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Describe the Frank Starling Mechanism
- ↑ LVEDP → ↑ SV
- The heart pumps the volume it receives
- (the wall of the ventricle gets stretched more and gets maximum overlap of myosin and actin filaments, and allows more tension generation and increases the SV)
- the ventricular wall tension at end of diastole
- The stretch of myocardial fibers (approximated to LVEDP)
- the ventricular wall tension during contraction (systole)
- Resistance ventricle must overcome in order to eject its contents & that gets approximated by systolic arteriole pressure
- Sometimes afterload is more formally defined as ventricular wall stress that develops during systolic ejection
the strength of contraction
Δ Volume/Δ Pressure
LVEDV/P = preload and is influenced by compliance
What three things contribute to SV?
Preload, Afterload, and contractility
- CO = HR x SV
- ↑ SV due to ↑ preload ↓ afterload ↑ contractility
LaPlace's law is used when talking about wall stress. Describe this as a compensatory mechanism
- wall stress or tension = pr/2h
- pressure= ventricular pressure
- radius =radius of the ventricle
- h = thickness of ventricular wal
- Ventricle wall stress or tension will increase in response to chronically high pressure (HTN) or increase chamber size.
- Increase wall thickness initially serves as a compensatory role because as that denominator of Laplace equation increases then wall stress/tension decreases because the forces gets distributed over a larger surface area.
How does a change in preload vs. a change in contractilty effect the Frank Starling curve?
Preload= moves up or down from a specific point on the FS curve, not changing the curve itself
Contractilty = shifts the curve up or down (LV function does this as well)
Increased Preload: SV increases, and ESV increases slightly because afterload increases (Vice versa is true)
Preload depends on compliance, so if LV compliance is decreased, (severe LV hypertrophy), the slope of the diastolic filling curve becomes steeper. (Point A to B, bottom curve on the loop).
- ↑afterload = ↓SV slighty (ESV and EDV sightly increase secondarily
- (vice versa as well)
Why does the the pressure that’s generated by the ventricle increase during ejection when afterload increases (like AS or HTN)?
because more work on part of ventricle needs to be expended in order to overcome the resistance to ejection that’s in place because of the increased afterload
There’s a nearly linearly relationship between afterload and ESV. The ESPVR. The line going up from 1 to 2 to 3. Interdependence among all these variables. When afterload ↑, as a result, ↑ ESV. That extra volume still in ventricle at systole gets added to normal EDV and so↑preload. So that secondary ↑preload, because of what that means w/Frank Starling, it will partially offset that ↓SV (caused by initial increase in afterload).
TRUE or FALSE. In the normal heart, an increase in afterload has little effect on SV
TRUE. Problem w/patient in HF, for them the EDV is pretty much maxed out so an increase in afterload that will significantly reduce SV.
usually, ↑afterload →↓SV →↑ESV which is added to EDV and FS kicks in to partially offset the initial decrease in SV caused by increased afterload
↑inotropy = ↑SV (↓ESV and EDV secondarily ↓ a sm. amt) EF increases. (Vice versa is true)
- ESPVR is a function of contractilty
- If contractility increases, the slope of that line goes up, goes from 1 to 2, so in going from 1 to 2 for any given preload and afterload the ventricle is going to empty completely (SV increases) so ESV decreases
ESV is dependent on what two things? What is it independent of?
Afterload against which the ventricle is contracting and the inotropic state.
But its independent of EDV just prior to contraction.
LVEDV depends on.....
Afterload & Contractility
NOT preload because LVEDV is preload!
What can cause HF?
- Impaired myocardial contractility (Ischemic heart disease & Cardiomyopathy)
- Valvular disease
- Congenital heart disease
- Diseases of the pericardium
- Pulmonary HTN (cor pulmonale)
Explain what forward (systolic) and backward (diastolic) HF is
- Forward failure (systolic): when heart can’t pump blood forward at whatever rate needed to meet metabolic demands.(failure to maintain good EF)
- Backward failure (diastolic): if the heart can only pump blood if cardiac filling pressures are abnormally high
- Both can also occur.
What can cause a significant increase in afterload leading to a reduced EF (systolic HF)?
