Heart Failure #1 Flashcards
A 45-year-old woman presents to the ED with complaints of worsening shortness of breath for the past week. The patient reports dyspnea on exertion after walking only 2 blocks, when walking upstairs, and sometimes at rest. Additionally, she is experiencing orthopnea and paroxysmal nocturnal dyspnea. She reports a viral illness 2 weeks ago, during which she had a runny nose and body aches. She took herbal tea for a few days, and the symptoms resolved. The patient denies any palpitation, fever, recent travel, sick contacts, or joint pains. Review of systems is otherwise unremarkable. She no past medical history, and past surgical history is significant for appendectomy. She denies use of tobacco, alcohol, or recreational drugs. She lives with her 2 kids and works for a software company. No significant family history is reported. She only takes cetirizine and multivitamins at home.
On arrival, her vital signs are stable, with a blood pressure of 127/70 mm Hg, pulse of 83 bpm, respiratory rate of 17 breaths/min, temperature of 37.1°C (98.8°F), and oxygen saturation of 96% on room air. PE is otherwise unremarkable except she appears lethargic. CV and resp examinations are unremarkable. Lab results show significantly elevated troponin and pro-B-type natriuretic peptide. ECG shows nonspecific ST/T–wave changes. Chest radiograph shows enlarged heart shadow. The patient is admitted to the telemetry floor for further workup.
How would you manage this case?
Orthopnea
paroxysmal nocturnal
Viral illness
young
Elevated biomarkers,
GET AN ECHO, so that you can look for wall abnormalities, dilated cardiomyopathy, ESSENTIAL to figure out.
Cardiomyopathy cause of heart failure
What does heart failure often mimic?
COPD
can hear crackles
Is heart failure a disease?
NO
it is a syndrome as a result of a disease process - which is why it is important to know the UNDERLYING cause if possible
What leads to heart failure?
clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.
eventually the compensatory mechanism does not work, and you get fluid overloaded
who has the highest risk of heart failure?
AA
What is the 5 year mortality rate of heart failure?
5 years :(
MC cause of death from heart failure?
Sudden cardiac death
Arrhythmias - stretched out LV can cause sudden death
Risk factors for heart failure
CAD / Atherosclerosis
DM
HTN
Metabolic syndrome / Obesity
labs for heart failure patients
HbA1c
lipids
TSH/T4
Biggest risk factor for heart failure
HTN!
in both men and women
2nd biggest risk factor for Heart failure in MEN
MI
Acute vs chronic heart failure
Acute: Symptoms began within last few days to weeks
Shortness of breath, PND, orthopnea, and RUQ pain
NOT compensated well in acute
Chronic: Symptoms present for months
Fatigue, anorexia, abdominal distention and edema
Can have an acute exacerbation in a chronic state
COMPENSATED well in chronic
(increased salt intake can cause acute on chronic)
How vs low output HF
High: heart is unable to meet the demands of the peripheral needs
Thyrotoxicosis, severe anemia, sepsis
Symptoms of reduced CO rather than volume overload
Low: insufficient forward output
Reduced EF, hypovolemia
HF with reduced LV EF vs HF with preserved EF
HFrEF → AKA HF with reduced EF (systolic)
EF ≤40% (lower or right at)
HFpEF → AKA HF with preserved EF (diastolic)
EF ≥ 50%
if 41-49%, it is harder to manage
How do you determine the ejection fraction (EF)?
ECHOOOOOO
it is interpreted by humans, so the EF may be +/- 5-10% (FYI)
Systolic HF is due to
decreased CONTRACTILITY because we are unable to get blood OUT
Diastolic HF is due to
What is the EF as a result?
STIFF ventricle
does not effect ejection fraction, because it has nothing to do with getting blood out of the ventricle to the aorta, meaning that EF is preserved!
What causes Left sided HF and what symptoms?
cardiomyopathies
Leads to DOE, PND, orthopnea, fatigue
because your body is not getting enough blood and you have less energy
What causes Right sided HF and what are the symptoms
Left sided HF!
(also
Often leads to ascities, JVD
Left vs right sided HF symptoms
Left: cool, pale extremeties, cyanosis
Right sided: ascities, weight, weight gain ect
How do you classify severity of heart failure?
