Lecture 3 (Cardio)-Exam 1

Question 1

American College of Cardiology defines Heart Failure as what?

Answer 1

“as a complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales”

Question 2

What is HF? Increased prevalence due to what?

Answer 2

• Pathophysiologic state in which abnormal cardiac function renders the heart unable to pump blood at a rate to meet the metabolic requirements of the tissues
• Increased prevalence due to aging population and prolongation of life

Question 3

Lower Yield

Epidemiology
* How many world wide?
* How many people over 65?
* Male vs Female?
* Improved therapeutic intervention for certain conditions has caused what?

Answer 3

Question 4

Lower Yield

Impact on Public Health
* Common or not?
* Can be what?
* How is it disabling?
* Increased mortality?

Answer 4

Question 5

What happens happen to the survival rate over the years?

Answer 5

“There have been modest improvements in survival rates for people with chronic HF over the past 70 years. Despite this, the 5-year survival rate is close to 50% and many people will die directly from HF or from related cardiovascular disease. Older populations are at the greatest risk of death, presenting a looming challenge to healthcare systems given changing global demographics”

Question 6

Cardiac Physiology
* Heart Rate is dependent on what?

Answer 6

is dependent on the conduction system as well as sympathetic and parasympathetic tone

Question 7

• Stroke volume is dependent on what?
• How do you get the Stroke volume?

Answer 7

Stroke volume is dependent on preload, afterload and ventricular contractility
* Not all of the blood that fills the heart by the end of diastole (end-diastolic volume or EDV) can be ejected from the heart during systole. Thus the volume left in the heart at the end of systole is the end-systolic volume (ES V). Thus, the stroke volume is not equal to the end-diastolic volume but the EDV- ESV

Question 8

What are factors what affect the HR and SV?

Answer 8

Question 9

Preload:
* What is it?
* Approximated by what?

Answer 9

Preload: The passive load or filling pressure of the LV.
* Approximated by the left ventricular end diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP)
* “Preload isproportional to the end-diastolic ventricular volume, or the amount of blood in the ventricles immediately before systole. Greater end-diastolic volumes of blood returned to the heart, increase the passive stretching of the heart muscles. This in turn results in the ventricles contracting with more force- a phenomenon called the Frank-Starling law of the heart”

Question 10

Afterload
* What is it?
* What is it estimated by?

Answer 10

Afterload: The resistance against which the LV contracts.
* Estimated by the systemic vascular resistance
* “Afterload represents all the factors that contribute to total tension during isotonic contraction.As such afterload can be related to the amount of systemic resistance the ventricles must overcome to eject blood into the vasculature. Afterload is proportionate to systemic blood pressures and is inversely related to stroke volume, unlike preload and contractility.”

Question 11

Contractility
* What is it?
* Approximated by what?

Answer 11

• Approximated by ejection fraction (EF)
• “Contractility describes the force of myocyte contraction, also referred to as inotropy. As the force of contraction increases,the heart is able to push more blood out of the heart, and thus increases the stroke volume”

Question 12

PATHOPHYSIOLOGY OF HEART FAILURE
* Compensatory mechanisms are trigged by what?
* Preload increases as a result of what?
* LV dilation occurs with what?
* Neuro-humoral mechanisms are activated when what happens?
* Vicisous cycle of what?

Answer 12

1. Compensatory mechanisms are trigged by an initial drop in cardiac output
2. Preload increases as a result of sodium retention
3. LV dilation occurs with a resultant increase in contractility (Frank-Starling relation)
4. Neuro-humoral mechanisms are activated when contractility begins to fail
5. Vicious cycle of failure, attempted compensation, failure, compensation…etc

Question 13

NEURO-HUMORAL COMPENSATORY MECH ANISMS
* What is released? What does that increase?
* What occurs to assure adequte organ perfusion?
* As heart failure worsens, what rises?

Answer 13

• Norepinephrine is released and increases heart rate and contractility
• Peripheral vascular vasoconstriction occurs to assure adequate organ perfusion
• As heart failure worsens, norepinephrine rises with a paradoxical decrease in organ perfusion

Question 14

Renin-Angiotensin-Aldosterone System
* Activated by what?
* Explain the pathway and the effects?

Answer 14

• Activated by Norepi levels, decreased renal perfusion, and increased PVR (peripheral vascular resistance)
• Renin secretion leads to formation of Angiotensin II
• Angiotension II causes vasoconstriction, increased afterload, and the release of aldosterone and vasopressin
• Aldosterone contributes to sodium and water retention
• Preload increases
• The pituitary releases vasopressin which causes fluid retention and vasoconstriction

Picture is extra if needed

Question 15

Answer 15

Question 16

Congestive Heart Failure Pathophysiology

Answer 16

Question 17

Frank-Starling law
* Relationship between what?
* Systolic contractile performance (stroke volume or CO) is proportional to what?
* What is normal heart?
* Failing heart: with exertion produces less what?
* When preload is low (at rest), there is little what?

