On a basic level, what does heart failure result from?
Some sort of LV dysfunction that reduces CO
What is compliance?
- -change in V / change in P
- -how easily the ventricle can be filled
T or F, SV only counts blood that is being pumped forward into the aorta?
False, it also includes blood that is being pumped backward into the atria
What value that we can easily measure approximates afterload?
What is the equation for wall stress?
- Law of LaPlace
- T= wall stress / tension
- P= ventricular pressure
- R= ventricular radius
- h= thickness of the ventricle
How is a change in preload seen in the Starling curves?
- The point moves along a specific Starling curve.
- -As preload increases, SV and LVEDP increase to the point moves up the Starling curve
How is a change in contractility seen in the Starling curves?
- We move to a different Starling curve.
- -With HF, SV decreases, so we move to the lower curve
What happens to SV and ESV as a result of increased preload (inotropy held constant)?
- SV increases
- ESV increases slightly because afterload increases (ie when you give IVF, BP increases)
What happens to SV and ESV as a result of increased afterload (inotropy held constant)?
- -decreased SV
- -ESV increases and EDV increases secondarily
What happens to the normal heart with increased afterload?
What about the heart in failure?
- -normal heart will have little change in SV as the heart can compensate and still pump the volume it recevies
- -with HF, the EDV is already at the max, so the heart can't compensate and SV is decreased
How does increased contractility affect SV, ESV, EF, and EDV?
- -SV increases
- -ESV decreases and as a result EDV is slightly decreased
- -EF increases
What 2 factors affect LVEDV?
An increase in which of the following will increase SV: afterload, preload, contractility?
increased preload and contractility
forward or systolic failure
- -heart can't pump enough blood forward to meet metabolic demands
- -decreased EF
occurs when the heart can only pump blood when the filling pressures are abnormally high
What major factors can contribute to systolic heart failure (reduced EF)?
- -impaired contractility (due to: CAD, chronic volume overload due to MR or AR, or dilated CMP)
- -increased afterload (chronic pressure overload due to severe AS or uncontrolled severe HTN)
What major factor can contribute to diastolic heart failure (preserved EF)?
-impaired diastolic filling (due to: LVH, rx CMP, myocardial fibrosis, transient MI, pericardial constriction or tamponade)
In the US, is systolic or diastolic HF more common?
About 50% of its fall into each category
What's the most common cause of right sided HF?
Left sided HF!!
How is the ESPVR line affected by reduced EF HF?
- -The line is decreased (decreased contractility)
- -Systolic emptying will stop at a higher than normal volume
Explain what happens to cause pulmonary congestion in reduced EF HF.
- -EF is reduced
- -ESV is increased
- -EDV is increased as a result
- -contractility is impaired so we can't compensate
- -blood backs up into LA then into pulmonary system
In HF with preserved EF, how is the PV loop affected?
-The ventricle fills at a higher than normal pressure (EDP at bottom of the loop is increased)
What are the effects of impaired filling in preserved EF HF?
-blood backs up into the pulmonary system and congestion results
Does diastolic or systolic HF prevalence increase with increasing age?
Diastolic, >50% of pts over age 70 have diastolic heart failure
What are the 4 classes of diastolic HF?
- Class 1- abn LV relaxation with normal LAP
- Classes 2, 3, 4- abn relaxation with decreased LV compliance and increased LVEDP, increased LAP
What factors can predispose the ventricle to decreased distensibility?
- -pressure overload
Are women or men more affected by diastolic HF?
How do the mortality and hospitalization rates for systolic and diastolic HF compare?
they are equal
What's considered to be a "preserved EF"?
EF > 40%
Is S4 more associated with diastolic or systolic failure?
Is S3 more associated with diastolic or systolic failure?
Is a prior MI more associated with systolic or diastolic HF?
Regardless of the cause of HF, what results?
What effects does ventricular remodeling have on heart function?
- -decreased EF
- -worsening HF
- -premature death
What non cardiac factors can contribute to ventricular remodeling?
SNS stimulation (causes vasoconstriction and Na+ retention by the kidneys)
What could cause new onset acute HF?
- -valve rupture
- -large MI
- -HTN crisis
What is the major clinical sign of acute HF?
- -decreased CO and BP
- -no peripheral edema
Is the RV or LV more compliant?
The RV, it can accept a wide variety of volumes with little change in pressure
Explain how L sided HF can cause R sided HF.
- -L sided HF with cause blood to back up in the pulmonary system
- -the R side will be confronted by this with increased PVR
- -RV failure due to a primary pulmonary process
- -can lead to R sided HF
Cardiac causes of R sided HF
- -left sided HF
- -pulmonary stenosis
- -RV infarct
Pulmonary parenchymal diseases that can cause R sided HF
- -chronic lung infection
Pulmonary vascular diseases that can cause R sided HF
- -primary pulmonary HTN
R sided HF s/sx
- -systemic congestion, manifested as:
- -peripheral edema
low output HF
-CO is ok at rest but does not respond adequately to stress
common causes of low output HF
- -valve disease
- -pericardial disease
high output HF
- -ventricle fails because there's both an increased HD burden and a direct myocardial toxicity
- -heart is overloaded by excess venous return
common causes of high output HF
- -AV fistula
- -severe hyperthyroidism
What are the 3 major compensatory mechanisms that will buffer the fall in CO to preserve perfusion to vital organs?
