated RHF
  • Physical exam
    • Loud P2 –> elevated pulmonary pressure
    • RV lift –> elevated RV pressure
    • Volume overload –> pulmonary HTN leading to RHF
26
Q

Lab Data

  • ECG
  • CXR
  • Echo
A
  • ECG
    • RAD
    • RA enlargement
    • RVH w/ strain
  • CXR
    • Enlarged RV w/ dimunition of the retrosternal air space
    • Peripheral hypovascularity (pruning)
    • :rominent hilar pulmonary arteries
  • Echo
    • Loss of normal circular shape of the LV
    • RV pressure & volume overload shifts the septum to produce a “D shaped” LV
    • Indicates pulmonary HTN
27
Q

Right Heart Failure

  • Catheterization hemodynamic assessment
  • RHF from pulmonary HTN
A
  • Catheterization hemodynamic assessment
    • Elevated pulmonary pressure
    • Normal pulmonary capillary wedge pressure
    • Elevated transpulmonary gradient & pulmonary vascular resistance
    • Elevated RA pressure
    • Diminished cardiac output
    • Consistent w/ RHF
  • RHF from pulmonary HTN
    • State of excessive afterload & preload
    • Mediated by neurohormonal pathways
    • Therapies target both the increased preload & afterload
28
Q

Pharmacotherapy of RHF

  • Fluid removal
  • Pulmonary vasodilators
    • Pulmonary arterial hypertension specific
    • Others
  • Inotropic agents
  • Once stabilized
A
  • Fluid removal
    • Often difficult due to “third spacing” & preload-dependence of the abnormal RV
  • Pulmonary vasodilators
    • Pulmonary arterial hypertension specific
      • Endothelin receptor antagonist
      • Phosphodiesterase type 5 inhibitor
      • Prostacyclines
    • Others
      • O2
      • Nitric oxide
  • Inotropic agents
    • Milrinone preferred for pulmonary vasodilating properties
  • Once stabilized
    • Re-institution of chronic therapy
    • Patient education

Cardiology (40 decks)

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