Answer 17

Question 18

Congestive Heart Failure: Frank-Starling Relationship
* Explain this chart

Answer 18

Normally (top curve), as preload increases, cardiac performance also increases. However at a certain point, performance plateaus, then declines. In heart failure (HF) due to systolic dysfunction (bottom curve), the overall curve shifts downward, reflecting reduced cardiac performance at a given preload, and as preload increases, cardiac performance increases less. With treatment (middle curve), performance is improved, although not normalized.

Question 19

KNOW

HF with reduced EF (HFrEF)
* Formerly know as what?
* Happens happens?

Answer 19

• formerly systolic HF
• Ventricle fails to contract properly. This is a pumping problem so the EF will be less than 40%

Can have combined CHF which has factors of both systolic and diastolic CHF

Question 20

KNOW

HF with preserved EF (HFpEF)
* Formerly known as what?
* What happens during this?
* Diagnosis of exclusion, how?

Answer 20

• formerly diastolic HF
• Ventricular muscles become stiff, causing impaired ventricular filling during diastole. Either impaired relaxation or increased stiffness of ventricles or both. LV EF will be normal (sometimes elevated)
• Diagnosis of exclusion: IF systolic function is normal and there is evidence of CHF

Can have combined CHF which has factors of both systolic and diastolic CHF

Question 21

What does systolic dysfunction and diastolic dysfunction look like?

Answer 21

Question 22

Answer 22

Question 23

HF with reduced ejection fraction (HFrEF)
* Also called?
* leads to what?
* What happens to EF?
* May have defects in what?

Answer 23

• Global LV systolic dysfunction
• Leads to increased diastolic volume and pressure
• Ejection fraction decreased (< or = 40%)
• May have defects in metabolism, electrophysiologic function, contractile elements, intracellular calcium modulation and cAMP production

Question 24

HF with reduced ejection fraction (HFrEF)
* May be due to what?

Answer 24

• May be due to CAD/MI (most common), valvular heart disease (valve not working so increase work or volume backed up), myocarditis/sarcoidosis (w/n wall), dilated cardiomyopathy, sustained arrhythmia such as AF, and sustained HTN (starts as LVH and diastolic heart failure, ending in systolic heart failure)
• May be due to LV or RV failure – if LV primary – can cause RV failure

Question 25

HF with Preserved Ejection Fraction (HFpEF) * What is the prior name? * **What is impaired? What does that result in?** * Usually has a norma what? * **What is normal?**

Answer 25

* Prior name: diastolic heart failure * **LV filling is impaired, resulting in – Increased LV end-diastolic pressure at rest or during exertion** * Usually has a normal LV end-diastolic volume * **Global contractility and ejection fraction remain normal (= or > 40%)**

Question 26

HF with Preserved Ejection Fraction (HFpEF) * **What are the causes?**

Answer 26

**HTN leading to myocardial hypertrophy (most common cause), Aging (normal), Obesity, DM (significant risk factor- associated with myocardial fibrosis), Valvular heart disease (AS and AI), Pulmonary HTN/MS, SLE, OSA**

Question 27

What are the different classfications of HF?

Answer 27

Question 28

Signs/Symptoms of HF * What are cardinal sxs? * What happens with breathing? * What type of congestions? What does that cause? * What are other breathing issues? (3)

Answer 28

* Cardinal symptoms – fatigue, SOB * Dyspnea with exertion in early disease, at rest in later disease * Pulmonary congestion with accumulation of interstitial or intra-alveolar fluid/Pulmonary edema (CXR changes) * Orthopnea * Nocturnal cough (non-productive), worse in recumbent position * Paroxysmal nocturnal dyspnea

Question 29

Signs/Symptoms of HF * What happens in 40% of late stages? * What happens with GI? * Neuro? * What happens to extremities?

Answer 29

* Cheyne-Stokes respiration - ~40% of patients with advanced HF * GI – anorexia, nausea, early satiety – abdominal bloating * Confusion and memory impairment in advanced HF (inadequate brain perfusion) * Diaphoresis and cool extremities at rest (NYHA class IV)

Question 30

What is the sx in acute left and right HF?

