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cardiology > heart failure > Flashcards

heart failure Flashcards

1
Q

what is ANP ( atrial natriuretic peptide)

A

ANP is released from monocytes in response to stretch. ANP induces diuresis, natriuresis, vasodilation and suppression of the renin-angiotensin system. ANP levels are increased in congestive cardiac failure

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2
Q

what is BNP (B-type natriuretic peptide)

A

secreted by ventricles in response to increased myocardial wall stress. BNP is increased in patients with heart failure

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3
Q

what is CNP ( C-type natriuretic peptide)

A

limited to vascular endothelium and CNS, similar effects to ANP and BNP

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4
Q

what system is activated in regards to heart failure

A

renin-angiotensin-aldosterone system

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5
Q

what are the pathophysiological changes in heart failure

A
  • ventricular dilation
  • myocyte hypertrophy
  • increased collagen synthesis
  • altered myosin gene expression
  • altered sarcoplasmic Ca2+
  • increased atrial natriuretic peptide secretion
  • salt and water retention
  • sympathetic stimulation
  • peripheral vasoconstriction
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6
Q

what is venous return (preload)

A

preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole

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7
Q

what is outflow resistance (afterload)

A

Afterload is the pressure that the heart must work against to eject blood during systole

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8
Q

effects that preload and afterload experience due to heart failure

A
  • preload - reduction of the volume of blood ejected within each heart beat and an increase in the volume of blood remaining after systole
  • afterload- an increase in afterload will decrease the cardiac output resulting in an increase of end diastolic volume and dilation of ventricle
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9
Q

how is salt and water retained due to heart failure

A
  • the increase of venous pressure that occurs when the ventricles fail will lead to retention of salt and water- the accumulation of salt and water in the interstitial will lead to the signs of heart failure
  • reduced cardiac output will lead to reduced renal perfusion which will activate the renin-angiotensin system and will then enhance salt and water retention
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10
Q

what is the role of calcium ion influx within myocytes (contraction) (relaxation) (in heart failure)

A
  • excitation of the myocyte cell membrane causes the rapid entry of calcium into the myocytes from the extracellular space via calcium channels. This triggers the release of intracellular calcium from the sarcoplasmic reticulum and initiates contraction
  • relaxation results from the uptake and storage of calcium by the sarcoplasmic reticulum controlled by the changes in nitric oxide
  • in heart failure there is the prolongation of the calcium current in association with prolongation of contraction and relaxation
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11
Q

what are some clinical syndromes of heart failure

A
  • heart failure with reduced ejection fraction
  • heart failure with preserved left ventricular ejection fraction
  • right ventricular systolic dysfunction
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12
Q

what are clinical features of heart failure

A
  • exertional dyspnoea
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • fatigue
  • tachycardia
  • elevated JVP
  • cardiomegaly
  • third and fourth heart sounds
  • Bi-basal crackles
  • pleural effusion
  • peripheral ankle oedema
  • ascites
  • tender hepatomegaly
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13
Q

what should the diagnosis of heart failure be based on

A
  • history
  • clinical findings
  • natriuretic peptide levels
    objective evidence of cardiac dysfunction
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14
Q

how are diuretics used in heart failure

A
  • they act by promoting the renal excretion of salt and water by blocking tubular reabsorption of sodium and chloride
  • loop diuretics and thiazide diuretics should be given in patients with fluid overload
    ie furosemide, bumetanide and bendroflumethiazide, hydrochlorothiazide
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15
Q

how are angiotensin converting enzyme inhibiters used in heart failure

A
  • improve symptoms and reduce mortality significantly
  • are recommended in all patients who are at risk of developing heart failure
  • should be introduced at a low dose and gradually titrated with regular monitoring of blood pressure and renal function
  • adverse effects = cough, hypotension, hyperkalaemia and renal dysfunction
  • ACE inhibitors dilate the blood vessels to improve your blood flow. This helps decrease the amount of work the heart has to do. They also help block a substance in the blood called angiotensin that is made as a result of heart failure. Angiotensin is one of the most powerful blood vessel narrowers in the body
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16
Q

how are angiotensin II receptor antagonists used in heart failure

A
  • eg candesartan, losartan, valsartan

- second line therapy for patients who are intolerant to ACE inhibitors

17
Q

how are beta blockers used in heart failure

A
  • Bisoprolol and carvedilol reduce mortality in ant grade of heart failure
  • Nebivolol is used in treatment of stable mild to moderate heart failure in patients over 70
  • Beta blockers cause your heart to beat more slowly and with less force, which lowers blood pressure. Beta blockers also help open up your veins and arteries to improve blood flow.
18
Q

how are aldosterone antagonists used in heart failure

A
  • eg spironolactone and eplerenone
  • helps reduce mortality in heart failure
  • can cause breast pain or gynaecomastia
  • Aldosterone receptor antagonists affect the balance of water and salts going into your urine and are weak diuretics. They help lower blood pressure, reduce congestion and thus protect the heart.
19
Q

how is angiotensin receptor neprilysin inhibitor used in heart failure

A
  • are a new class of drug that produce dual inhibition of the angiotensin receptor and the natriuretic system
20
Q

how are cardiac glycosides used in heart failure

A
  • eg digoxin
  • indicated in patients with atrial fibrillation with heart failure
  • it is infrequently used in patients ass an add on therapy if they are already using ACE inhibitors
21
Q

how are vasodilators and nitrates used in heart failure

A
  • reduces preload and afterload

- is used in patients intolerant to ACE inhibitors or ARAs

22
Q

what are the stages of heart failure and what drugs should be used at each stage

A

A= high risk with no symptoms = risk factor reduction, patient and family education, treat hypertension, diabetes, dyslipidemia