- Advanced AS
- Uncontrolled severe HTN
What kinds of things can lead to impaired diastolic filling leading to failure with a preserved EF (diastolic failure)
- LV hypertrophy
- Restrictive cardiomyopathy
- Myocardial fibrosis
- Transient myocardial ischemia (could be sys too)
- Pericardial constriction or tamponade
What is more prevalent in the US, systolic or diastolic HF?
Trick Question. In US about 50% of patients fall into each category
She repeated it over and over... Most common cause of RV failure is............
Why are we seeing an increased incidence of heart disease?
d/t aging of population and a lot of interventions that prolong survival, see more people along continuum that we would have before.
What are some causes of impaired contractility leading to reduced EF and systolic HF?
- CAD (myocardial infarction or transient myocardial ischemia)
- Dilated cardiomyopathy (DCM)
- Chronic pressure overload (AS & Chronic HTN)
- Chronic volume overload (Regurgitant valve lesions & High output failure)
Describe how there can be a loss of contractility at the cellular level
but the loss of contractility can be from destruction of myocardial cells (completely destroyed or not functioning normally) and there may be fibrosis
Why are patients with systolic HF prone to arrhythmias?
- Higher risk for conduction defects because of abnormal myocardial cells
- LBBB is common
- Because of the problem w/conduction system, ventricular arrhythmias patient w/systolic HF are at high risk for sudden death.
- Systolic HF. The line, ESPVR, shifts down from 1 to 2 so that systolic emptying stops at higher than normal ESV.
- Ventricle trying to contract but can’t contract all that volume. So more volume is left in ventricle at end of systolle and ↓SV, when the normal blood returning from the pulmonary venous system gets added to ↑ESV we now have a higher than normal EDV (moving to right) this increases preload and according to frank starling, would cause an increase in SV. But problem is now we have defect in contractility, normal compensatory mechanism isn’t effective and we end up w/increased in ESV to an increase EDV that backs up into LA and pulmonary veins causing pulmonary congestion
Which kind of HF has increased prevalence with increasing age?
- Diastolic HF
- The prevalence of this type increases w/age, more than 50% of patient over age 70 have diastolic HF.
What causes diastolic HF?
Impaired relaxation & ↑ stiffness of ventricular wall
**Relaxation is also an active process (energy dependent process).
What kind of defects cause diastolic HF?
- Transient or chronic defect
- Acute MI (transient inhibition of energy delivery & diastolic relaxation)
- LV hypertrophy, Fibrosis, &Restrictive cardiomyopathy (keeps LV walls chronically stiff and unable to relax)
- Pericardial diseases (tamponade), pericardial constriction of some sort that externally limits filling. Pressure from outside the heart, nothing wrong w/ventricle wall of heart itself.
Diastole failure: the LV fills in higher than normal pressure (shift up from 1 to 2). So a patient w/diastolic dysfunction show signs of vascular congestion because that EDP gets transmitted up to LA and pulmonary veins and over to systemic veins as well.
Diastolic failure can be divided into 4 classes, what are they?
- Class 1 – abnormal LV relaxation with normal LAP
- Class 2, 3, 4 – abnormal relaxation plus decreased LV compliance →↑ LVEDP (When this happens chronically, the LAP ↑ in a compensatory way, because ↑LAP that allows for ventricular filling even though the pressure within the LV is increased itself)
Three are most common causes of diastolic HF:
- ischemic heart disease
- longstanding essential HTN
- progressive AS
In contrast to systolic HF, ____more affected that_____ for diastolic HF, but hospitalization and mortality rates are equal for both.
women are more affected than men for diastolic HF
What are the ages for diastolic and systolic HF?
- diastolic: frequently elderly
- systolic: 50-70yrs
What's more common according to sex for diastolic or systolic HF?
- Diastolic: frequently females
- Systolic: more likely male
Describe the EF for diastolic and systolic HF
- Diastolic: presevered (≥40%)
- Systolic: depressed (≤40%)
Describe the LV cavity size for diastolic and systolic HF
- diastolic: usually normal
- systolic: usually dilated
What are the CXR findings for diastolic and systolic?