Answer 30

Question 31

* **New York Heart Association (NYHA) functional classification system is a widely used tool for assessing what?** * What are the categorization? (general)

Answer 31

* **New York Heart Association (NYHA) functional classification system is a widely used tool for assessing the severity of heart failure symptoms and functional limitations** * Categorizes HF patients into 1 of 4 classes based on the degree of physical activity limitations experienced

Question 32

# KNOW What is NYHA Class 1?

Answer 32

**no limitations of physical activity** – able to carry out usual activities without experiencing fatigue or other symptoms

Question 33

# KNOW What is NYHA Class 2?

Answer 33

**slight limitations of physical activity** – comfortable at rest or with mild exertion but experience symptoms such as fatigue, dyspnea or angina with moderate exertion

Question 34

# KNOW What is NYHA Class 3?

Answer 34

NYHA Class III – **marked limitations of physical activity** – significant symptoms of heart failure that result in marked limitations of physical activity. Comfortable at rest but experience symptoms of fatigue, dyspnea, and angina with less than ordinary exertion (mild exertion like walking short distances)

Question 35

# KNOW What is NYHA Class 4?

Answer 35

NYHA Class IV – **unable to carry out any physical activity without discomfort** – have severe symptoms of heart failure that severely limit physical activity – happen at rest and are unable to carry out any physical activity without experiencing significant discomfort

Question 36

New York Heart Association Functional Classification

Answer 36

Question 37

# KNOW What are the major sx of Right sided heart failure?

Answer 37

Right sided HF: **Ascites, congestive hepatomegaly, pedal edema, decreased bowel perfusion, jugular venous distension, and weight gain. Appears like hepatic dysfunction.** ## Footnote SYSTEMIC ISSUES

Question 38

Cor Pulmonale * **What is it?** * Progresses into what?

Answer 38

**Cor pulmonale is right ventricular enlargement secondary to a lung disorder that produces pulmonary artery hypertension**. * Progresses to right ventricular failure follows.

Question 39

Cor Pulmonale * What are the Physical exam findings? (systemic vs **cardiac**) * What is the txt?

Answer 39

* Systemic- Findings include peripheral edema, neck vein distention, hepatomegaly, * Cardiac - **Palpable left the parasternal lift, loud S2 (accentuation of the pulmonary component of the second heart sound) narrow splitting of S2, a holosystolic murmur of tricuspid regurgitation at the left lower sternal border, right-sided S4 heart sound** * Treatment is directed at the cause.

Question 40

Cor Pulmonale * Alteration of what? * usually what? * May be caused by what?

Answer 40

* Alteration of right heart structure or function * Usually chronic, may be acute and reversible * May be caused by any disease which leads to elevated pressure in the lungs

Question 41

Again, what is cor pulmonale?

Answer 41

Question 42

What are the cor pulmonale sx?(6)

Answer 42

* Asymptomatic at first * Dyspnea * Exertional fatigue * Edema * Chest pain * Syncope

Question 43

What are Cor Pulmonale PE Findings?

Answer 43

* Left parasternal systolic lift * Loud pulmonic component of the 2nd heart sound (S2) * Murmurs of functional tricuspid * Right sided S3 gallop * JVD * Hepatomegaly/Ascites * Lower extremity edema

Question 44

Cor Pulmonale PE Findings * pHTN is caused by what? * Elevated what? What does that cause?

Answer 44

Pulmonary hypertension * Increased afterload in RV, similar to what occurs in LV failure Elevated end-diastolic, central venous pressure * ventricular hypertrophy and dilation

Question 45

Cor Pulmonale Diagnostic testing * What do you see on EKG? * What do you see on CXR?

Answer 45

EKG * RVH and strain * tall peaked P waves (P-pulmonale), * Right axis deviation * RBBB CXR: * Enlargement of pulmonary arteries * Dilation of the right atrium * Dilation of right ventricle

Question 46

Cor Pulmonale Diagnostic testing * What od you see on Echo? (4)

Answer 46

Question 47

Cor Pulmonale Diagnosis * **What is the gold standard to dx**? What does it provide? * What are the values?

Answer 47

Right heart catheterization * **Invasive hemodynamic assessment with right heart catheterization is considered the gold standard for diagnosing pulmonary hypertension and cor pulmonale.** RHC provides direct measurements of right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output, which are essential for confirming the diagnosis and guiding treatment. * Elevation of pulmonary artery (mean greater than 25mmHg), RV and RA pressures

Question 48

How does COPD and unresolved PE cause cor pulmonale?

Answer 48

Question 49

Cor Pulmonale Treatment * What is the txt for the cause? * What is the txt for the symptoms?

