Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FCM Physiology > 2 LOBS > Flashcards

2 LOBS Flashcards

1
Q

Explain the pathophysiology of congestive heart failure – link into physical exam findings.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Develop a differential diagnosis for dyspnoea.

A
  • pneumonia,
  • asthma and
  • chronic obstructive pulmonary disease (COPD).
    ?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does cardiac failure effect the function and release of hormones? (This can be
related to the rationale for medication for CHF)

A

bnp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name 4 common heart murmurs

A

Aortic stenosis
Pulmonary stenosis
Tricuspid regurgitation
Mitral stenosis/regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

explain the anatomy and basic
pathophysiology of Aortic stenosis

A

this is a type of heart valve disease (valvular heart disease). The valve between the lower left heart chamber and the body’s main artery (aorta) is narrowed and doesn’t open fully. This reduces or blocks blood flow from the heart to the aorta and to the rest of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

explain the anatomy and basic
pathophysiology of Pulmonary stenosis

A

this is a narrowing of the valve located between the lower right heart chamber (right ventricle) and the lung arteries (pulmonary arteries). In a narrowed heart valve, the valve flaps (cusps) may become thick or stiff. This reduces blood flow through the valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

explain the anatomy and basic
pathophysiology of Tricuspid
regurgitation

A

this occurs when the valve’s flaps (cusps or leaflets) do not close properly. Blood can leak backward into the atrium from the leaky tricuspid valve, causing your heart to pump harder to move blood through the valve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

explain the anatomy and basic
pathophysiology of Mitral stenosis/regurgitation

A

this occurs when the mitral valve in your heart narrows, restricting blood flow into the main pumping chamber. Your mitral valve may also leak, causing blood to flow back through the valve each time the left ventricle contracts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the CXR findings for congestive heart failure.

A
  • Alveolar oedema (perihilar/bat-wing opacification)
  • Kerley B lines (interstitial oedema)
  • Cardiomegaly (cardiothoracic ratio >50%)
  • Dilated upper lobe vessels
  • Effusions (e.g. pleural effusions – blunted costophrenic angles)

?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

relevant bedside investigations of acute heart failure. (include side effects + contraindications.)

A
  • Vital signs: may show hypoxia (often SpO2 < 90%), tachycardia, and tachypnoea. The systolic blood pressure may be normal, elevated, or reduced (hypotension is associated with cardiogenic shock and poor prognosis). The pulse pressure may be narrow (<25% of the sBP).
  • ECG: the ECG is rarely normal. Abnormalities (e.g. signs of ischaemia or arrhythmias) are very common in AHF and an alternative diagnosis should be considered if the ECG is completely normal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pharamacological
management of acute heart failure
(include side effects + contraindications.)

A
  • oxygen
  • loop diurectics
  • nitrates
  • Non-invasive ventilation (NIV)
  • Cardiogenic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When is a loop diuretic considered in the management of heart failure?

A
  • All ‘WET’ patients will require diuretics as the cornerstone of their management.
  • Patients with chronic kidney disease and those already on oral diuretics will need a greater dose.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Understand the impact of a cardiovascular diagnosis on a family, and the future implications for the family

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Understand the mechanism of action, side effects and contraindications for loop and potassium-sparing diuretics.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are idiopathic and iatrogenic?

A

Idiopathic disease: any disease which is of uncertain or unknown origin, arising spontaneously.
Examples: acute idiopathic polyneuritis, diffuse idiopathic skeletal hyperostosis, idiopathic pulmonary fibrosis, idiopathic scoliosis.

Iatrogenic disease: disease induced by drug/s prescribed by a physician and/or diagnostic or therapeutic procedures undertaken on a patient. With the multitude of drugs prescribed to a single patient adverse drug reactions are bound to occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define dyspnoea

A

difficult or laboured breathing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Differentials diagnosis for dyspnoea

A
  • Asthma
  • COPD
  • Heart failure
  • Pneumonia
  • mental disorders
  • lung cancer
  • cystic fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes pallor?

A

Pallor- paleness. Caused by reduced blood flow and oxygen or by a decreased number of red blood cells. Can be a symptom of serious medical conditions such as anaemia, bloodstream infection, frostbite, leukaemia, low BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is paroxysmal nocturnal dyspnoea (PND)?

