What is heart failure
A complex clinical syndrome Result of any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood NOT necessarily “congestive” heart failure HF is a progressive disorder There is tremendous clinical heterogeneity
Poor prognosis of outcomes for heart fail pts:
repeat hospitalizations
What intrinsic factors contribute to CO?
Contractility and heart rate
What extrinsic factors contribute to CO?
Preload and Afterload
Heart Rate effects of Cardiac Output Tachycardia______ diastolic filling time.
decreases --> issue bc in heart fail we increase HR bc we need more blood but this will decrease diastolic fill time thereby reducing CO
Why is it an issue for pts with diastolic dysfunction to have tachycardia?
bc the heart fills with blood during diastole, if we have tachycardia, we decrease time spent in diastole.
In heart fail pts, impaired contractility leads to inability to handle volume thus ______ increases
CVP
What is La Places law?
Wall stress = Pressure x radus/ 2x wall thickness
In heart fail, pt experiences increase pressure, as a result what happens to the heart?
(think about La Place's Law)
wall stress = Pxr/2h
h is wall thickness, as P increases, we would increase wall stress. To resist increase in wall stess, the heart with increas it's wall thickness, h, via hypertrophy. After a certian point, it cannot hypertrophy anymore and we end up with decreased CO
CO = HR x SV thus as heart beast faster, we should increase CO. But this isn't quite the case... why?
as HR increases, it has a shortened diastole, thus HR can affect SV (bc SV is determined by diastolic filling time)
If HR is increased enough to decrease SV, what happens to preload and afterload?
Preload will decrease in response to decreased SV... afterload can change to compensate for decreased SV
When does active reuptake of Ca+ back into teh SR occur?
Diastole
How can increase in HR be a bad thing for pt with heart fail?
Pt with tachycardia and heart fail is bad because these pts depend on a longer diastolic filling time to generate adequte SV. When we see heart fail pt with tachycardia, it means they have no other way to generate CO except increase in HR
The amount a contracting heart must overcome to eject blood into the vasculature
afterload
Assuming no change in CO, when vasculature is contracted, more blood remains in arterial circulation... What happens to venous pressure?
Venous pressure decreases with each stroke
When afterload is reduced via vasodialation, flow across the systemic circulation is enhanced and central venous pressure will....
Increase
As a failing heart dilates ts wall stress increases. _________ is a compensatory mech for chamber dilation
Ventricular hypertrophy
Diuretics work to decrease __________ in order to decrease afterload in heart fail pts with compensatory hypertrophy
LV end diastolic pressure
•Sodium content in diet
• Excessive fluid intake
• Renal failure
all contribute to increased:
Preload
• Uncontrolled Hypertension
• Pulmonary embolism
• Severely dilated ventricle
all contribute to
increased AFterload
•Increased metabolism
•Fever
• Infection
• Anemia
• Tachycardia
• Hyperthyroidism
• Pregnancy
•Slow heart rate
all contribute to
increased HR
Acute MI
• Negative
Inotrope
• Alcohol
all contribute to
decreased contractility
What are the key components of the cycle of congestion in AHF
Myocardial ischemia--> worsening HF--> elevated LVEDP--> increased wall stress adn increased functiona MR--> myocardial oxygen deman--> back to ischemia
Role of the physician in Acute Heart Fail pts.
1. Identify the etiology of acute heart failure
2. Appropriately treat acute heart failure to achieve a stable hemodynamic equilibrium.
3. Reverse (if possible) the exacerbating stimulus.
Assesment we need to perform on pt with AHF
• History and Physical Examination
• Laboratory Testing
• Echocardiogram (Non-Invasive Imaging)
• Swan-Ganz Catheter (Invasive hemodynamics)
What are some key questions to ask for in pt history in pt with AHF?
What do you eat for breakfast, lunch, dinner, snack, restaurants?
Do you weigh yourself every day?
How far can you walk?
How many pillows do you sleep with? Do you wake up short of breath?
Any recent changes to your medication?
Do you have chest pain?
What types of murmurs will we hear on pt with AHF?