Answer 49

Question 50

# She has the big section of CCB, i think it is low yield What is the role of CCB for pHTN?

Answer 50

Calcium channel blockers (CCB) were the first vasodilator agents to gain popular acceptance in the treatment of pulmonary arterial hypertension (PAH). They have been shown to be particularly effective in patients who show a significant immediate hemodynamic response to pulmonary vasodilators ("responders"). The application of CCB is currently restricted to "responders" only. It is believed that no more than 5% of PAH patients will benefit from CCB long term. The response rate of most non-idiopathic forms of PAH is considered to be even lower. The "non-responders" as well as "responders" who fail to benefit from CCB should be treated with newer agents, collectively called "advanced PAH therapy." The basis of this consensus rests on empiric experience gained in the PAH community over the years. However, the cut-points where advanced agents are more effective than CCB and where there is no additional role for CCB remain unknown.

Question 51

Cor Pulmonale Prognosis * What is the prognosis? * What is it a marker of?

Answer 51

* In patients with lung disease, the development of cor pulmonale is associated with poor prognosis * Usually a marker of severe end-stage lung disease

Question 52

# KNOWWWW What are the left sided heart failures?

Answer 52

L sided HF: Paroxysmal nocturnal dyspnea, orthopnea, crackles at lung bases, dullness to percussion, decreased urine output, palpitations, and chronic cough. High risk for pleural effusion

Question 53

What is the most common cause of right sided heart failure?

Answer 53

Left sided heart failure

Question 54

Physical Exam findings for HF * What is going on with the heart? (think HR, Sounds, veins and displacement)

Answer 54

Question 55

Physical Exam findings for HF * What is going on with the lungs?

Answer 55

* Pulmonary crackles * Diminished breath sounds (pleural effusion)

Question 56

PHYSICAL EXAM of HF (BODY) * What is going on with the liver? * Peripheral? * What is in severe chronic HF?

Answer 56

* Hepatomegaly – important sign – late in disease, ascites present due to increased pressure in the hepatic veins * Jaundice is a late sign * Peripheral edema is a cardinal sign – but non-specific and does not happen with adequate diuretic use * In severe chronic HF – marked weight loss or cardiac cachexia may be present

Question 57

* Right side failure, think what? * Left side failure, think what?

Answer 57

* Right side failure, think systemic * Left side failure, think pulmonary

Question 58

What is going on with the Physical exam in terms of neuro?

Answer 58

Cerebral symptoms, especially common in elderly * Confusion * Anxiety * Headaches * Delirium * Insomnia * Secondary to poor perfusion

Question 59

Heart Failure – diagnostic testing * What does the EKG show?

Answer 59

LVH, check for myocardial infarction (MI), screen for Arrhythmias, Q waves (old infarct)

Question 60

Heart Failure – diagnostic testing * What do the labs show?

Answer 60

CBC, CMP (check LFTs), TSH, Lipid panel, troponin, A1C and BNP * Hyponatremia * Hypokalemia-diuretics * Hyperkalemia- low cardiac output leads to renal insufficiency, ACEI use, K-sparing diuretics * Elevated LFTs – liver congestion

Question 61

Heart Failure – diagnostic testing: BNP * What is it secreted by? * When are there higher levels? * What are the classes (3) * Used for what?

Answer 61

Question 62

Heart Failure – diagnostic testing on CXR?

Answer 62

Cardiomegaly Pulmonary edema * Increased pulmonary vasculature * Diffuse bilateral opacities Pleural effusions Kerley B lines Indicate interstitial edem

Question 63

What are these?

Answer 63

Heart Failure – * Right: Intersitital markings * Left: Kerley B lines

Question 64

What does this show?

Answer 64

Pleural effusion

Question 65

# KNOW Heart Failure – Diagnostic testing * What is the dx test of choice? * What does it show?

Answer 65

Question 66

Heart Failure – DiAGOSTIC testing * What is MUGA? * What does it provide?

Answer 66

MUGA (multi-gated acquisition scan) scan * Provides measurement of left and right ventricular EF * Useful when Echo is technically suboptimal * Nuclear scan calculating EF

Question 67

Heart Failure – diagnostic testing: Stress test * What is it used for? * Identifies what? * Quantitates what? * Can help differentiate what? * Assess what?

Answer 67

Stress test: This is mainly for risk stratification and class placement. * Identifies if ischemia present * Quantitates level of conditioning * Can help differentiate cardiac versus pulmonary etiology of dyspnea * Assess dynamic responses of HR, rhythm, BP

Question 68

Heart Failure – diagnostic testing * **If ischemia is a possible contributing factor then get what**? What does it tell

Answer 68

**If ischemia is a possible contributing factor then get cardiac angiography** * Quantitative information regarding systolic and diastolic dysfunction * Excludes CAD as underlying cause of CHF

Question 69

HF: Treatment * What med guidelines? * What about risk factors? * Diet? * Moving? * Fluid?

