CHD therapeutics Flashcards

1
Q

what is the BNP?

A
  • -Brain natriuretic peptide (half-life: 4–8 hours) and its precursor N-terminal pro-B-type BNP (half-life 2–3 days) are hormones that are produced by the cardiac ventricles. BNP is a systemic vasodilator and diuretic. The level of BNP is proportional to ventricular volume and pressure overload.
  • -High levels of BNP in patients with classic symptoms of CHF confirm the diagnosis (high predictive index
  • -A mild increase in BNP levels is difficult to interpret. BNP may be increased slightly in elderly patients, chronic renal disease, atrial fibrillations, or sepsis (low positive predictive value). In obese patients, BNP levels may be lower than in patients without obesity.
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2
Q

what is the left axis deviation?

A

An electrocardiographic finding in which the mean angle of ventricular depolarization (i.e., the QRS complex) is between -30º and -90º. LAD is present if the QRS complex is upright in lead I and down in lead II. Common causes for LAD include: left ventricular hypertrophy, left bundle branch block, and old inferior myocardial infarction.

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3
Q

what is the significance of Q waves on ECG?

A

An ECG finding that represents the beginning of ventricular depolarization. Normal Q waves are narrow (≤ 40 ms). Pathologic Q waves are abnormally wide (≥ 40 ms) and/or abnormally deep (≥ 2 mV or > 25% of the R wave amplitude) and can develop due to myocardial injury.

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4
Q

what are the causes of pathologic Q waves?

A

1) Myocardial injury or replacement
- -Myocardial infarction
- -Cardiac infiltrative disease (e.g., sarcoidosis, amyloidosis)
2) Ventricular enlargement
- -Acute pulmonary embolism
- -Hypertrophic cardiomyopathy
3) Altered ventricular conduction
- -Left bundle branch block
- -Wolff-Parkinson-White syndrome

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5
Q

what is the Ejection fraction?

A
  • -The percentage of blood pumped by the left ventricle during each contraction (i.e., stroke volume divided by end diastolic volume). Normally ∼ 55%.
  • -Serves as an index of myocardial contractility: e.g., ↓ myocardial contractility → ↓ EF (seen in systolic heart failure, where EF is < 40%)
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6
Q

what is the alveolar edema?

A
  • -A type of pulmonary edema in which the majority of fluid collects in the alveoli. Presents on chest x-ray with a positive air bronchogram and bilateral opacities that extend outward from the hilum (bat wing pattern). Common causes include heart failure, acute myocardial infarction, pulmonary embolism, and pneumonia.
  • -The radiologic signs of pulmonary congestion can be remembered with “ABCDE”: A = Alveolar edema (bat’s wings), B = Kerley B lines (interstitial edema), C = Cardiomegaly, D = Dilated prominent pulmonary vessels, and E= Effusions!
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7
Q

what is the congestive heart failure (CHD)?

A

A condition in which the heart is unable to pump enough blood to meet the metabolic needs of the body. Ventricular dysfunction results in low cardiac output, which in turn causes congestion of blood (backward failure) and poor systemic perfusion (forward failure).

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8
Q

what are the 3 main causes of heart failure?

A

The three main causes of CHF are coronary heart disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which results in blood congestion (backward failure) and poor systemic perfusion (forward failure). CHF is classified as either left heart failure (LHF) or right heart failure (RHF), although biventricular (global) CHF is most commonly seen in clinical practice.

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9
Q

systolic vs diastolic dysfunction?

A
  • -Systolic dysfunction: CHF with reduced stroke volume and ejection fraction (EF)
  • -Diastolic dysfunction: CHF with reduced stroke volume and preserved ejection fraction (The ejection fraction is not reduced because both the left ventricular end-diastolic volume and the stroke volume are reduced.)
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10
Q

RHF vs LHF?

A
  • -Right heart failure (RHF): CHF due to right ventricular dysfunction; characterized by backward heart failure
  • -Left heart failure (LHF): CHF due to left ventricular dysfunction; characterized by forward heart failure
  • -Biventricular (global) CHF: CHF in which both the left and right ventricle are affected, resulting in simultaneous backward and forward CHF
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11
Q

what is the consequence of systolic and diastolic dysfunction?

A

1) Forward failure: reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction)
2) Backward failure
- -Increased left-ventricular volume and pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema
- -Reduced cardiac output → systemic venous congestion → edema and progressive congestion of internal organs
- -Resulting macroscopic findings: nutmeg liver (Hepatic venous congestion leads to ischemia and fatty degeneration, causing the liver to resemble the inside of a nutmeg seed.)

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12
Q

what are the causes of systolic dysfunction?

A
  • -Reduced contractility: Damage and loss of myocytes reduce ventricular contractility and stroke volume.
  • -Increased afterload: increase in mean aortic pressure, outflow obstruction
  • -Increased preload: ventricular volume overload
  • -Cardiac arrhythmias
  • -High-output conditions
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13
Q

what are the causes of diastolic dysfunction?