B= structural heart disease, no symptoms = ACE inhibitors or ARAs in all patients, beta blockers in selected patients

C= structural disease, previous or current symptoms = ACE inhibitors and beta blockers in all patients, dietary sodium restriction and diuretics and digoxin, cardiac resynchronisation if bundle branch block present, ravascularisation and mitral valve surgery, consider multidisciplinary team, aldosterone antagonist, nesiritide

D= refractory symptoms requiring special intervention = Inotropes, VAD and transplantation, Hospice

23
Q

what are example of ACE inhibitor drugs

A
  • Ramipril
  • Enalapril
  • Captopril
  • Candesartan
  • Lisinopril
  • Valsartan
  • Losartan
24
Q

what are examples of beta adrenoceptor blocking drugs (beta blockers)

A
  • Bisoprolol
  • Carvedilol
  • Metoprolol succinate
  • Nebivolol
25
Q

what are non-pharmacological treatment of heart failure

A
  • revascularisation
  • hibernating myocardium and myocardial stunning
  • cardiac resynchronisation therapy
  • implantable cardioverter-defibrilator
  • cardiac transplantation
26
Q

what is revascularization

A

revascularization is the restoration of perfusion to a body part or organ that has suffered ischemia. It is typically accomplished by surgical means. Vascular bypass and angioplasty are the two primary means of revascularization.

27
Q

what is hibernating myocardium

A

reversible left ventricular dysfunction due to chronic coronary artery disease that responds positively to inotropic stress and indicates the presence of viable heart muscle that may recover after revascularization.

  • it is caused by reduced myocardial perfusion
  • it results from repetitive episodes of cardiac stunning that occur
28
Q

what is myocardial stunning

A

is reversible ventricular dysfunction that persists following an episode of ischaemia when the blood flow has returned to normal , there is a mismatch between flow and function.

29
Q

what is cardiac resynchronisation therapy

A

simultaneous placing of both ventricles using a lead placed in the right ventricle and another in the coronary sinus to pace the left ventricle. Resynchronisation may reverse the process of ventricular remodelling, reduce functional mitral regurgitation and improve left ventricular function

30
Q

what is the definition of heart failure

A

The state in which the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or do so only at a high pressure

31
Q

what is a common physical exam to find heart failure

A
  • neck exam: elevated JVP
  • auscultation of the lungs: Rales crackles
  • auscultation of the heart: third or fourth heart sounds, murmurs
  • oedema in dependant areas: sacrum, feet/ankles/lower legs
32
Q

what is ejection fraction

A

Its the percentage blood that is pumped out of the heart during each beat. Normally it is >50%. Heart failure with an EF of <40% is known as heart failure with reduced ejection fraction (HFrEF)

33
Q

what is the distinction between HRrEF and HRpEF

A

In HRrEF the LV is unable to eject an adequate amount of blood during systole whereas in the HRpEF less blood is able to fill the LV in diastole, due to myocardial stiffness. Thus the LV has less blood to eject during systole

34
Q

what are pharmacological measures that will prolong survival of heart failure

A
  • RAS inhibitors - ie ACE inhibitors and ARII antagonists - push to the maximum dose tolerated
  • Beta blockers to block sympathetic symptoms - start at a low dose and slowly up-titrate to the highest dose tolerated
  • Aldosterone antagonists - ie spironolactone and eplerenone
  • Vasodilators - Hydralazine and nitrates combined for those who cannot tolerate ACE inhibitors
  • Sinus node blocker
35
Q

what are pharmacological measures that will improve symptoms of heart failure

A
  • Digoxin

- Frusemide

36
Q

what can be the aetiology of acute heart failure

A
  • ischaemic heart disease
  • valvular heart disease
  • hypertension
  • acute and chronic kidney disease
  • atrial fibrillation
37
Q

what is the structured assessment for the clinical diagnoses of acute heart failure

A
  • A 12 lead ECG
  • Blood investigations
  • Plasma BNP of NT-proBNP (BNP>100pg/ml or NT-proBNP>300pm/ml is suggestive of heart failure)
  • TTE (echocardiogram)
38
Q

what are ventricular assist devices

A

Mechanical systems that replace or help the failing ventricles in delivering blood around the body

  • LVAD = left ventricular assist device receives blood for the left ventricle and delivers it to the aorta
  • RVAD = receives blood at the right ventricle and delivers it to the pulmonary artery
39
Q

what are pharmacological therapies for acute heart failure

A
  • Myocardial oxygenation = ensures airway is patent and maintain arterial saturation at 95-98%
  • Opiate eg morphine = use in an agitated patient and it relieves dyspnoea, venous and arterial dilation
  • Antithrombin eg low weight molecular heparin = used in patients with AHF, ACS or atrial fibrillation
  • Vasodilators eg glyceryl trinitrate = reduces pulmonary congestion: at low doses causes venodilation, reducing preload: at high doses it can cause arterial vasodilation, reducing afterload
  • Diuretic eg furosemide = low doses produce vasodilation, reduce right atrial pressure
  • Inotropes eg dopamine = produce vasodilation and may improve diuresis. A medium dose acts on beta receptors to increase myocardial contraction and cardiac output. A high dose can act on alpha receptors causing vasoconstriction and increasing total peripheral resistance
  • Vasopressor eg noradrenaline = stimulates alpha receptors. Increases total peripheral resistance and BP
  • Digoxin inhibits myocardial sodium and potassium ATPase leading to increased calcium and sodium exchange. Increases cardiac output and slows AV conduction

cardiology (13 decks)

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