Lecture 13: Heart Failure 1 Flashcards
Define Heart Failure.
It is a complex clinical syndrome that RESULTS from any structural or functional impairment of ventricular filling or ejection of blood.
AHA/ACC definition
Characterized by s/s of reduced CO and volume overload
What is the rate of mortality, hospitalization and readmission for patients with HF
- 5 year survival rate - 50%
- Severe disease could mean 1 year mortality as high as 40%
- 83% of pts are hospitalized at least once
- 20-25% chance of readmission in 60 days, 50% chance at 6 months
What are the MCC of death in people with HF?
Progressive HF or SCD.
Arrhythmia is common as the left ventricle keeps stretching.
What are the risk factors for HF?
- CAD/Atherosclerosis
- DM
- HTN
- Metabolic syndrome/Obesity
What is the #1 risk factor for HF in both genders?
HTN!
What are the common symptoms of acute HF?
- SOB
- PND
- Orthopnea
- RUQ pain
acute = symptoms began w/i last few days/weeks
What are the common symptoms of chronic HF?
- Fatigue
- Anorexia
- Abdominal distension
- Edema
You can have an acute exacerbation still.
chronic = symptoms present for months
What is high output HF?
- Unable to meet demands of peripheral needs.
- Thyrotoxicosis, severe anemia, sepsis
- Symptoms of reduced CO.
What is low output HF?
Insufficient forward output
* reduced EF, hypovolemia
What is the difference between HF w/ reduced left ventricular EF (HFrEF) and HF with preserved EF (HFpEF)?
- HFrEF is systolic HF with reduced EF <= 40%
- HFpEF is diastolic HF with normal EF >= 50%
What are the classifications of HF?
- Type I - HFrEF (EF </=40%)
- Type II - HFpEF (EF >/= 50%)
- Type a - HFpEF, borderline (EF 41-49%)
- Type b - HFpEF, improved (EF >40%)
What is the MC type of HF? what does this type of HF lead to?
- Left sided systolic HF/HFrEF
- Leads to DOE, PND, orthopnea, fatigue
What is the MCC of right sided HF? How does it present?
- Left sided HF
- presents with JVD, hepatic congestion, ascites, anorexia, LE edema
Isolated is rare unless lung disorder is present.
How does left-sided HF typically present? Right-sided?
- Left-sided: DOE, PND, Orthopnea, fatigue
- Right-sided: JVD, hepatic congestion, ascites, anorexia, LE edema
What do NYHA classes quantify?
- The functional limitation caused HF to estimate severity of disease.
- Assesses effort needed to elicit symptoms in a HF patient.
Class I-IV
Describe the 4 classes of NYHA severity for HF.
- Class I = no limitation of activity/ ordinary activity does not cause HF symptoms
- Class II = Slight limitation with symptoms upon ordinary activity but not at rest
- Class III = Marked limitation with symptoms upon less than ordinary activity but still NOT at rest
- Class IV = Complete inability to do activity with symptoms at rest
Limitation varies by patient based on their baseline.
What is the main difference between ACC/AHA staging and NYHA classes?
- AHA Describes the evolution of heart failure
- AHA are progressive stages and CANNOT change
- AHA Helps define appropriate therapeutic approach and determine prognosis
Define Stages A-D for the ACC/AHA stages of HF.
- A = At risk but no disease or symptoms.
- B = Structural disease but no S/S.
- C = Structural dsease with prior or current S/S
- D = Refractory HF that requires specialized interventions (Usually class IV patients)
comparison pic of NYHA/ACC/AHA stages combined
What are the two neurohumoral compensatory mechanisms in HF?
- Vasoconstriction to maintain systemic pressure
- Increased myocardial contractility and HR to restore CO
These mechanisms/adaptations occur with systolic and diastolic dysfunction
Why is hyponatremia common in HF?
- Poor renal perfusion due to poor CO causes the RAAS system to activate.
- RAAS will cause us to retain fluid and therefore dilute our sodium.
this is enochs card, i actually have no clue whats going on here ahahahaha. good luck
What is one of the first responses to low cardiac output? what does this do?
- activation of the SNS!
- Increases release and decreases uptake of NE –> increased ventricular contractility and HR
- Also leads to vasoconstriction and enhanced venous tone, increasing preload
What occurs in the kidney due to SNS stimulation in HF?
- Increased proximal tubular sodium reabsorption, which contributes to sodium retention in HF.
- Increases plasma concentration of NE, which correlates to the severity of HF and inversely w/ survival.
What stimulates RAAS?
- Decreased glomerular filtration
- Increased Beta-1 adrenergic activity
what are the results of activation of RAAS system
- increases sodium reabsorption
- Induces systemic renal vasoconstriction
- Can act directly on myocytes to promote pathologic remodeling via hypertrophy, apoptosis, necrosis
What cell type can RAAS affect?
Myocytes. it causes them to develop more AT receptors which results in cell apoptosis.
What is the order of events that triggers ADH release and what is the effect of ADH release?
- Low CO
- Activates carotid sinus and aortic arch baroreceptors
- Release of ADH
- Promotes water retention and stimualtes thirst
- increases SVR
- leads to reduced sodium (via dilution). degree of hyponatremia parallels the severity of HF
What are the two natriuretic peptides released by the heart and what triggers each?
- ANP: response to atrial volume expansion, rises eary in HF.
- BNP: response to high ventricular filling pressures, long half-life. Present in chronic or advanced HF.
- BNP: Reduces SVR and central venous pressure and increases natriuresis to reduce afterload.