A
  • -Decreased ventricular compliance: increased stiffness or impaired relaxation of the ventricle → reduced ventricular filling and increased diastolic pressure → decreased cardiac output ( long-standing arterial hypertension or aortic stenosis resulting in left ventricular hypertrophy, restrictive pericarditis, pericardial tamponade)
  • -Increased afterload: increase in pulmonary artery pressure
  • -Increased preload: ventricular volume overload
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14
Q

what are the compensatory mechanisms in CHF?

A

1) ↑ Adrenergic activity → increase in heart rate, blood pressure, and ventricular contractility
2) Increase of renin-angiotensin-aldosterone system activity (RAAS): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output
- -↑ Angiotensin II secretion → vasoconstriction → ↑ systemic blood pressure → ↑ afterload
- -Kidney: vasoconstriction of the efferent arterioles and, to a lesser degree, the afferent arterioles → ↓ net renal blood flow and ↑ intraglomerular pressure to maintain GFR
- -↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload
3) Brain natriuretic peptide (BNP): ventricular myocyte hormone released in response to increased ventricular filling and stretching
- -↑ Intracellular smooth muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary wedge pressure

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15
Q

what are the general features of heart failure?

A
  • -Nocturia (In the supine position, cardiac output increases and renal vasoconstriction decreases, leading to an increase in filtered urine and nocturia.)
  • -Fatigue
  • -Tachycardia, various arrhythmias (Due to an increase in sympathetic tone)
  • -Heart sounds S3/S4 gallop (An S3 gallop indicates rapid ventricular filling, while an S4 gallop indicates ventricular hypertrophy (reduced compliance). Other heart sounds may indicate valvular disease as a potential cause of CHF.)
  • -Pulsus alternans (A physical finding characterized by alternating strong and weak pulses (with a regular pulse rhythm) caused by alterations in cardiac output. Associated with left ventricular failure and cardiac tamponade.)
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16
Q

what are the clinical features of left-sided heart failure?

A
  • -Dyspnea , orthopnea (Initially exertional dyspnea; as CHF progresses, also dyspnea at rest)
  • -Pulmonary edema in severe cases of acute decompensated heart failure (see below)
  • -Bilateral basilar rales may be audible on auscultation.
  • -Paroxysmal nocturnal dyspnea: nocturnal bouts of coughing and acute shortness of breath (Supine position at night increases pulmonary venous congestion)
  • -Cardiac asthma: increased pressure in the bronchial arteries results in airway compression, leading to bronchospasm
  • -Laterally displaced apical heartbeat (precordial palpation beyond the midclavicular line)
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17
Q

what are the clinical features of right-sided heart failure?

A

1) Peripheral pitting edema
2) Signs of increased central venous pressure (CVP)
- -Jugular venous distention: visible jugular venous congestion, also seen in biventricular heart failure
- -Hepatojugular reflux: jugular venous congestion (Rise in central venous pressure leading to visible swelling of neck veins (upper body venous congestion))induced by exerting manual pressure over the patient’s liver → ↑ volume load on the right side of the heart → right heart is unable to pump additional blood volume → visible jugular venous distention persists for several seconds
3) Hepatic venous congestion
- -Hepatosplenomegaly
- -Abdominal pain
- -Jaundice
- -Ascites
4) Congestion of other organs, e.g., congestive gastritis or gastropathy (nausea, loss of appetite), renal congestion

18
Q

what is the high-output HF?

A

heart failure secondary to conditions associated with a high-output state, in which cardiac output is elevated to meet the demands of peripheral tissue oxygenation

19
Q

what are the causes of HOHF?

A
  • -Anemia
  • -Systemic arteriovenous fistulas (Blood is shunted from the arterial high pressure system to the venous low pressure system. This decreases systemic vascular resistance, which in turn increases heart rate, stroke volume, and subsequently cardiac output)
  • -Sepsis
  • -Hyperthyroidism
  • -Multiple myeloma
  • -Glomerulonephritis
  • -Polycythemia vera
  • -Wet beriberi (vitamin B1 deficiency)
  • -Physiological causes: pregnancy, fever, exercise
20
Q

what are the clinical features of HOFH?

A
  • -Symptoms of low-output CHF; particularly tachycardia, tachypnea, low blood pressure, and jugular distention with an audible hum over the internal jugular vein
  • -Pulsatile tinnitus
  • -Bounding peripheral pulses
  • -Laterally displaced apical heart beat
  • -Midsystolic murmur, S3 gallop (indicates rapid ventricular filling)
21
Q

What therapies are used in the management of acute heart failure?