A

Sensation of shortness of breath that awakens a patient after 1-2 hours of sleep, usually relieved in the upright position. Caused by failure of left ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is orthopnoea?

A

Sensation of breathlessness whilst lying down, relieved by sitting or standing. Usually occurs when heart isn’t strong enough to pump out all the blood sent from the lungs. Heart failure, build-up of fluid in lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is jugular venous pressure and what happens if it is distended?

A

Jugular venous pressure provides an indirect measure of central venous pressure. Jugular vein distention is the bulging of the major veins in the neck. Increased pressure of the superior vena cava causes the jugular vein to bulge. Key symptom of heart failure and other circulatory problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the mechanism for ventricular hypertrophy?

A

Left ventricular hypertrophy is induced by an increased filling pressure of the left ventricle, otherwise known as diastolic overload. This condition is caused by changes in genes that cause the heart muscle to thicken. The thickening makes it harder for the heart to pump blood. It can occur even without high blood pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the pathophysiology of congestive heart failure

A

Heart failure develops when there are changes to the structure of the heart muscle and it can’t pump blood as efficiently as it should. When this happens blood can back up and fluid may build up in the lungs or arms and legs, indicating congestive heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does the FBC indicate?

A

Full blood count. This is a test to check the types and numbers of cells in your blood, including red blood cells, white blood cells and platelets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does high BNP indicate?

A

Brain natriuretic peptide (BNP)- hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume.
BNP levels go up when the heart cannot pump the way it should. A result greater than 100 pg/mL is abnormal. The higher the number, the more likely heart failure is present and the more severe it is.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

chest x-ray interpretation A to E

A

The ABCDE approach can be used to carry out a structured interpretation of a chest X-ray:
Airway: trachea, carina, bronchi and hilar structures.
Breathing: lungs and pleura.
Cardiac: heart size and borders.
Diaphragm: including assessment of costophrenic angles.
Everything else: mediastinal contours, bones, soft tissues, tubes, valves, pacemakers and review areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is interstitial oedema?

A

Caused by accumulation of fluid in the extracellular spaces of the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Understand the relationship between sodium levels and oedema

A

High quantities of sodium consumption can lead to an electrolyte imbalance, causing hypertension or oedema. Oedema, known as water retention, occurs when you consume large amounts of sodium relative to your water intake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

When are chest drains a suitable management?

A

You need a chest drain if you have an air leak (pneumothorax), a collection of fluid (pleural effusion), pus (empyema) or blood (haemothorax) in the pleural space. Any of these can cause problems with breathing and can stop the lungs from working properly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why are loop diuretics used in heart failure?

A

Due to their greater effectiveness, loop diuretics, such as furosemide, are the mainstay of diuretic therapy in HF. Loop diuretics produce more intense and shorter diuresis than thiazides, which results in more gentle and prolonged diuresis

Loop- fast acting
Thiazide diurectics - - gentle and more prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the common heart murmurs and the pathophysiology of each of them?

A

Aortic stenosis, mitral regurgitation, aortic regurgitation, mitral stenosis, mitral valve prolapses, tricuspid regurgitation, pulmonary stenosis, pulmonary regurgitation, tricuspid stenosis,

(incomplete)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is LVEF and the normal range?

A

LVEF is the fraction of chamber volume ejected in systole (stroke volume) in relation to the volume of the blood in the ventricle at the end of diastole (end-diastolic volume).
The left ventricle is the heart’s main pumping chamber. It pumps oxygen-rich blood up into your body’s main artery (aorta) to the rest of the body.
A normal ejection fraction is about 50% to 75%.
A borderline ejection fraction can range between 41% and 50%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is spironolactone and how does it work?

A

Diuretic to treat oedema, high BP, hormone conditions. Spironolactone is also used to lessen the need for hospitalisation for heart failure.

Unlike other types of diuretic, spironolactone does not make your body lose potassium.
It works by stopping aldosterone (a hormone made by the adrenal glands) from working in a part of the kidneys called the distal tubules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is available in the community for cardiac rehab?