Mitral regurgitation (Don’t rule out papillary rupture)
Crescendo-decrescendo murmur of Aortic stenosis
S3 Gallop
P2 “knock” suggests RV volume or pressure overload
P2 “knock” suggests
RV volume or pressure overload
Crescendo-decrescendo murmur is classic for:
Aortic stenosis
What are findings seen in AHF pts as far as:
jugular veins
pulmonary exam
pulse rates
Distended jugular veins
Pulmonary: Tachypnea, inspiratory crackles
Lower extremity edema
Decreased pulses intermittent pulses
Your attending tells you to get the BP of a pt recently admitted for AHF, you get a SBP of 110mmHg... is this concerning?
Hypotension: SBP <115 mmHg predictive of increased mortality on presentation
Pt with ACF will be
hot and sweaty or cold and clammy
Bradycardic or tachypnic
Cold clammy skin
Tachycardia
What are the two best predictors of event free survival in AHF pts?
third heart sound and JVP... if we can't make these go away, prognosis is very bad.
What is Brain natiuretic peptide or Nt-pro-BNP a marker of
Produced in the atria and ventricles in response to stretch.
When we get a basic metabolic panel in AHF pts, what are we assessing? What are our key markers?
Assess renal function and electrolyte imbalance
Elevated BUN (>43mg/dL) and elevated Creatinine most predictive of increased risk of mortality.
Why do we perform a CBC in AHF?
Evaluate for anemia or hemoconcentration
Chest X Ray is taken in pt with AHF to check for:
pulmonary edema
When we need to find out the mixed venous O2 saturation, where do we draw it from?
Drawn from PA catheter, <70%
Troponin levels are used for what purpose in AHF labs?
Risk Stratification and Diagnostic tool
Elevated troponin levels in HF are common and predictive of death
What is the significance of getting an Echo in pts with acute decompensation?
Assists in identifying the cause: Wall motion, valve dysfunction
Assist in patient risk stratification.
Can give some estimates of hemodynamics:
Monitor progress of therapy.
Ejection Fraction can give a rough idea about cardiac function, however a
patient can have a “normal “ EF and be in acute decompensated heart
failur
What hemodynamic estimates do echo's provide?
Right Atrial Pressure
Cardiac Output
Left Atrial Pressure ( E/ e’)
Left ventricular dimensions and volumes
How beneficial is knowing EF in a heart fail pt?
Ejection Fraction can give a rough idea about cardiac function, however a patient can have a “normal “ EF and be in acute decompensated heart failure
When do we consider a PA catheter?
• Uncertain fluid status, perfusion, systemic or
pulmonary vascular resistance
• Hypotension or worsening renal function with empiric therapy
• Evaluation of candidacy for VAD or transplant
• Presumed Cardiogenic Shock
• Severe clinical decompensation with uncertain
hemodynamic profile
• Apparent inotrope dependence or refractory
symptoms
Key signs and symptoms of congestion or 'wet' symptoms
Orthopnea/PND, JVD, Ascities, edema, rales
Evidence of low perfusion or 'cool' symptoms
narrow pulse pressure, sleepy, low serum Na+, cool extremeties, hypotensive w/ ACE inhibitor, renal dysnfunction
Wedge pressure translates to:
LV end diastolic volume
High Wedge pressure =
Too much volume in Left Ventricle
Too much volume in Left Ventricle =
a. Too much preload
b. Not enough stroke
volume
Key findings in 'Dry' patient
PCWP < 18 AND RA PRESSURE < 8
key findings in 'wet' pt
PCWP > 18 OR RA PRESSURE > 8
Warm patient will have cardiac index:
WARM= CARDIAC INDEX> 2.2
Cold pt will have cardiac index:
COLD= CARDIAC INDEX < 2.2
Hemodynamic goal for Right Atrial Pressure:
< 8 mm Hg
Hemodynamic goal for Pulmonary Capillary Wedge
< 16 mmHg
Hemodynamic goal of Systolic Blood Pressure
> 80 mmHg
What is our hemodynamic goal for SVR?
SVR – not a goal in itself, but if diastolic filling
pressures are high consider reducing to 1000-
1200 dynes/sec/cm.