BOTH have congestion and/or cardiomegaly
What abnormal heart sounds do you hear with diastolic vs. systolic HF? (gallop rhythm)
- Diastolic: S4
- Systolic: S3
Describe HTN & Diabetes in diastolic and systolic HF
- Diastolic: +++
- Systolic: ++
Describe rate of prior MI for diastolic and systolic HF
- Diastolic: +
- Systolic: +++
Describe rate of obesity for diastolic and systolic HF
- Diastolic: +++
- Systolic: +
Is chronic lung disease characteristic of diastolic or systolic HF?
Is sleep apnea more associated with diastolic or systolic HF?
EQUAL IN BOTH! (++)
Is dialysis more characteristic of diastolic or systolic HF?
Describe AF in diastolic and systolic HF
- Diastolic: (+) usually paroxysmal
- Systolic: usually persistant
Regardless of the cause of LV dysfunction, what is the pathophysiology of HF?
- Results in progressive LV remodeling. The remodeling leads to a ↓ EF, dilation w/arrhythmias, progressive HF and premature death likely.
- Non-cardiac factors (like SNS stimulation, vasoconstriction, Na retention by the kidneys) that can be stimulated by LV dysfunction and then contribute to LV remodeling that goes on. Also contribute to symptoms like dyspnea, fatigue, all characteristic of CHF.
What is acute HF?
- Change in Sx requiring emergency treatment
- Sudden ↓ CO → ↓BP but no signs of peripheral edema
What are the 3 clinical entities of acute HF?
- Worsening chronic failure
- New-onset (Valve rupture, Large MI, Hypertensive crisis)
- Terminal heart failure
What is chronic HF?
- Present in patients with long-standing heart disease
- BP usually maintained but venous congestion
What are the causes of RIGHT heart failure?
- Cardiac causes (Left HF, PV stenosis, & RV infarction)
- Pulmonary parenchymal diseases (COPD, Interstitial lung disease (sarcoid), ARDS, &Chronic lung infection)
- Pulmonary vascular diseases (Pulmonary embolism, Primary pulmonary HTN)
Which ventricle is thinned walled and much more compliant, accepts blood at low pressure and ejects against relatively low vascular resistance?
RIGHT (PVR is relatively low)
RV has little difficulty accepting a wide range of volumes, highly compliant, but also very susceptible to failure to sudden increases in afterload like an _________________
acute pulmonary embolism
clinical s/s of heat failure are due to .....
increased ventricular pressure and subsequent accumulation of fluid upstream from affected ventricle
Isolated RV failure is less common, usually reflects ........
- increased ventricular afterload from some sort of pulmonary disease
- If RV disease develops from primary pulmonary process that’s what’s called Cor Pulmonale and that can lead to RV failure.
What are the most common manifestations of RV failure?
Peripheral edema and congestive hepatomegaly
Most common causes of low output HF...
- CAD, cardiomegaly, HTN, valve disease, and pericardial disease.
- CO may be essentially normal at rest but doesn’t respond adequately during stress.
Most common causes of high output HF....
- anemia, pregnancy, AV fistulas, severe hyperthyroidism.
- In this case the ventricle fails because of increased HD burden and also often direct myocardial toxicity possibly by thyrotoxicosis and myocardial anoxia from anemia.
What are the three compensatory mechanism for HF?
- Frank Starling
- Ventricular remodeling
- Neural hormonal changes (SNS, etc.)
Frank Starling will help compensate to a point, why is it limited?
- If HF severe, contractile markedly depressed, curve may be almost flat.
- So any augmentation of CO because of preload is somewhat decreased in its ability to help the situation and of course that additional volume gets reflected back into LA and lungs and pulmonary congestion results. Moving up on the curve will further increased in EDV will just lead to pulmonary congestion
Ventricular remodeling and hypertrophy is helpful to a point, but then what happens?
- Increased muscle mass is stiff and less compliant.
- So initial benefits come at the expense of higher than normal diastolic pressure (LVEDP), and again back up in LA, pulmonary veins, and so on.
Neural Hormonal system consist of what 5 things?