A

Cardiac rehabilitation often involves
- exercise training
- emotional support
- education about lifestyle changes to reduce your heart disease risk, such as eating a heart-healthy diet, maintaining a healthy weight and quitting smoking.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Define heart failure

A

It is a complex syndrome in which the ability of the heart to maintain the circulation of blood is impaired as a result of structural or functional impairment of ventricular filling or ejection

In other words:
When the heart is unable to circulate blood around the body as a result of impairment of ventricular filling or ejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name the different types of heart failure

A
  • Acute versus chronic
  • Right-sided versus left-sided
  • Systolic (HFrEF) versus diastolic (HFpEF)
  • High output versus low output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the risk factors and causes of heart failure

A
  • coronary heart disease (myocardial infarction, atrial fibrillation, heart block)
  • hypertension.
  • smoking,
  • excess alcohol intake and
  • recreational drug use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the classification used for heart failure

A

Time-course of heart failure
 Acute vs Chronic

When the Ejection fraction
 LVEF ≤ 35-40%
 Heart failure with reduced ejection fraction (HF-REF)
 Heart failure with preserved ejection fraction (HF-PEF)

Symptomatic severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the symptoms of heart failure

A

CHF:
- Dyspnoea on exertion
- Fatigue limiting exercise tolerance
- Orthopnoea: the patient may be using several pillows to reduce this symptom.
- Paroxysmal nocturnal dyspnoea (PND): attacks of severe shortness of breath in the night that are relieved by sitting up (pathognomonic for CHF).
- Nocturnal cough with or without the characteristic ‘pink frothy sputum’.
- Pre-syncope/syncope
- Reduced appetite
- shortness of breath
- ankle swelling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Explain how to diagnose heart failure

A

investigations required for diagnosis include ECG, NT-proBNP and echocardiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causes of new-onset AHF include:

A

Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Acute valve dysfunction
Arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the management of heart failure and recognise some of the common medications used to treat heart failure

A

Management involves a combination of lifestyle modification, pharmacological therapies and in some cases surgical intervention.

pharmacological therapies include:
- Diuretics
- ACE inhibitors
- Beta-blockers eg. bisoprolol
- Angiotensin-II receptor antagonists (ARBs) eg. candesartan
- Mineralocorticoid/aldosterone receptor antagonists (MRAs) eg. spironolactone or eplerenone
- Sodium-glucose cotransporter-2 (SGLT2) inhibitors eg. dapagliflozin

lifestyle modification:
- Fluid and salt restriction
- Regular exercise
- Smoking cessation
- Reduced alcohol intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is chronic HF

A

(CHF) is a clinical syndrome involving reduced cardiac output because of impaired cardiac contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is acute HF

A

rapid onset or worsening of the signs and symptoms of heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

causes of heart failure

A
  • coronary heart disease (myocardial infarction), - atrial fibrillation,
  • valvular heart disease,
  • hypertension.

Other causes of heart failure include:
- Endocrine disease: hypothyroidism, hyperthyroidism, diabetes, adrenal insufficiency, Cushing’s syndrome

Medications:
- calcium antagonists,
- anti-arrhythmics,
- cytotoxic medication,
- beta-blockers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

symptoms of Chronic HF

A

shortness of breath, fatigue and ankle swelling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

causes of HF

A

HIGH-VIS
- Hypertension (common cause)

  • Infection/immune: viral (e.g. HIV), bacterial (e.g. sepsis), autoimmune (e.g. lupus, rheumatoid arthritis)
  • Genetic: hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM)
  • Heart attack: ischaemic heart disease (common cause)
  • Volume overload: renal failure, nephrotic syndrome, hepatic failure
  • Infiltration: sarcoidosis, amyloidosis, hemochromatosis
  • Structural: valvular heart disease, septal defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

syncope

A

fainting or passing out

49
Q

Orthopnoea

A

the sensation of breathlessness in the recumbent (lying down) position, relieved by sitting or standing

50
Q

Paroxysmal nocturnal dyspnea (PND)

A

is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position.

51
Q

cardiomyopathy

A

a disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body. Cardiomyopathy can lead to heart failure.