Cold and Dry is EXTREMELY RARE PRESENTATION
* REQUIRES PA CATHETER PLACEMENT TO
EVALUATE FILLING PRESSURE
– PCWP<12 AND RA<6:
– PCWP >16:
– PCWP 12-16 + RA PRESSURE NORMAL:
– PCWP<12 AND RA<6: DC DIURETICS, PO FLUIDS
– PCWP >16: PROFILE C
– PCWP 12-16 + RA PRESSURE NORMAL:
• VASODILATORS , IABP, AND INOTROPE ARE
TEMPORARY FIX
• NEEDS VAD/ TRANSPLANT EVALUATION
• 27 YO F, presents to PCP with 2 weeks of “no energy”, abdominal bloating, early satiety.
• Had an completed an uneventful pregnancy 8 weeks prior
• Vitals: BP 86/62, HR 110 BPM, RR 18, afebrile, BMI 20
• PE: Tachycardic, regular, soft S1, prominent P2, II / IV HSM L MSB, PMI diffuse and laterally displaced
• No edema, pulses +1
• Labs reveal Na+ 129, ALT 134, AST 189, rest normal
Diagnosed with likely cholecystitis, RUQ US ordered.
On hospital day 2, develops respiratory distress, desaturates to 88% O2 sat
on BiPap.
• Subsequently requires intubation and mechanical ventilation
What do you want to do next?
STAT Echo shows LVEF 18%, moderate – severe mitral regurgitation, LVEDd
7.2cm.
• PA Catheter placed:
You place a PA cath in a pt and get these results; which are concerning?
• PA Catheter placed:
• RA 25
• RV 55/28
• PA 54/32
• PAWP 30
• SVO2 28%
• PA Catheter placed:
• RA 25; normal is 0-5; this is elevated = wet
• RV 55/28; 28 correlates with RA ressure and this is fine
• PA 54/32: this is slightly elevateed
• PAWP 30; normal is 6-12; this is elevated meaning high filling pressure
• SVO2 28%; mixed CO; this is super low (normal is 70% or higher) so blood is circulating slow
Pt presents and your attending says he is in AHF; and it is Cold and Wet
What do you expect the PCWP to be?
What do you expect the CI to be?
WET = CONGESTION (PCWP>18)
COLD = INADEQUATE PERFUSION (CI<2.2)
Tx for patient with ACF defined as Cold and Wet
YOU MAY NEED TO WARM THEM UP BEFORE
DRYING THEM OUT
Diuresis to improve CO, but may not be possible if renal perfussion is severely impaired
Use: vasodialtor (maybe inotrope) and check SVR and look at BP
For AHF pt we use the follow drugs, why?
Diuretics:
Vasodialtors:
Ionotropes:
Diuretics reduce fluid volume
VasoD will decrease preload or afterload
Ionotropes will augment contractility
Key drugs to tx 'wet' symptoms
Vasodialators: nitroprusside, nitroglycerin and nesiritide
Pt is 'Cold and Wet' with PCWP low or normal and decreased CI... what do you tx with?
Ionotropic drugs: dobutamine, milrinone, Ca sensitizers
Ionotropes are not always a great choice in AHF pts... what three things would suggest use of ionotropes?
1. Advanaced systolic HF + low output syndrome + hypotension
2. Vasodialtors are either ineffective or contraindicated
3. Fluid overload and non-responsive to diuretics or they get deteriorating renal dysnfuction
Why do we consider ionotropes 'double edeged swords' when tx heart fail pts?
Heart failure leads to impaired calcium handling
Inotropes to increase calcium ... YET increased Calcium leads to increased work and arrhythmia
Phosphodiesterase inhibitor administered as an iv infusion
Considered an inodilator because it is an inotrope and a vasodilator
Increases contractility and decreases afterload
No significant increase in myocardial oxygen consumption
Milrinone
Side effects of Milrinone
Hypotension: Can be attenuated by with holding
bolus, Arrhythmia, Tachycardia
Ultimately milrinone will:
Increases contractility and decreases afterload