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.