52
Q

Clinical findings on cardiovascular examination for Chronic HF

A
  • Tachycardia at rest
  • Hypotension
  • Narrow pulse pressure
  • Raised jugular venous pressure
  • Displaced apex beat (due to left ventricular dilatation)
  • Right ventricular heave
  • Gallop rhythm on auscultation (pathognomic for CHF)
  • Murmurs associated with valvular heart disease (e.g. an ejection systolic murmur in aortic stenosis)
  • Pedal and ankle oedema
53
Q

Clinical findings on respiratory examination for Chronic HF

A

Tachypnoea
Bibasal end-inspiratory crackles and wheeze on auscultation of the lung fields
Reduced air entry on auscultation with stony dullness on percussion (pleural effusion)

54
Q

Clinical findings on abdominal examination for Chronic HF

A

Hepatomegaly
Ascites

55
Q

Tachypnoea

A

abnormally rapid breathing.

56
Q

bedside investigations for Chronic HF

A
  • ECG: should be performed on all patients with suspected heart failure. An ECG may identify evidence of previous myocardial infarction (e.g. ‘Q’ waves) or arrhythmias (AV block or atrial fibrillation). A normal ECG makes heart failure unlikely.
  • Urinalysis: may show glycosuria (diabetes) or proteinuria (renal disease)
57
Q

ECG findings associated with heart failure include

A
  • Tachycardia
  • Atrial fibrillation (due to enlarged atria)
  • Left-axis deviation (due to left ventricular hypertrophy)
  • P wave abnormalities (e.g. P.mitrale/P.pulmonale due to atrial enlargement)
  • Prolonged PR interval (due to AV block)
  • Wide QRS complexes (due to ventricular dyssynchrony)
58
Q

Tachycardia

A

a heart rate over 100 beats a minute

59
Q

laboratory investigations for Chronic HF

A
  • FBC: anaemia
  • U&Es: renal failure, electrolyte abnormalities due to fluid overload (e.g. hyponatraemia)
  • LFTs: hepatic congestion
  • Troponin: if considering recent myocardial infarction
  • Lipids/HbA1c: ischaemic risk profile
  • TFTs: hyperthyroidism/hypothyroidism
  • Cardiomyopathy screen
  • N-terminal pro-B-type natriuretic peptide
60
Q

Classification based on severity of symptoms and limitation of physical activity (due to HF)

A

Class 1- no severe symptoms
Class 5- most severe

  • Class I: no symptoms during ordinary physical activity
  • Class II: slight limitation of physical activity by symptoms
  • Class III: less than ordinary activity leads to symptoms
  • Class IV: inability to carry out any activity without symptoms
61
Q

Complications of HF

A
  • Cardiac arrhythmias
  • Atrial fibrillation
  • Ventricular arrhythmias
  • Depression
  • Cachexia (wasting)
  • Chronic kidney disease
  • Sexual dysfunction
    -Sudden cardiac death
62
Q

Causes of acute decompensation of CHF include:

A
  • Infection
  • Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
  • Uncontrolled hypertension
  • Arrhythmias
  • Worsening chronic valve disease
  • Non-adherence with drugs/diet
  • Change in drug regimen
  • Withdrawal/reduction of heart failure medications inappropriately
  • Initiation/increase of rate-control medications inappropriately
  • Other medications: steroids, non-steroidal anti-inflammatories, pioglitazones
63
Q

Typical symptoms of HF:

A
  • Breathlessness: on exertion, at rest, on lying flat (orthopnoea), nocturnal cough, or waking from sleep (paroxysmal nocturnal dyspnoea)
  • Fluid retention (ankle swelling, bloated feeling, abdominal swelling, or weight gain
  • Fatigue, decreased exercise tolerance, or increased recovery time after exercise.
  • Light headedness or history of syncope
64
Q

Signs of HF:

A
  • Tachycardia
  • Laterally displaced apex beat, heart murmurs, and third and fourth hart sounds (gallop rhythm)
  • Hypertension
  • Raised jugular venous pressure
  • Enlarged liver (due to engorgement)
  • Respiratory signs such as tachypnoea, basal crepitations, and peripheral effusions.
  • Dependent oedema (legs, sacrum), ascites
  • Obesity
65
Q