- Adrenergic Nervous System
- Renin-Angiotensin-Aldosterone System
- Natriuretic Peptides
- Other Peptide
Overall, how does the neural hormonal system work?
- Increase systemic vascular resistance which will help maintain perfusion to vital organs even in setting of decreased CO.
- (BP = CO x total peripheral resistance) so help to balance & maintain BP in early stages of HF.
- These neurohormonal changes will also result in Na & H20 retention, ↑ intravascular volume and preload, goes to maximize SV (FS)
What is important to remember about the neural hormonal changes?
These neural hormonal changes are acutely beneficial but often harmful to failing heart and ultimately contribute to a more progressive downhill course.
How does the adrenergic NS system help comepensate
- ↓CO gets sensed by baroreceptors in carotid sinus and the aortic arch.
- (sense ↓ BP, so ↓rate of firing, a signal goes to vasomotor control center in medulla, & get a sympathetic discharge and a ↓ parasympathetic tone).
- ↑HR, ↑ contractility, (which ↑ CO)
- and vasoconstriction from alpha stimulation.
- If we get venoconstriction, ↑venous return, ↑preload, ↑ SV (FS).
When is the adrenergic NS not going to help compensate?
- Works as long as heart is able to function on ascending part of curve, if we get on flat part of curve, its’ not going to help SV.
- So constriction can be venous or arteriolar. Arteriolar will increase SVR. That will help maintain perfusion pressure and direct circulation to vital organs (heart and brain) at the expense of things like the skin.
How does the RAAS get activated in HF?
- Activated early in patient w/HF.
- Stimuli for renin secretion:
- 1) (juxtaglomerular cells in kidney) ↓renal artery perfusion pressure from low CO
- 2) ↓Na delivery to macula densa (because of altered HD within the kidney ↓ perfusion)
- 3) Direct stimulation of beta 2 receptors in kidney by the activated SNS.
How does the RAAS compensate for HF?
- Renin secreted, goes though RAAS
- Angiotensin II is potent vasoconstrictor, ↑
- resistance and helps maintain BP.
- Angiotensin II also does a few things to ↑
- IV volume : 1. Hypothalamus, stimulate thirst so ↑H2O intake 2.↑ aldosterone secretion from adrenal cortex, which causes Na and H2O reabsorption.
- ↑ preload, (FS),↑CO.
- IF patient is on ascending part of the curve
How does ADH help compensate for HF?
- Baroreceptors sense, and then send signal. Release ofADH causes water pores to be inserted, ↑ water reabsorption from renal tubules, again ↑ preload and CO.
- Also it’s a vasoconstrictor and that will ↑BP.
- Initially good. But result in adverse consequences. Patient in HF don’t’ want retaining water so eventually these things become counter productive
How do the natriuretic peptides
- Hormones secreted in HF (ANP & BNP).
- The action of these hormones (mediated by specific receptors) is opposite to the other hormone systems that get activated.
- Result in excretion of Na and water, vasodilation, inhibition of renin, and they’re antagonistic to the effect of angiotensin II on aldosterone and vasopressin levels.
- Helpful but not enough to overcome the deleterious effects of the other hormones.
Where is ANP and BNP stored and when are they released?
- ANP is stored in atrial cells, released from atrial distention.
- BNP is not detected in normal hearts but is produced when myocardium of the ventricle is subjected to stress of some sort (like HF or MI) relationship between serum BNP levels and clinical severity of HF.
Sue listed Endothelin I under other peptides for the neural hormonal compensation. How does Endothelin I work?
- Endothelin I = potent vasoconstrictor
- Comes from endothelial cells that line all the blood vessels.
- In HF patients, the plasma concentrations of Endothelial will correlate w/severity of disease and w/adverse outcomes.
- Develop some drugs to try and offset the effects of endothelin but long term benefits haven’t been demonstarted yet
What two ways do we get myocyte loss and cellular dysfunction in HF?
What two things can cause cell necrosis and cause myocyte loss and cellular dysfunction in HF?
- Myocardial infarction
- Cardiotoxic drugs (Doxirubicin)
What is apoptosis and what triggers this?
