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
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)?
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
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?
- CAD?
- 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
- Cough, dyspnea on exertion (DOE), & edema
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)
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

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)”)
8
Q

A
- Pulmonary edema
- Cardiac enlargement
- Compatible w/ dilated cardiomyopathy
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
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
- Pros
- 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
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
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
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
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
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
- Catheter is balloon-tipped & flow-guided

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
- No IABP
- 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
- Increase LVEDV –> increase LVEDP
- 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
- Pulmonary arterial hypertension specific
- Inotropic agents
- Milrinone preferred for pulmonary vasodilating properties
- Once stabilized
- Re-institution of chronic therapy
- Patient education