Answer 69

Question 70

According to the 2022 American College of Cardiology/American Heart Association/Heart Failure Society of America heart failure (HF) guidelines, initiation of what is the first step of txt of HFrEF?

Answer 70

initiation of quadruple therapy with renin-angiotensin-system inhibitors including angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blockers (ARBs)/angiotensin and neprilysin inhibitor (ARNI), beta-blocker, mineralocorticoid receptor antagonist (MRAs), and sodium-glucose cotransporter 2 inhibitors (SGLT2is)

Question 71

# Medications * Patients with tachycardia, active ischemia, recent myocardial infarction, or ventricular ectopy may be initiated on what? * Patients with significant congestion and volume overload may be initiated on what?

Answer 71

* Patients with tachycardia, active ischemia, recent myocardial infarction, or ventricular ectopy may be initiated on beta-blocker. * Patients with significant congestion and volume overload may be initiated on SGLT2i or MRA after diuretics. 

Question 72

When should quadruple therpy happen?

Answer 72

There is evidence of early benefit with GDMT in patients with HFrEF, as early as within the first 30 days of treatment with SGLT2i or ARNI, and within 2 weeks of initiation of SGLT2i in patients with HFrEF or HFpEF. It is therefore important for quadruple therapy to be initiated within the first 4 to 6 weeks.

Question 73

After initiation and optimization of doses of quadruple therapy, the following steps are important to consider in patients with HFrEF. * What is indicated in African-American patients with NYHA functional class III-IV HFrEF? * For patients with symptomatic stable chronic HFrEF in sinus rhythm with a heart rate of ≥70 beats/min despite beta-blocker, what can be useful?

Answer 73

* Hydralazine and nitrates are indicated in African-American patients with NYHA functional class III-IV HFrEF.  * For patients with symptomatic stable chronic HFrEF in sinus rhythm with a heart rate of ≥70 beats/min despite beta-blocker, ivabradine can be beneficia

Question 74

* In patients with symptomatic HFrEF, what can be considered to decrease hospitalizations for HF? * In selected high-risk patients with HFrEF and recent worsening of HF, what can be used? * In patients with LVEF <35% and NYHA functional class II-III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year, what is recommended?

Answer 74

* In patients with symptomatic HFrEF, digoxin might be considered to decrease hospitalizations for HF. * In selected high-risk patients with HFrEF and recent worsening of HF, vericiguat may be considered to reduce HF hospitalization and cardiovascular death. * In patients with LVEF <35% and NYHA functional class II-III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year, implantable cardioverter-defibrillator therapy is recommended.

Question 75

* Patients with left bundle branch block and wide QRS interval also have indications for what? * Important additional considerations include appropriate treatment strategies for comorbidities, such as what?

Answer 75

* Patients with left bundle branch block and wide QRS interval also have indications for cardiac resynchronization therapy. * Important additional considerations include appropriate treatment strategies for comorbidities, such as iron deficiency, atrial fibrillation, ischemic heart disease, valvular heart disease, sleep apnea, and diabetes, and treatment of specific etiologies, such as cardiac amyloidosis or sarcoidosis

Question 76

What is the evoluion of HF txt?

Answer 76

Question 77

Guideline Directed Therapy * What has it reduced?

Answer 77

GDMT : proven to reduce mortality and morbidity

Question 78

Guideline Directed Therapy: Beta-blocker * What is the MOA? * **What does it decrease?** * Improves sx of what? * **Off loads what?**

Answer 78

Beta-blockers: decrease catecholamine levels and dysrhythmias * **Decreases mortality for all classes** * Improves symptoms of CHF * **Off loads the work of the heart, decrease heart rate which decreases forcefulness of contraction**

Question 79

Beta-blockers * What are the receptors? What does it cause? * May slow progression of what? * Contraindicated while what? * Which BB are more effective?

Answer 79

Question 80

HFrEF: * What are the standard therapies? * What are additional interventions? * What is the follow up? * What should you also treat?

Answer 80

Question 81

GDMT: Carvedilol (Coreg) * Preferred when? * Reduced all what? * Contraindicated for who?

Answer 81

* Preferred beta-blocker in patients with HFrEF and NYHA II-IV symptoms * Carvedilol reduced all-cause mortality compared to metoprolol tartrate (COMET Trial) * Contraindicated for acute/decompensated heart failure due to acute negative inotropic effects

Question 82

GDMT: ACEI * What is the MOA? * In addition, ACE inhibitors increase what? What does that cause? * What does it reduce?