- Programmed cell death (genetic instructions that will activate various pathways in the cell that will cause cells to fragment and undergoes phagocytosis from other cells without a preceding inflammatory response)
- Triggers include: ↑ catecholamines, Angiotensin II, Inflammatory cytokines, & Mechanical strain from wall stress.
TRUE or FALSE. Even viable myocardium in HF is abnormal.
TRUE. (ultrastructural and molecular level)
All of this neurohormonal activation and inflammatory cytokines are believed to alter the genetic expression of the contractile proteins (those ion channels) & receptors, that are important in the excitation retraction coupling. So they alter the energy production involved w/excitation contraction coupling.
What two things are important in myocyte loss and cellular dysfunction?
- Decreased ability to maintain Ca+ homeostasis
- Changes that occur in both production and energy utilization (ATP).
- Not completely clear how it all fits in, it’s an area of current research
What are the 6 Factors Precipitating Symptoms in Chronic Compensated Heart Failure?
- 1. Increased metabolic demands (Fever, infection, anemia, ↑HR, pregnancy, hyperthyroidism)
- 2. Increased circulatory volume (↑ preload d/t ↑Na intake, administer too much IVF, & renal failure)
- 3. Conditions that increase afterload (uncontrolled HTN and PE)
- 4. Conditions that impair contractility (neg. inotropes, MI, chronic alcohol abuse)
- 5. Failure to comply with medication regime
- 6. Excessive bradycardia
What are the clinical manifestations of Left HF?
- Paroxysmal nocturnal dyspnea
- Tachycardia, Tachypnea
- Loud P2 (pulmonic component of S2)
- S 3 gallop (systolic dysfunction)
- S 4 gallop (diastolic dysfunction)
What are the clinical manifestations of RIGHT HF?
- Peripheral edema
- RUQ discomfort (from hepatic enlargement)
- Clinical Findings:
- Peripheral edema
What are some other signs of low forward flow that Sue mentioned in class?
- Altered or dull mental status (from ↓ cerebral perfusion)
- ↓u/o from ↓ renal blood flow
- Nocturia (blood flow redistributed to kidney in supine position)
- Fatigue because less flow to skeletal muscles, patient feels weak and fatigued.
What causes Paroxysmal nocturnal dyspnea?
Severe breathlessness wakes patient up from sleep, from fluid reabsorption d/t supine position (usually 2-3 hrs after falling asleep)
Normal LAP is 10, if the LAP is 15mmHg or more what will you see on the CXR?
- CXR shows upper zone vascular redistribution.
- The vessels supplying the upper lobes are larger than those supplying the lower lobes.
- Edema is more prominent in lung bases, where hydrostatic pressure is highest
What are Kerley B lines? when do they show up on CXR?
- Short linear markings in periphery of lower lung fields and indicate intralobar edema.
- Show up when LAp exceeds about 20mmHg and represent interstitial edema.
- Can progress (if Lap exceeds 25-30) can be opacity of air spaces.
How do patients w/chronic HF accomodate higher pressure w/out changes in CXR?
There’s often increased lymphatic drainage, Relationship w/LAp and CXR findings is somewhat altered or attenuated in the patient w/chronic HF.
CXR findings of pulmonary edema can lag about ___ hrs behind clinical evidence.
BNP is important marker, BNP assays will correlate well w/degree of LV dysfunction and prognosis. Elevated BNP can distinguish HF from other cause of dyspnea like pulmonary lung disease. What are the level ranges and what do they indicate?
- Plasma BNP levels of less than 100 = HF unlikely.
- If level is between 100-500 = intermediate probability for HF
- If level is above 500 = consistent w/diagnosis of HF.
What are the 4 New York Heart Association Classifications of Chronic Heart Failure?
- I: No limitation of physical activity
- II: Slight limitation of activity. Dyspnea & fatigue with moderate exertion (i.e. walking upstairs quickly)
- III: Marked limitation of activity. Dyspnea
- with minimal exertion (i.e. slow walking upstairs)
- IV: Severe limitation of activity. Symptoms
- are present even at rest
Why are the NY heart association classifications helpful?
because severity symptoms has excellent correlation w/survival and quality of life.