As we get increased diastolic pressures in HF, what occurs in our lung?
- Pulmonary vascular congestion
- Peripheral edema
What does increased afterload do in HF?
- Depress cardiac function
- Enhance deterioration of the heart
What two hormones can promote myocyte loss and result in cardiac remodeling?
- Catecholamines
- Angiotensin II
Catecholamine-stimulated contractility and increased HR can worsen coronary ischemia
Define preload, contractility, and afterload.
This is VERY IMPORTANT TO KNOW for all heart stuff
- Preload: venous return and EDV (end-diastolic volume)
- Contractility: force generated at any given EDV.
- Afterload: Aortic impedance, SVR, and wall stress.
These three are the major determinants of the LV stroke Volume
Afterload is essentially the pressure the heart must overcome during systole.
What happens to myocardial contractility in systolic dysfunction?
Decreased contractility, assocaited with a decreased SV and therefore CO.
CO = HR x SV
How does the body compensate for reductions in CO and SV?
- SNS will activate first, increasing contracility and HR.
- Salt and water retention will also occur to raise blood volume and therefore EDV.
What are the cardinal symptoms of HF?
- Dyspnea
- Fatigue
- Fluid retention
fluid retention presents as LE edema
these symptoms are d/t low CO and fluid accumulation
What are common general PE findings in HF?
- Resting sinus tach
- narrow PP (< 25 mm Hg)
- Diaphoresis
- Peripheral vasoconstriction
What are some positive findings when doing a volume assessment on PE
- pulmonary congestion - inspiratory rales or dull breath sounds at bases
- peripheral edema - LE, scrotum, ascites
- Elevated jugular venous pressure - present if edema is d/t HF
How do you properly assess for LE edema?
Start at the feet then work your way proximally to see how far the edema extends.
DONT FORGET ABOUT SCROTAL AREAS
How is pitting edema graded?
0-4
1. mild pitting (2mm depression)
2. moderate pitting (4mm depression that disapears in 10-15s)
3. moderate/severe - (6mm depression that last >1 min)
4. severe - (8mm depression lasting >2 min)
What is a pathognomonic finding in severe LV failure?
Pulsus alternans
Evenly spaced strong and weak peripheral pulses
what PE finding would suggest LV enlargement
laterally displaced apical impulse
what PE finding would suggest Pulmonary HTN
parasternal lift of RV on precordial palpation
What HFs are associated with S3 and S4?
- S3: systolic (because it occurs in early diastole)
- S4: diastole (because it occurs in late diastole/early systole)
S3S
what is the goal of diagnostic studies in HF patients
not only to confirm that symptoms are d/t heart failure but also to determine the cause of HF
What is the main purpose of an EKG in HF?
- can detect findings that specify a cause of HF
- can show arrhythmias that is the cause or result of HF
What CXR findings suggest HF?
- Pulmonary vascular congestion
- KERLEY B lines
- cardiomegaly
- Pleural effusions
Kerley B lines CXR image
Horizontal lines that begin in the periphery and extend to the pleural surface.
Suggests pulmonary edema.
What is the primary treatment for reducing pulmonary vascular congestion?
Lasix
what are the initial tests in evaluation of HF
- CBC - anemia, pericarditis, leukocytosis
- CMP - electrolytes, BUN, Cr, Mg, LFTs
- Coag studies
- fasting BG
- Lipid panel
CXR and EKG are also initial
what are additional lab tests that could be done in evaluation of HF when supporting or determining the etiology of HF
- TFTs
- Iron studies
- ANA
- Viral Serology
- Genetic testing
what is the BEST test for HF evaluation
- BNP and NT-proBNP
- used when excluding HF as a dx due to its high negative predictive value
- also good for establishing severity of disease
what is BNP and NT-proBNP
a biomarker released from the ventricles while in HF
Between BNP and NT-proBNP, which range is higher?
NT-proBNP can go up to 300 before considering it as positive.
BNP only needs to be higher than 100 to be positive.
What is the primary difference between NT-proBNP and BNP?
NT-proBNP has a longer half-life.
What are the limitations of BNP and NT-proBNP
- pt may present with more than one cause of their symptoms
- pts with chronic severe HF may have persistently elevated levels of BNP
- there can be other causes of elevated BNP aside from HF (will be covered on next card)
What can cause elevated BNP?
- ACS
- LVH
- Pulmonary HTN
- Afib
- S/P Cardioversion
- PNA
- Sepsis
- Severe burns
- Increased age
- Severe anemia
- Renal failure
- Chronic HF
It is a poor indicator in patients with chronic HF.
Why can trops be elevated in HF that does not have CAD or ischemia?
suggestive of ongoing myocardal injury or necrosis
Suggests increased mortality rate.
what imaging is always indicated in new onset HF patients
Echoooo
What infromation can be given with an echo
- Ventricular size and function
- LV diastolic function
- Regional wall motion abnormalities
- Pericardial Thickening or effusion
- Valvular disease
- RV function and pulmonary pressure measurements
How do we rule out CAD in HFrEF?
- Stress testing
- Even if stress test is normal, coronary angiography should be considered
- May also perform left ventriculogram during cardiac cath to evaluate LV function
Denial of symptoms is NOT exclusion of CAD.
what additional diagnostic evaluations for HF can be considered if necessary
- cardiac MRI
- Cardiac CTA
- endomyocardial biopsy
What is most clinical evidence regarding HF based on? (Which HF type?)
HFrEF patients
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