Immediate management for HF

A
  • Review the person’s medication and if appropriate reduce or stop any drugs that may cause or worsen heart failure.
    Eg. CCBs
  • If symptoms are sufficiently severe, start a loop diuretic such as:
    Furosemide/bumetanide/torasemid
  • Arrange admission if the person has severe symptoms
  • Seek specialist advice/ arrange admission for pregnant women (or women who have given birth within 6 months) (this is to avoid late diagnosis of peripartum cardiomyopathy)
66
Q

What is Brain natriuretic peptide (BNP)

A

is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. ///
Predominantly secreted by the ventricles in response to increased myocardial wall stress

N-terminal (NT)- proBNP is an inactive protein that is cleaved from pro-BNP to release BNP.
Both are increased in patients with HF, and levels correlate with ventricular wall stress and the severity of heart failure.

67
Q

Other tests to consider to check for aggravating factors (to HF) and exclude other conditions. Possible tests include:

A
  • Chest X-ray
  • U&Es, eGFR, FBC, TFT, LFT, HbA1c, fasting lipids
  • Urine dip for blood and protein.
  • Lung function tests (peak flow and/or spirometry)
68
Q

Diagnosis of HF:

A
  • If the BNP level is above 400pg/mL (116pmol/L) or the NT-pro-BNP level is above 2000pg/mL (236pmol/L), refer for specialist assessment and echocardiography to be seen within 2 weeks.
  • If the BNP level is between 100–400pg/mL (29–116pmol/L) or the NT-pro-BNP level is between 400–2000pg/mL (47–236pmol/L), refer for specialist assessment and echocardiography to be seen within 6 weeks.
  • If BNP levels are normal (less than 100pg/mL [29pmol/L]) or NT-pro-BNP is less than 400pg/mL (47pmol/L), a diagnosis of heart failure is unlikely. Consider referral if a clinical suspicion of heart failure persists and conditions are present which may cause a false negative result.

Echocardiography is the gold standard investigation to confirm a diagnosis of heart failure

69
Q

Natriuretic peptide levels may be elevated by:

A

Age over 70 years.
Female gender.
Left ventricular hypertrophy, myocardial ischaemia, or tachycardia.
Hypoxia.
Pulmonary hypertension.
Pulmonary embolism.
Chronic kidney disease (estimated glomerular filtration rate less than 60 mL/min/1.73m2
Sepsis.
Chronic obstructive pulmonary disease (COPD).
Diabetes mellitus.
Liver cirrhosis.
Tachycardia
Left ventricular hypertrophy

70
Q

Natriuretic peptide levels may be reduced by:

A
  • Body mass index (BMI) greater than 35 kg/m2.
  • Drugs including diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-II receptor antagonists (AIIRAs), beta-blockers, and aldosterone antagonists (such as spironolactone).
71
Q

LVEF

A

is the percentage of blood that enters the left ventricle in diastole that is subsequently pumped out in systole.

72
Q

CHF management is to improve…

A
  • cardiac function
  • quality of life
  • prevent hospitalisation
  • reduce mortality.
73
Q

Lifestyle management strategies include:

A
  • Fluid and salt restriction
  • Regular exercise
  • Smoking cessation
  • Reduced alcohol intake
74
Q

medications which may be harmful in the context of heart failure such as:

A
  • Calcium channel blockers (e.g. verapamil, diltiazem)
  • Tricyclic antidepressants
  • Lithium
  • NSAIDs and COX-2 inhibitors
  • Corticosteroids
  • QT-prolonging medications
75
Q

patients with chronic heart failure require monitoring of:

A
  • Functional capacity, fluid status, cardiac rhythm, cognitive status and nutritional status
  • Renal function
76
Q

Why are Diuretics prescribed for HF?

A

to relieve symptoms of fluid overload (e.g. shortness of breath, peripheral oedema).

77
Q

Pharmacological management for HF involves:

A
  • ACE inhibitors
  • Diuretics
  • Beta-blockers
  • Angiotensin-II receptor antagonists (ARBs)
  • Mineralocorticoid/aldosterone receptor antagonists (MRAs)
  • Sodium-glucose cotransporter-2 (SGLT2) inhibitors
78
Q

Why are ACE inhibitors prescribed for HF?