What are the 4 stages of Stages of Chronic Heart Failure? (these help guide treatment)
- A: Patient who is at risk of developing heart failure but has not yet developed structural cardiac dysfunction (i.e. patient with CAD, HTN, or family history of cardiomyopathy)
- B: Patient who has structural heart disease associated with heart failure but has not yet developed symptoms
- C: Patient who has current or prior symptoms of heart failure associated with structural heart disease
- D: Patient who has structural heart disease and marked heart failure symptoms despite maximal medical therapy and requires advanced interventions (i.e. cardiac transplantation)
Prognosis of HF is dismal in the absence of correctable cause. Progressive disease unless something identified that’s correctable. 5 year mortality after dx is ____%.
Naturally patients w/worst or most severe symptoms (NYHA 3 and 4) do the worst and have a 1yr survival rate of only ___%.
Greatest cause of mortality is ________ HF, many die from associated _______arrhythmias
Which is worse, diastolic or systolic HF?
- They actually have similar rates of hospitalization, in hospital complications and mortality.
- Systolic is not necessarily worse in this case.
What lab tests can help identify HF?
- ↑BUN & creatinine levels
- ↓ Na and ↓ K levels
- High BNP
- Severely depressed EF
- Limited exercise tolerance, and often multifocal PVCs.
Treatment of Heart Failure with ↓ EFSystolic Heart Failure. 5 Main goals of treatment are:
- 1. Identify & correct underlying cause (Replacing incompetent valve or coronary revascularization, aggressively tx untreated HTN, or d/c alcohol consumption)
- 2. Eliminate acute precipitating factors (Infection or arrhythmia. ↓ Na intake. Maybe medication adjustment. d/c NSAIDS!)
- 3. Symptom management (Na+ restriction, diuretics, promote forward flow w/vasodilators & inotropic support)
- 4. Modulate neuroendocrine response (Limit the progression of remodeling and LV dysfunction)
- 5. Prolong long-term survival
How do diuretics help tx HF? Why should we use caution?
- Relieve the vascular congestion in the pulmonary and peripheral edema ( faster than any other drug) by ↓ preload and EDP.
- ↓hydrostatic force causing pulmonary congestion to begin with.
- Use diuretics carefully so they don’t significantly ↓ SV And CO.
- In HF, on flatter part of curve,so not substantially ↓ SV & CO by ↓ preload.
- If you overly diurese, on steeper part of curve and will effect SV and CO.
Which diuretics are most potent?
- Diuretics that act primarily on loop of Henle (Lasix) are most potent.
- Thiazide (hydrochlorothiazide) are useful but less effective especially in setting of decreased renal perfusion.
Why are we worried about arrhythmias w/diuretics?
Diuresis can also cause electrolyte abnormalities (low K and low Mg) can cause arrhythmias in patient already prone to arrhythmias.
Nitrate is a vasodilator, how does it work?
- Venous dilators, ↑ venous capacitance, ↓venous return & ↓preload.
- Improve the pulmonary congestion as long as patient is on flat part of the curve.
- If patient is on steeper part of curve, venodilation may have too much of impact on HR, SV, CO and BP
Hydralazine is a vasdilator, how does it work?
- Pure arteriolar vasodilators. ↓ SVR & afterload → ↑ SV & shift curve up.
- Although an arterial vasodilator would ↓BP (don’t want if pt is already hypoTN) this doesn’t usually happen.
- The ↓SVR usually results in an ↑ CO so BP is constant or only slightly decreased.
RAAS inhibitors (ACE I and ARBs) are vasodilators. How doe they work?
- ACE I specifically have been found to limit ventricular remodeling. They will improve stamina, ↓ need for hospitalization and extend survival in pt w/HF and ↓ EF.
- ARB provide more complete inhibition of whole system but not shown to be more beneficial so usually reserved for pt that can’t tolerate ACE I (cough).
- Can get balanced vasodilation if you combine one of the nitrates w/hydralazine but in general the RAAS inhibitors are superior
_____are the standard 1st line chronic therapy in pt w/LV systolic dysfunction.
Who are inotropes good for?
- Shifts curve up to point C.