Answer 82

* **ACE Inhibitors**: work by preventing ACE from converting angiotensin I to angiotensin II in the lungs. This prevents an elevation in blood pressure, reduces sodium reabsorption, and reduces ventricular remodeling. * In addition, ACE inhibitors increase bradykinin and prostaglandin levels, which leads to vasodilation of the arterioles, **decreasing afterload and SVR** (Decrease BP) * **ACEI reduce mortality (CONSENSUS and SOLVD) trials**

Question 83

GDMT: ACEI * What are the positvies of this drug? * Class effect so you can use any medication within what? * Dosage? Monitor what?

Answer 83

* Prolong survival, increase quality of life by alleviating symptoms in mild, moderate and severe CHF * Class effect so you can use any medication within the class to reduce overall mortality.  Both ACEI or ARB * Always start low dose to prevent hypotension * Monitor BUN and Creatinine

Question 84

GDMT: ARB * What is it? * Used in patients who cannot take what? * Should not replace what? * Help limit the growth of what? * What is not advisable?

Answer 84

Angiotensin II receptor blockers (ARBs) * Used in patients who cannot take ACEI due to dry cough side effect * **Should not replace ACEI if patient can tolerate it** * **ARB’s can help limit the growth of aneurysms** (ex. Losartan) * **Combination ACE inhibitor + ARB is not advisable** and places patients at risk for side effects such as hyperkalemia

Question 85

GDMT: Aldosterone antagonists * What is aldosterone? What does it help control? (2)

Answer 85

* Aldosterone -  A steroid hormone made by the adrenal cortex(the outer layer of the adrenal gland) * Helps control the balance of water and salts in the kidney by keeping sodium in and releasing potassium from the body * Aldosterone also helps control the amount of water your kidney reabsorbs; this increases blood volume and also impacts blood pressure

Question 86

GDMT: Aldosterone antagonists * Blocking aldosterone helps what? * Decreases what? * Spironolactone and eplerenone will do what? * They have been shown to do what?

Answer 86

* Blocking aldosterone helps to increase sodium and water excretion * Decreases mortality * **Spironolactone and eplerenone** (less endocrine side effects than spironolactone – use this in males) will reduce preload and increase sodium/water excretion. * **These have been shown to reduce mortality in Class III and class IV patients**.

Question 87

GDMT: SGLT-2 Inhibitor * What do they do?

Answer 87

SGLT2 inhibitors **reduce sodium and glucose flow into the blood, reduce fluid load, and exert an indirect osmotic diuretic effect.** Also with myocardial energy supply affect to decrease oxygen consumption and cardiac sympathetic nerve activity

Question 88

SGLT-2 INHIBITOR * What does the meta-analysis confirm?

Answer 88

“The results of this meta-analysis confirm the growing evidence in the literature of the favorable profile of SGLT2 inhibitors in cardiovascular outcomes and mortality in patients with heart failure regardless of the baseline diabetes status.”

Question 89

SGLT2 inhibitors: * What are the MOA? * What are the examples?

Answer 89

Question 90

SGLT2 inhibitors: * What are the major advantages? * What is contraindications?

Answer 90

Question 91

SGLT2 inhibitors: * What are the common side effects and important toxicities?

Answer 91

Question 92

GDMT: NEPRILYSIN INHIBITOR (ARNI) * What is an example? * Decreases what? * What is the MOA? When combined with ARB, it can improve what?

Answer 92

* **Sacubitril/Valsartan (Entresto)** * Decreases mortality * Sacubitril is a **neprilysin inhibitor** (First FDA approved NI). * **When combined with an ARB, this can improve blood pressure, HR, and EF**. ->relax blood vessels and decrease sodium and fluid in the body.

Question 93

GDMT: Neprilysin inhibitor (ARNi) * **For what disease?** * **Can be used in place of what?** * Reduces what? * **What do you need to before initating therapy?**

Answer 93

* **For use in chronic heart failure with reduced EF (<40%) – not enough data to use in HFpEF** * Can be used in place of ACE inhibitor monotherapy and/or if an ACE inhibitor isn’t tolerated (cough). **This medication is better than ARB monotherapy**. * Reduces the risk of cardiovascular death and hospitalization (NYHA class II-IV) with reduced ejection fraction * **Must allow at least 36 hours after the last ACEI dose before initiating therapy**

Question 94

GDMT others: Loop Diuretics * Used for what? * What does loop diuretics do? * What is the MOA?