New York Heart Association (NYHA) functional classes
It is based on effort needed to elicit symptoms in a HF patient
What are the different classifications of severity
Patient can change classifications
1: Heart disease but no limitation of physical activity
2: Heart disease and symptoms with ACTIVITY
3: Heart disease and symptoms with ACTIVITY
4: Heart disease with symptoms at rest.
not going to ask to differentiate between 1 and 2
What are the stages of heart failure?
Progressive and DO NOT change, because this has to do with the physical structure of the heart
What are the ACC/AHA stages of heart failure
A: At risk for HF but NO STRUCTURAL disease or symptoms of HF
B: Structural heart disease WITHOUT s/s of HF.
C: Structural HF symptoms at some point
D: Refractory HF (have difficult functioning
symptoms of heart failure
increased symptathetic NS
Pulmonary and systemic venous congestion
Cardiac dilation and hypertrophy
increased preload
sodium and water retention
increased afterload
Neurohormonal adaptations of heart failure
Compensatory mechanisms used by the body in an attempt to adjust for a reduction in cardiac output
Maintain systemic pressure by vasoconstriction
Restores cardiac output by increasing myocardial contractility and heart rate
Occurs with systolic and diastolic dysfunction
What does the RAAS system do?
Try to increase volume through
Renin
angiotensin
aldosterone
Allows you to increase preload so that you can have more blood flow
Epinephrine increases the heart’s contractility
How to combat the RAAS system?
ACE/ARBs
problem with compensatory mechanism of heart failure
It is good short term to increase preload and blood to the heart, but overtime the heart will lose myocytes d/t being overworked
1st response of low cardiac output
activation of the SNS
increased released and decreased uptake of NE
leads to Increases ventricular contractility and heart rate
Also leads to vasoconstriction and enhanced venous tone, increasing preload
What does the SNS d/t the kidneys and blood?
Stimulates proximal tubular sodium reabsorption, contributing to sodium retention in HF
Results in an increase of plasma NE concentration, which correlates to the severity of HF and inversely with survival
How does ADH lead to
Low cardiac output → activation of carotid sinus and aortic arch baroreceptors → release of ADH and stimulation of thirst
May lead to increase in systemic vascular resistance
Promotes water retention
Increased water retention and increased thirst, leads to reduced sodium level (due to dilution)
The degree of hyponatremia parallels the severity of HF
What is the long name for ANP and BNP?
Atrial (ANP) and Brain (BNP)
What releases ANP and when does it rise?
ANP
Released from the atria in response to volume expansion
ANP rises early in HF
What releases BNP and when does it rise?
BNP
Released from the ventricles in response to high ventricular filling pressures
Present in chronic or advanced HF
Reduces systemic vascular resistance and central venous pressure, while increasing natriuresis, which reduces afterload
What is a high BNP and what does it tell you?
> 100
tells you the more fluid you have taken in
What is the maladaptive cycle of CHF?
decrease O2 to heart
decrease contractility
decrease CO
decrease BP
decrease O2 to tissues
cycles through these
What is afterload?
Left over blood in the ventricle after systole, which then backs up into the left ventricle
this can lead to more myocyte death
aortic impedance, vascular resistance, wall stress
Afterload affects a normal heart minimally, but small changes in afterload in a failing heart can lead to large changes in SV
maladaptive consequences
Elevation in diastolic pressures are transmitted to the atria and pulmonary & systemic venous circulations
Results in pulmonary vascular congestion and peripheral edema
The increased afterload can depress cardiac function and enhance deterioration
Catecholamine-stimulated contractility and increased heart rate can worsen coronary ischemia
Catecholamines and angiotensin II promote myocyte loss, resulting in cardiac remodeling
what is preload?
how much blood goes from atria to the ventricle
what is contractility?
the force generated at any given end-diastolic volume
Why is increase in afterload worse for a patient with HF?
We are not able to keep up with it
LV is already stretched out and then this can get even worse
What reduces our SV and CO?
With systolic dysfunction, there is a reduction in myocardial contractility, leading to reduction in SV and CO
volume is not getting out as fast.
What are the symptoms of heart failure due to?
Symptoms due to low CO and fluid accumulation
Cardinal symptoms:
Dyspnea
Fatigue
Fluid retention
Lower extremity edema
What is the ROS that may be a problem with HF?
Chest pain, flu-like symptoms, HTN, alcohol use, hx of heart murmurs
Family hx (risk factors)
Changes in medications (chemo, calcium channel blockers, flecainide)
PMH of autoimmune disorders, thyroid disease, DM, CAD, etc.
what are the PE findings of heart failure?