- -Starling mechanism
- -hypertrophy / remodeling
- -neurohormonal influences
Explain how the Starling mechanism can be compensatory in HF.
- -increased EDV will increase SV to preserve CO
- -but only to a point!
Explain how hypertrophy can be compensatory in HF.
- -can be in response to increased volume or pressure
- -increased LV wall mass results
- -this will help to maintain CO
- -but it is also stiff and noncompliant
- -so increased LVEDP results, which gets transmitted to LA, then to pulmonary veins
What neurohormonal changes are at play in attempting to compensate for HF.
- -adrenergic nervous system
- -natriuretic peptides
- -other peptides
What effect do the natriuretic peptides have in compensating for HF?
- -secreted in response to increased pressures
- -cause Na+ and water excretion, VD, inhibition of renin, antagonize effects of angio 2 and aldosterone
- -they are helpful, but not enough to overcome deleterious effects of other neurohormonal changes
What does it mean to be "stuck on the flat part of the curve" in HF?
- -LVEDP increases with no increase in SV
- -worsening heart failure as move along flat section of the heart failure Starling curve
What factors can precipitate HF symptoms?
- -increased metabolic demands
- -increased circulatory volume (increased preload)
- -increased afterload
- -impaired contractility
- -bradycardia (decreases CO)
- -medication non-compliance
Are you more likely to hear S3 and S4 in L or R sided HF?
L sided HF
What signs indicative of CHF might be seen on a CXR?
- -increased width of vascular pedicle
- -perihilar haze
What are Kerley B lines?
- -appear in the lower lung fields on CXR
- -indicate interlobar edema
- -show up when LAP > 20 mmHg
Why may a CXR not be indicative of what's going on with CHF at that exact moment?
-CXR findings lag 12 hours behind clinical evidence
Why do LA pressures and CXR findings often not correlate in CHF?
-with chronic CHF, there's increased lymphatic drainage so higher pressures can be accommodated without CXR changes
What level BNP is indicative of HF?
What does a BNP of 100-500 mean?
Intermediate likelihood of CHF
NY Heart Association Functional Classification of chronic HF
- class 1- no limitation of physical activity
- 2- slight activity limitation, dyspnea with moderate exertion
- 3- marked activity limitation, dyspnea with minimal exertion
- 4- severe activity limitation, symptoms at rest
HF 5 year mortality rate
Stages of chronic HF (A-D)
- A- risk for HF but no structural dysfunction
- B- structural dz assoc with HF but no symptoms
- C-structural dz assoc with HF and current or prior symptoms
- D- structural dz assoc with HF and marked symptoms despite maximal med therapy, requires advanced interventions (transplants)
T or F, elevated norepi levels can predict decreased survival in HF?
What are the 5 goals of treatment in reduced EF HF?
- 1- identify and correct underlying cause
- 2- eliminate acute precip factors
- 3- symptom management
- 4- modulate neuroendocrine responses
- 5- prolong LT survival
What drug classes are indicated in the treatment of systolic HF?
- -vasodilators (hydral, nitrates, RAAS inhibitors)
- -aldosterone antagonists
cardiac resynchronization therapy
-what is it?
-what pts is it indicated for?
- -can improve function as both ventricles will contract simultaneously
- -pts with EF < 35% or prolonged QRS duration or symptoms of continued failure despite maximal drug therapy
Drug therapy in diastolic failure
- -limited to diuretics
- -need to be careful not to under fill LV as it is stiff and needs higher than normal pressures
- -if overdiurese can decrease SV
Goals of treatment in preserved EF HF
- -relief of pulmonary and systemic congestion
- -address correctable causes (HTN and CAD)
Can BB, CCB, and digoxin be used in diastolic HF?
- -yes, but they have no demonstrated improvement in mortality
- -can help to allow adequate filling by slowing the HR
How is acute HF classified (what symptoms)?
- 1) presence or absence of volume overloading- wet or dry
- 2) presence or absence of decreased CO- warm or cold
Describe acute HF profile A- warm and dry.
- -CO normal
- -LV filling pressures normal (absence of systemic or pulmonary congestion)
- -normal HD
- -cardiopulmonary symptoms not due to HF but to lung disease or MI
Describe acute HF profile B- warm and wet.
- -normal CO
- -symptoms of pulmonary and systemic congestion, increased LV filling pressures
- -JVD, rales, peripheral edema
- -warm extremities
Describe acute HF profile C- cold and wet
- -decreased CO
- -elevated LV filling pressures
- -marked peripheral VC
Describe acute HF profile L- cold and dry
- -reduced CO
- -normal LV filling pressures
- -volume depletion or limited cardiac reserve in absence of volume overload
Is acute cardiogenic pulmonary edema due to L or R sided HF?
What acute HF profiles are associated with cardiogenic pulmonary edema
B and C
Treatment of Acute HF (LMNOP)
- -life threatening
- -preload- decrease it with diuretics
What is the single most important risk factor for predicting peri-op M & M?
Anesthesia management of HF meds during surgery
- -d/c diuretics day of surgery
- -d/c ACEI / ARB
- -con't BB and dig
Anesthesia for HF pt
- -Use of PEEP can improve oxygenation
- -opioids are beneficial (inhibit adrenergic activation)
- -all anesthetic agents can be used in HF, but dose may need to be adjusted
What are some issues with a transplanted heart?
- -it's denervated and increased HR can only be achieved with a direct acting beta agonist like epi
- -LT immunosuppression