- For given preload, SV And CO would be increased.
- So drugs useful for patient w/decreased EF but not really effective if EF is already well preserved.
Beta agonist (inotrope) is only used for temporary support, why?
One reason they can only be given IV and another reason continued administration causes down regulation of adrenergic receptors so the effectiveness of the IV administration declines overtime.
What is a common phosphodiesterase inhibitor (inotrope) and why is it's use limited?
Milrinone. It’s limited to treating acute HF because even though it’s given IV (thought there was a promising PO version of the drug but it hasn’t proven to be so promising)
Digoxin (inotrope) is still used. What is it good for?
Digoxin is old but still useful. IV or PO. Digoxin improves symptoms but doesn’t really improve long term survival. Also useful if patient is in AF.
How are BB good for tx HF?
- Historically contraindicated because of negative inotropes.
- But new studies say they have some benefit in augmenting CO and improving survival.
- Not clear how it works but maybe decreasing HR is beneficial.
- Also blunting chronic SNS activation that as we know is initially good then not so good.
How are Aldosterone antagonist,such as Spirolactone (Aldactone), good for treating HF?
- Evidence that aldosterone itself contributes to cardiac fibrosis and remodeling.
- Need to follow K carefully, esp. if on ACE I.
- Trials show if patient already taking ACEI and diuretics, and aldosterone antagonist was added, that mortality decreased & symptoms improved.
Why are statins useful in HF?
Anti inflammatory, lipid lowering effect may decrease morbidity and mortality n patients w/systolic failure.
- Failing heart – point “a”
- Diuretics – point “b”(Also venous dilation)
- Inotropes – point “c”
- Vasodilator (balanced or arteriolar) – point “d”
- Inotrope + vasodilator – point “e”
Chronic anticoagulation is used in HF, why?
Prevent intracardiac thrombus formation if systolic dysfunction is severely impaired. It is somewhat controversial if not another reason for anticoagulation. But it has been tested in clinical trials. If EF is seriously decreased
___________ is anti-arrhythmic is most effective in suppressing ventricular arrhythmias and least likely to provoke other rhythms disorders but not improved survival benefit from it.
Patients may benefit from an implantable cardio defibrillator even if they don't have a history of arrhythmias, why?
- Particularly indicated if patient has chronic ischemia or non-ischemic cardiomyopathy (dilated) and at least moderately reduced EF (less than or equal to 35%).
- So an ICD may be helpful even if patient doesn’t have arrhythmias because it decreases the likelihood of sudden death in this patient population.
What is cardiac resynchronization therapy?
- Patient also have intraventircular conduction defects: L bundle is common. So fact L and R ventricle aren’t coordinate will contribute to cardiac symptoms. So if you can re-coordinate so ventricles contract together, it help can help LV systolic dysfunction.
- Referred to as cardiac resynchronization therapy (appropriate for select patients w/ advance diastolic dysfunction like EF less than or equal to 35% or pt w/prolonged QRS or continued symptoms of failure on maximum drug therapy.
ACCHA guidelines for tx of Stage A HF
High Risk with no symptoms so lifestyle modification (diet Na restriction, weight control, control blood sugar, reduce alcohol consumption) patient and family education
ACCHA guidelines for tx of Stage B HF?
- Structural heart disease, no symptoms
- Tx HTN, diabetes, dyslipidemia, ACEI or ARBs
- (BB for select patients in the next step)
ACCHA guidelines for tx for Stage C HF?
- ACEI and BB in ALL Patients
- Dietary Na restriction, diuretics, and digoxin
- Cardiac resynchronization (if BBB present)
- Revascularization (MV surgery)
- Consider multi-disciplinary team
- Aldosterone antagonist, nesiritide
ACCHA guidelines for tx of Stage D HF?
Treatment of Heart Failure with Preserved EF (Diastolic Failure) Goals:
- Goals of treatment: Relief of pulmonary & systemic congestion and Address correctable causes (HTN &CAD)
- Treatment: Diuretics. Careful not to under fill LV (it’s stiff and needs higher than normal pressures). So if we excessively diurese, decreased ventricular filling, decreased SV.