A

given to all patients with left venticular dysfunction
- to improve ventricular function

79
Q

Who are ACE inhibitors prescribed for

A

patients with CHF and a reduced ejection fraction (≤40%)

80
Q

Who are Beta-blockers prescribed for

A

Beta-blockers (e.g. bisoprolol) should be prescribed for all patients with symptomatic heart failure and reduced LVEF (≤40%)

81
Q

Why are Beta-blockers prescribed for HF

A

decrease heart rate, myocardial oxygen demand and RAAS activation

82
Q

Contraindications for ACE inhibitors

A

Contraindications include
- a history of angioedema,
- bilateral renal artery stenosis,
- hyperkalaemia (>5 mmol/L),
- severe renal impairment (serum creatinine >220 μmol/L)
- and severe aortic stenosis.

83
Q

Contraindications for Beta-blockers

A

Contraindications include
- asthma,
- 2nd or 3rd degree AV block,
- sick sinus syndrome and
- sinus bradycardia.

84
Q

When are Angiotensin-II receptor antagonists (ARBs) prescribed?

A

If a patient is unable to tolerate an ACE inhibitor (usually due to persistent cough) an ARB (e.g. candesartan) should be prescribed as an alternative.

Patients must have normal serum potassium and adequate renal function to commence an ARB.

85
Q

When are Mineralocorticoid/aldosterone receptor antagonists (MRAs) prescribed?

A

A low-dose aldosterone antagonist (e.g. spironolactone or eplerenone) should also be prescribed if a patient continues to have symptoms of heart failure despite diuretics, ACE inhibitors and beta-blockers.
(e.g. spironolactone or eplerenone)

86
Q

When are Sodium-glucose cotransporter-2 (SGLT2) inhibitors prescribed

A

SGLT2 inhibitors (e.g. dapagliflozin) can be used as add-on therapy in patients with a reduced LVEF (<40%).
eg. dapagliflozin and empagliflozin.

87
Q
A
88
Q

congestive symptoms include

A
  • Shortness of breath with activity or when lying down
  • Fatigue and weakness
  • Swelling in the legs, ankles and feet
  • Rapid or irregular heartbeat
  • Reduced ability to exercise
  • Persistent cough or wheezing with white or pink blood-tinged mucus
  • Swelling of the belly area (abdomen)
  • Very rapid weight gain from fluid buildup
  • Nausea and lack of appetite
  • Difficulty concentrating or decreased alertness
  • Chest pain if heart failure is caused by a heart attack
89
Q

Where symptoms of fluid overload are present, what needs to be prescribed?

A

loop diuretic such as
- Furosemide 20–40 mg daily.
- Bumetanide 0.5–1.0 mg daily.
- Torasemide 5–10 mg daily.

90
Q

why are loop diuretics prescribed for people with HF

A

to relieve them of congestive symptoms and fluid retention

91
Q

what medications should be avoided for heart failure?

A

dihydropyridine CCBs such as verapamil, diltiazem and short-acting dihydropyridine agents

92
Q

What do all patients with HF get prescribed as part of their management plan?

A

a beta-blocker once established on an ACE inhibitor, unless there is a contraindication based on bradycardia, reactive airway disease, and unstable or low-output heart failure.

93
Q

management for HF exceptions where symptoms can worsen:

A
  • An ACE-inhibitor if the person has diabetes mellitus or has signs of fluid overload (a beta-blocker may make the symptoms of heart failure worse).
  • An ACE-inhibitor should not be initiated in a person with a clinical suspicion of haemodynamically significant valve disease, until the valve disease has been assessed by a specialist.
  • If the person is unable to tolerate an ACE-inhibitor (usually due to persistent troublesome cough), prescribe an angiotensin-II receptor antagonist (AIIRA).
94
Q

What do you offer if ACEi and BB not adequately controlling symptoms?

A

a mineralocorticoid receptor antagonist aka aldosterone antagonist (spironolactone), + an ACE inhibitor (or ARB) and beta-blocker, to people who have heart failure with reduced ejection fraction if they continue to have symptoms of heart failure.