A

1) Oxygen Therapy
- -Inhaled oxygen
* recommended when O2 saturation <90%
* aim SaO2 of 94-96%.
- -+/- Ventilatory support
* Continuous positive airways pressure (CPAP)
* Non-invasive positive pressure ventilation (NIPPV)
* Mechanical ventilation with endotracheal intubation
2) Diuretics for fluid retention
- -Initially loop diuretics such as furosemide 20-40mg as IV bolus.
- -Where the response is insufficient consider:
- -Higher dose loop diuretic
- -Addition of a thiazide, thiazide-like diuretic (metolazone) or spironolactone
3) Anticoagulation to reduce the risk of deep vein thrombosis
- -sub-cutaneous heparin
4) Vasodilators such as IV glyceryl trinitrate or nesiritide relieve pulmonary congestion, through balanced vasodilation of venous and arterial sides of the circulation, thereby reducing left ventricular preload and afterload and increasing stroke volume.
5) Inotropic agents are indicated where there is marked hypotension (shock), evidence of tissue hypo-perfusion or resistant pulmonary edema – bear in mind the risk of arrhythmias, myocardial ischemia, and longterm dysfunction.
- -Sodium-potassium-ATPase inhibition (Digoxin - mainly used in the presence of atrial fibrillation).
- -Beta-adrenoceptor stimulation (Dobutamine, Dopamine)
- -Phosphodiesterase inhibition (Type III), (Milrinone )
- -Calcium sensitization (Levosimendan)

22
Q

what are the lifestyle modifications in CHF?

A
  • -Salt restriction (< 3 g/day)
  • -Fluid restriction in patients with edema and/or hyponatremia
  • -Weight loss and exercise
  • -Cessation of smoking and alcohol consumption
  • -Immunization: pneumococcal vaccine and seasonal influenza vaccine
23
Q

what are the indications of diuretics in CHF?

A
  • -Begin treatment with loop diuretics (furosemide) to treat volume overload
  • -Thiazides may be added for a synergistic effect
24
Q

what are the indications of ACE inhibitors in CHF?

A
  • -initiate treatment with ACE inhibitors to reduce preload, afterload, and improve cardiac output
  • -If the patient does not tolerate drug (e.g., dry cough develops) → substitute with AT2-receptor blocker
25
Q

what are the indications of Beta-blocker in CHF?

A
  • -Add a beta blocker once the patient is stable on ACE inhibitor
  • -Particularly beneficial for patients with hypertension and post-myocardial infarction
26
Q

what is the role of aldosterone antagonists in CHF?

A
  • -In select patients, an aldosterone antagonist may be beneficial.
  • -If EF < 35%, and after myocardial infarction
  • -Spironolactone; eplerenone as an alternative
27
Q

what are the indications of digoxin in CHF?

A

–In heart failure with reduced ejection fraction
If symptoms persist despite treatment with beta blocker, ACE inhibitor, diuretics, and aldosterone antagonists
–May be given to control ventricular rate in atrial fibrillation (if beta blockers are contraindicated)

28
Q

what are the indications of ARNI (angiotensin receptor-neprilysin inhibitor) in CHF?

A
  • -Persistent or worsening symptoms despite adequate treatment regimen with first-line drugs
  • -Administered as combination valsartan-sacubitril
  • -Valsartan is an AT1-receptor blocker, while sacubitril is a neprilysin inhibitor. Neprilysin is an endopeptidase that degrades natriuretic peptides such as BNP. Inhibiting neprilysin results in a longer BNP effect.
29
Q

what are the drugs that improve the prognosis in CHF?

A

drugs that improve prognosis: beta blockers, ACE inhibitors, and aldosterone antagonists!

30
Q

what is the role of vasodilators in CHF?

A

Vasodilators such as IV glyceryl trinitrate or nesiritide relieve pulmonary congestion, through balanced vasodilation of venous and arterial sides of the circulation, thereby reducing left ventricular preload and afterload and increasing stroke volume.

31
Q

what is the milrinone?

A
  • -PDE3 inhibition → ↑ cAMP
  • -In the myocardium: ↑ cAMP → activation of calcium channels → cardiostimulatory effects (e.g., ↑ contractility)
  • -In peripheral vessels: ↑ cAMP → smooth muscle relaxation → vasodilation with reduced cardiovascular preload and afterload
  • -In platelets: ↑ cAMP → inhibition of platelet aggregation
  • -Acute treatment of decompensated cardiac failure with cardiogenic shock
32
Q

what is the indication of IV morphine in CHF?

A

indicated with severe dyspnoea and agitation

33
Q

ACEI and BB are not indicated in the early stabilization of patients with acute heart failure. T/F

A

True

34
Q

what is the warm dry vs warm wet CHF patient based on clinical features?

A

1) no congestion or hypoperfusion

2) congestion but no hypoperfusion

35
Q

cold wet vs cold dry?

A

1) hypoperfusion and congestion

2) hypoperfusion but no congestion

36
Q

what is the treatment of the wet and warm patients?

A

1) Hypertension predominates: vasodilator, diuretic

2) congestion predominates: diuretic, vasodilator, ultrafiltration

37
Q

what is the treatment of the wet and cold patient?

A

1) SBP <90: inotrops, vasopressor, diuretics, mechanical circulatory support
2) SBP>90: vasodilator, diuretic, consider inotropic

38
Q

what is the treatment of the dry and warm patient?

A

adjust oral therapy

39
Q

what is the treatment of dry and cold patients?

A

fluid challenge, inotrope

40
Q

what are the discharge prescriptions for a patient with CHF?

A
  • -ACEI and BBs, still symptomatic?–
  • -aldosterone antagonist, still symptomatic and EF <35%–
    1) ARNI
    2) CRT if QRS >130
    3) ivabradine if HR >70
  • -still resistant?–
  • -digoxin, H-ISDN, MVAD, heart transplantation