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
AKA inability to have proper ventricular output or filling.
Ultimately means we have poor cardiac output.
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
What are the common symptoms of chronic HF?
- Fatigue
- Anorexia
- Abdominal distension
- Edema
You can have an acute exacerbation still.
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, such as reduced EF or hypovolemia
What are HFrEF and HFpEF?
- HFrEF is systolic HF with reduced EF <= 40%
- HFpEF is diastolic HF with normal EF >= 50%
What is the MC type of HF?
Left sided systolic HF/HFrEF
What is the MCC of right sided HF?
Left sided HF
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 by HF.
- The effort needed to elicit symptoms in a patient.
Class I-IV
Describe the 4 classes of NYHA severity for HF.
- Class I = no limitation
- Class II = Slight limitation with symptoms upon ordinary activity.
- Class III = Marked limitation with symptoms upon less than ordinary activity.
- Class IV = Complete limitation with symptoms at rest
Limitation varies by patient based on their baseline.
What is the main difference between HF staging and NYHA classes?
- Staging cannot CHANGE.
- It stages the structural changes of the heart.
Progresses.
Define Stages A-D for the 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)
What are the two neurohumoral compensatory mechanisms in HF?
- Vasoconstriction to maintain pressure
- Increased myocardial contractility and HR to maintain CO
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.
How does the sympathetic NS boost vasoconstriction and enhance venous return?
Increased release of NE, which also increases ventricular contractility and HR
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 Plasma NE.
What stimulates RAAS?
- Decreased glomerular filtration
- Increased Beta-1 adrenergic activity
What cell type can RAAS affect?
Myocytes, causing remodeling of the heart.
Also increases the # of AT2 receptors in the heart.
What is the pathway that triggers ADH release and what is the effect of ADH release?
- Low CO
- Activates carotid sinus and aortic arch baroreceptors
- Release of ADH and stimulates thirst
- Increased SVR
- Promotes water retention
What are the two natriuretic peptides released by the heart and what triggers each?
- ANP: response to volume expansion, rises earlier.
- BNP: response to high ventricular filling pressures, long half-life.
- BNP: Reduces SVR, and increases natriuresis to reduce afterload.
As we get increased filling pressures/diastolic pressures, 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 cardiac remodeling?
- Catecholamines
- Angiotensin II
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.
Afterload is essentially the pressure the heart must overcome during systole.
What happens to myocardial contractility in systolic dysfunction?
Decreased contractility, aka 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 contractility and HR.
- Salt and water retention will also occur to raise EDV.
What are the cardinal symptoms of HF?
- Dyspnea
- Fatigue
- Fluid retention
What are common vitals seen in HF?
- Resting sinus tach
- narrow PP (< 25 mm Hg)
- Diaphoresis
- Peripheral vasoconstriction
What lung sounds might be heard in a volume assessment for HF?
- Inspiratory rales
- Dull breath sounds at the bases
How do you properly assess for LE edema?
Start at the feet then work up
How is pitting edema graded?
0-4, with 0 being none and 4 being a lot.
Also note when the pitting edema stops
What is a pathognomonic finding in HF?
Pulsus alternans
Evenly spaced strong and weak peripheral pulses
Also seen in DCM along with tach and LBBB
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)
S4 = diAstole (4 = A and d is the 4th letter)
What is the main purpose of an EKG in HF?
Looking for arrhythmias or underlying causes of the HF.
What CXR findings suggest HF?
- Diffuse infiltrates
- KERLEY B lines
- Waterbottle heart
- 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 is the primary use of BNP tests?
Excluding HF due to its high negative predictive value
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 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?
Remodeled myocytes can be irritated more easily and is suggestive of ongoing injury.
Suggests increased mortality rate.
What measurements does an echo give that we want to know about in a patient with HF?
- Ventricular size and function
- Regional wall motion abnormalities
- Thickening
- RV function and pulmonary pressure estimates
How do we rule out CAD in HFrEF?
- Stress testing
- Potentially coronary angiography
Denial of symptoms is NOT exclusion of CAD.
What is most clinical evidence regarding HF based on? (Which HF type?)
HFrEF patients