Answer 94

Used for symptom control only, does not decrease mortality Loop Diuretics: Decrease blood pressure and removes excess fluid. * inhibiting the sodium-potassium-chloride (Na+/K+/2Cl) co-transporter in the thick ascending loop of Henle (hence the name loop diuretic), which is located in the kidneys. * This reduces or abolishes sodium, chloride, and potassium reabsorption, leading to increased loss of sodium, chloride, and potassium into the nephron (the functional unit of a kidney). As a result, water is also drawn into the nephron and urine volume increases

Question 95

GDMT others: Loop Diuretics * **Can cause what levels to decrease?** * beware of what? * **Does not improve what?** * What should you remember?

Answer 95

* **Can cause hypokalemia and reduced magnesium levels** * Beware over-diuresis, orthostatic hypotension; worsening renal insufficiency * **Does not improve LV contractility (only reduces preload – prevent pulm edema)** * **Remember: patients with diastolic dysfunction need elevated filling pressures(HOCM, severe AS)- care when using diuretics**

Question 96

Gdmt Add-Ons: Hydralazine + Nitrates (isosorbide dinitrate) * Reduces what? * Hydralazine does what? * This medication combo is especially effective in who?

Answer 96

Reduces mortality * Hydralazine dilates arteries and Nitrates will dilate veins and decrease preload. * This medication combo is especially effective in African Americans.

Question 97

Gdmt Add-Ons: Hydralazine + Nitrates (isosorbide dinitrate) * Used if cannot tolerate what? * Not as effective as what? * Dosage?

Answer 97

* Used IF cannot tolerate ACEI/ARB * Not as effective as ACEI * Inconvenient dosage schedule (TID)

Question 98

GDMT: more add-ons (digoxin) * What is the MOA? * What are the mechanical affects? * What are the electrical affects? * What are the toxicity issues?

Answer 98

* Selectively and reversibly inhibits the Na-K ATPase ion transport system (increased sodium inside the cell slows it down and calcium builds which triggers myocyte- increases force of contraction) * Mechanical affects: increases contractility, EF, CO * Electrical affects: decrease heart rate, increase PR interval, decrease QT interval, increases refractory period at AV node (Afib therapy) * Toxicity issues – check dig levels, digibind. Also interacts with lots of other medications

Question 99

GDMT: more add-ons (Ivabradine) * Belongs to what drug class? * Is works by what?

Answer 99

* Belongs to drug class: hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blockers * It works by slowing the heart rate so the heart can pump more blood through the body each time it beats

Question 100

# - Acute Decompensated heart failure (ADHF) * What are the Acute Onset or Worsening of Symptoms? * What happens with volume?

Answer 100

* **Acute Onset or Worsening of Symptoms:** Patients with ADHF typically present with a sudden onset or exacerbation of symptoms related to heart failure, such as **dyspnea (often orthopnea or paroxysmal nocturnal dyspnea), fatigue, exercise intolerance, peripheral edema, and/or weight gain.** * **Volume Overload:** ADHF is characterized by volume overload, which may manifest as **pulmonary congestion (pulmonary edema)** leading to dyspnea, orthopnea, and cough, or systemic congestion leading to peripheral edema, ascites, and hepatic congestion. Patients may exhibit signs of fluid overload, such as jugular venous distention (JVD), hepatomegaly, and ascites.

Question 101

Acute Decompensated heart failure (ADHF) * When are they hemodynamic instable? * What are preipating factors?

Answer 101

* **Hemodynamic Instability**: Patients with ADHF may exhibit hemodynamic instability, including hypotension, tachycardia, and/or evidence of end-organ hypoperfusion (e.g., altered mental status, cool extremities). In severe cases, patients may present with cardiogenic shock, characterized by severe hypotension and evidence of tissue hypoperfusion. * **Precipitating Factors**: ADHF often occurs in the setting of precipitating factors or triggers, such as myocardial ischemia/infarction, uncontrolled hypertension, arrhythmias (e.g., atrial fibrillation/flutter), infection, medication non-adherence, dietary indiscretion (e.g., excessive sodium intake), or exacerbation of comorbid conditions (e.g., chronic kidney disease, chronic obstructive pulmonary disease).

Question 102

Heart failure requiring inpatient admission:Acute decompensated heart failure (ADHF) * What are the five goals?

Answer 102

* Manage oxygenation, ventilation * Treat unstable dysrhythmias if present * Preload reduction, fluid removal * Afterload reduction, lower BP and work of the heart * Improve contractility

Question 103

Treatment of ADHF * The first goal is oxgenation ventilation, what are the different types and how they help?