- Unlike patients w/impaired systolic function, BB, RAAS-I have not shown mortality benefit. Inotropes don’t’ work because EF preserved
Diastolic Heart Failure Management Strategies
- Prevent development by ↓ing risk factors (Treat CAD, HTN, DM & Weight control)
- Allow adequate LV filling by ↓ing HR (Beta blockers, calcium channel blockers, & digoxin)
- Control volume overload (Diuretics, long-acting nitrates, low sodium diet)
- Restore & maintain SR (Cardioversion, amiodarone, & digoxin)
- Decrease ventricular remodeling (ACEI, statins)
- Correct precipitating factors (AVR, coronary revascularization)
What is the eitiology of acute HF?
- Previously asymptomatic pt with CAD, severe HTN, or acute valve regurg
- Compensated pt decompensates
What are the treatment goals in acute HF?
- Normalize filling pressures
- Restore tissue perfusion
- Identify appropriate profile for the patient and that helps guide treatment in terms of need for diuretics, vasodilators, and so on
What are the 4 types of acute HF?
- Profile A: warm & dry
- Profile B: warm & wet (↑LV filling pressures, congestion)
- Profile C: cold & wet (↑LV filling pressures, congestion, ↓CO, & vasoconstriction)
- Profile L: cold & dry ( ↓CO, & vasoconstriction) but don’t have signs of vascular congestion. So this patient may be volume depleted or have limited cardiac reserve but in the absence of volume overload.
Acute Pulmonary Edema Cardiogenic
- Cause is cardiac in origin pulmonary edema (As opposed to negative pressure pulmonary edema)
- Can appear suddenly in asymptomatic patient
What causes acute pulmonary edema (of cardiogenic origin)?
- left-sided heart failure↑ capillary hydrostatic pressure →fluid accumulation in interstitium & alveolar spaces
- If LVEDP > 25 mmHg if normal oncotic pressure
What are the s/s of acute pulmonary edema (of cardiogenic origin)?
- Hypoxemia due to shunt
- Severe dyspnea & anxiety
- Profiles “B” & “C” (Frothy sputum, Rales & wheezes)
- (Cold clammy increased SNS stimulation = profile C)
What is the treatment of acute pulmonary edema "LMNOP"?
- Lasix (↓preload→↓PCWP)
- Morphine (↓anxiety & ↓venous return)
- Nitrates (NTG)
- Oxygen (via FM)
- Position (↑HOB to↓venous return)
Is acute pulmonary edema a life threatening emergency?
What is the goal of treatment for acute pulmonary edema?
- Improve oxygenation
- Eliminate underlying cause
What is another treatment option for acute pulmonary edema of cardiac origin if LMNOP doesn't work?
Mechanical devices – IABP, LVAD
What is the single most important risk factor for predicting perioperative cardiac M & M
Heart Failure!!! Wouldn't do elective surgery on someone in CHF or acute pulmonary edema
Pre-operative anesthesia considerations include identify precipitating causes & treat aggressively pre-op (before elective surgery) and medication management. What would you do for med management?
- D/C diuretics day of surgery
- Continue beta blockers (BB decrease morbidity and mortality)
- D/C ACEI/ARB --controversial.Can usually be d/c day of or day before. Increased risk of intraoperative hypotension. ACEI-given to decrease risk of ventricular remodeling in HF and prevent renal dysfunction in diabetic pt, stopping for 1 day won’t have huge impact on that.
- Digoxin-continue day of surgery.
- All lab tests, particularly electrolytes need to be carefully evaluated.
What is the intraoperative management of CHF?
- Adjust drug dosing
- Opioids beneficial – inhibition of adrenergic activation
- Positive pressure ventilation & judicious PEEP improves oxygenation
- Monitor according to complexity
- Regional + OK
- Additional cautions with transplanted heart
With a transplanted heart, what are some other intraop considerations we need to think about?
- long term immunosuppression
- The transplanted heart is denervated, increased HR can only be achieved w/direct acting beta agonist like Epi.
What should we do for post-op management for a pt w/HF?
- Treat pain aggressively
- Restart usual meds ASAP
What would you like to do?
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