Resting sinus tachycardia, narrow pulse pressure (< 25 mmHg), diaphoresis, and peripheral vasoconstriction
Suggests severity of cardiac dysfunction
Pulmonary congestion – Inspiratory rales or dull breath sounds at the bases
Peripheral edema – lower extremities, scrotum, ascites
Elevated jugular venous pressure – present if edema is due to HF
what direction do you check pitting edema?
distally and then
what can scrotal edema lead to?
poor peeing
what is Pathognomonic of severe LV failure on EKG?
Pulsus alternans
Why do you hear S3 and S4 for HF?
S3 hear blood going into LV
S4 atrial kick (tries to get blood across the mitral valve)
Why do you have decreased peripheral pulses?
d/t decreased perfusion
What can you see on skin of PE of HF?
can sometimes see fluid leaking out of skin
Why do we look at thyroid for HF?
Secondary cause to r/o thyrotoxicosis
What are the diagnostics for HF?
EKG (MI, LVH, etc)
ECHO
BNP or proBNP
Troponin
CBC (r/o anemia)
TSH/F4
CMP to make sure they don’t have hyponatremia or Bun/Cr (elevate)
CXR (look for cardiomegaly, diffuse congestion and not specific area, curly B-lines)
Coag studies (to plan surgery)
Lipid panel
ANA (autoimmune disorder)
based on differential
Use for severity and cause NOT to confirm typically
How is HF diagnosed?
Typically clinically, but we use labs to find underlying cause
What do you often see on CXR of HF?
Cardiomegaly
Pulmonary vascular congestion (looks like diffuse spider webs typically. Ask URI symptoms fever/chills, that would NOT be seen in CHF)
Curly B-lines (thickening of septa d/t fluid build up)
what do kerley B lines confirm?
There is fluid overload
thickened interlobular septa) are thin, 1-2 cm lines, virtually always at the lungs bases and at the lung periphery lying perpendicular to the pleural surface to which they contact.
What test MUST you order?
BNP and NT-proBNP
if it is NOT elevated, you for surely do NOT have heart failure
It is not solely diagnosed for CHF
What levels of BNP and NT-proBNP is normal and concerning?
Normal value for BNP is < 100 pg/mL (NT-proBNP <300)
used in an acute or chronic setting rather than serioal
the higher the number, the more likely they have CHF
NT-proBNP has a _____ half life than BNP
longer
if this is >100, it is not diagnostic of CHF
Limitations of BNP and NT-proBNP
Limitations exist
Pt may present with more than one cause for dyspnea, ex. PNA and HF
Pts with severe chronic HF may have persistently elevated levels of BNP
Other causes for elevated BNP
ACS, LVH, valvular disease, Afib, S/P Cardioversion
Increased age, Severe anemia, Renal failure
PNA, Pulm HTN
Sepsis, Severe burns
when is BNP not as useful?
It may be chronically high
Why can troponins be elevated if they do not have ischemia from IHD?
This suggests ongoing myocardial injury or necrosis (even if not an ischemic process)
Associated with increased mortality rate, whether present in acute or chronic HF
what does echo tell you for CHF?
ventricular size and function
Also detects LV diastolic function
Can detect regional wall motion abnormalities
Usually suggests CAD, but segmental abnormalities are possible with nonischemic dilated cardiomyopathies
Pericardial thickening or effusion can be seen
Valvular disease is evaluated
RV function and pulm pressures can be measured
Detection of CAD in CHF?
CAD typically needs excluded, especially in pt’s with new reduced LVEF and no other identifiable causes
Denying chest pain is not reason enough to exclude CAD
Stress testing is useful
Even if stress test normal, if no other cause is identifiable, coronary angiography should be considered
May also perform left ventriculogram during cardiac catheterization to evaluate LV function
If your echo is inconclusive, what can cardio order for CHF?
Cardiac MRI
Cardiac CTA
Endomyocardial biopsy
what is class I medication?
Is indicated for sure, negligent if you do not order
what is a class II medication?
Should/may be considered
what is class III medication?
DON’T give
Why do we treat CHF?
We cannot reverse the heart failure
we want to:
keep them out of the hospital
relieve symptoms
promote independence
prevent death
medication is specifically for LOW ejection fraction and dyastolic is not known whether or not to treat.