Answer 103

Question 104

Treatment of ADHF * Goal 2: How do you Treat any unstable dysrhythmias

Answer 104

* Unstable brady dysrhythmias: pace * Unstable tachy dysrhythmias: shock * Afib RVR, slow down/convert

Question 105

Treatment of ADHF * Goal 3: How do you reduce Preload?

Answer 105

* Nitroglycerine * Loop diuretics

Question 106

Treatment of ADHF * How do you reduce afterload?

Answer 106

* IV milrinone * High dose NTG works, tricky with BP and headaches * ACE-inhibitors * Nitroprusside/Nipride (can lead to brain edema from vasodilation; prolonged use can also lead to cyanide toxicity)

Question 107

Treatment of ADHF * How do you improve contractility?

Answer 107

Question 108

HF Treatment: IV medications used in hospital during ADHF-> dobutamine * What class of CHF? * Positive what? * Improves what? * Used in txt of what? * Used to assess what?

Answer 108

* Class IV CHF * Positive inotropic agent * Improves LV contractility and cardiac output * Used in treatment of acute decompensated CHF hospital admission * Used to assess cardiac contractile reserve | Proarrhythmic

Question 109

HF Treatment: IV medications used in hospital during ADHF-> milrinone * What class of CHF? * Positive what? * What does it cause/decrease * Improves what?

Answer 109

* Class IV CHF * Positive inotropic agent * Vasodilator, decreases afterload (decrease BP) * Improves LV contractility and cardiac output

Question 110

Medications are great but also need to treat comorbidities * Why do we need to tx a-fib? * What are the two types of control? * Restoration to what? * What are the txt?

Answer 110

* Afib leads to atrial cardiomyopathy, fibrosis, and heart failure * Rate control vs rhythm control * Restoration to NSR is key * Treatment: antiarrhythmic drugs, dccv, surgery

Question 111

What is the process of afib? What are the risk factors?

Answer 111

Question 112

HF treatment: Device Therapy Late Stage Management * When is ICD a good rec? * Used to prevent what? * Improves what?

Answer 112

* Implantable cardioverter-defibrillator (ICD) – rec’d for patients with good life expectancy (at least 1 year) if they have sustained v tach or v fib or unexplained syncope or are symptomatic with an EF less than 35% and on meds * Used to prevent arrhythmias/sudden cardiac death Improves survival | Appropriate for some patients

Question 113

Device Therapy * Biventricular pacemaker (cardiac resynchronization therapy - CRT) may help with what?

Answer 113

may help with symptoms and decrease hospitalizations for HF patients with LVEF less than 35% and a widened QRS complex with left bundle branch block (NYHA Class III).

Question 114

Many CRT devices also have ICD function and indicated if what (3)?

Answer 114

* Ejection fraction  <30%, in normal sinus rhythm, and QRS >150ms.  * Optimizes diastolic function by reducing mismatch between atria and ventricles. * Allows both ventricles to contract together

Question 115

Cardiac Resynchronization Therapy (CRT) * **CRT improves symptoms of heart failure in about 50% of patients who have been treated how?** * Improves what? (2)

Answer 115

* **CRT improves symptoms of heart failure in about 50% of patients who have been treated maximally with medications but still have severe or moderately severe heart failure symptoms**. * Improves survival, quality of life, heart function, the ability to exercise, and helps decrease hospitalizations in select patients with severe or moderately severe heart failure. * Improves NYHA class

Question 116

Device Therapy: MCS (Mechanical circulatory support) * What are the different types and what do they do? (3)

Answer 116

Question 117

What is the intra-aortic balloon pump?

Answer 117

Question 118

LVAD – Left ventricular assist device * What is ti? * What type of pump? * Helps with what?

Answer 118

* Pump used for patients who have reached end-stage heart failure * Battery operated, mechanical pump * Helps the left ventricle pump blood to the rest of the body

Question 119

LVAD – Left ventricular assist device * Can be used as what? (2)

Answer 119

* **Bride to transplant therapy** – used while patients awaiting heart transplant * **Destination therapy** – for patients that are not candidates for heart transplants

Question 120

Surgical Intervention: Heart transplantation * Choice of txt for who? (3)

Answer 120

* patients under age 60 with severe refractory HF, have no other life threatening conditions and are highly adherent to treatment regimens * End stage heart failure * Severe CAD, not amenable to CABG or PCI

Question 121

Heart transplantation * What is the survival? * When was the first heart transplant? * How many are performed each year?

Answer 121

* Survival is 85-90% at 1 year, 75% at 5 yrs * The world's first human heart transplant was on December 3, 1967 * Worldwide there are 5,000 heart transplants performed every year

Question 122

What are Factors that affect eligibility for Heart Transplantation?

Answer 122