95
Q

other management options:

A
  • Antiplatelet if indicated
  • Statin if indicated
  • Screen for depression and anxiety
  • If suitable, ensure the person has been offered referral to a supervised exercise-based group rehabilitation programme for people with heart failure
  • Ensure the person is offered an annual influenza vaccine and a once-only pneumococcal vaccination
  • advising the person to monitor their weight at home to detect fluid retention of worsening heart failure, if practical
  • Give advice about:
    ~ Salt consumption and diet
    ~ Maintaining fluid balance
    ~ What to do if acutely unwell (for example diarrhoea and vomiting) (sick day rules)
    ~ Smoking cessation if relevant
    ~ Alcohol consumption
    ~ Physical activity
    ~ Nutritional status
    ~ Sexual activity
    ~ DVLA
    ~ Air travel
96
Q

Follow up:

A
  • Assess and monitor symptoms and signs of heart failure
  • Ask about palpitations, shortness of breath, presence of oedema, syncopal and presyncopal symptoms.
  • Check the person’s pulse rate and rhythm and examine the heart
  • Assess fluid status (body weight, oedema, raised JVP, lung crepitations, hepatomegaly, postural drop in BP)
  • Assess functional capacity (NYHA)
  • Assess cognitive status and any psychosocial needs
  • Provide self-management plan
  • Assess nutritional status
  • Review medications
  • Ensure the person has been offered a supervised group exercise-based heart failure rehabilitation programme.
  • Ensure immunizations are up-to-date.
  • Monitor the serum urea, electrolytes, and estimated glomerular filtration rate (eGFR) every 6 months.
  • Consider if referral is indicated.
  • Provide women of child-bearing age with advice about contraception and pregnancy
97
Q

What is Ivabradine used for?

A

to treat adults who have chronic heart failure to reduce their risk of hospitalization for worsening heart failure

98
Q

What is ARNI (angiotensin receptor and neprilysin inhibitor) used for?

A

is made up of two drugs put together to treat heart failure. It contains an ARB (angiotensin II receptor blocker) and a neprilysin inhibitor.

99
Q

what does coronary artery bypass grafting involve?

A

taking a blood vessel from another part of the body (usually the chest, leg or arm) and attaching it to the coronary artery above and below the narrowed area or blockage. This new blood vessel is known as a graft.

100
Q

Complications of CHF include:

A
  • Arrhythmias: atrial fibrillation and ventricular arrhythmias
  • Depression and impaired quality of life
  • Loss of muscle mass
  • Sudden cardiac death
101
Q

what is Congestive heart failure (CHF)

A

is a common clinical disorder that results in pulmonary vascular
congestion and reduced cardiac output.

102
Q

aortic stenosis

A

is a type of heart valve disease (valvular heart disease). The valve between the lower left heart chamber and the body’s main artery (aorta) is narrowed and doesn’t open fully. This reduces or blocks blood flow from the heart to the aorta and to the rest of the body

103
Q

who are WET patients

A

Congestion in the pulmonary or systemic circulation. Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia.

104
Q

who are COLD patients

A

Hypoperfusion of vital organs as the cardiac output is reduced. These patients are ‘COLD’.

105
Q

Hypoperfusion

A

“a reduced amount of blood flow”

106
Q

ACH causes (pathology)

A

Hypoperfusion and congestion

107
Q

Causes of new-onset AHF include:

A

Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Acute valve dysfunction
Arrhythmias

108
Q

Causes of acute decompensation of CHF include:

A
  • Infection
  • Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
  • Uncontrolled hypertension
  • Arrhythmias
  • Worsening chronic valve disease
  • Non-adherence with drugs/diet
  • Change in drug regimen
    Withdrawal/reduction of heart failure medications inappropriately
    Initiation/increase of rate-control medications inappropriately
    Other medications: steroids, non-steroidal anti-inflammatories, pioglitazones
109
Q

Typical symptoms of acute heart failure include

A

Dyspnoea
Reduced exercise tolerance (classify using the New York Heart Association classification)3
Ankle swelling (clarify how high and whether this is progressing)
Fatigue
Pink frothy sputum
Orthopnoea (ask about the number of pillows used)
Paroxysmal nocturnal dyspnoea

110
Q

Typical symptoms of acute heart failure include

A

Dyspnoea
Reduced exercise tolerance (classify using the New York Heart Association classification)3
Ankle swelling (clarify how high and whether this is progressing)
Fatigue
Pink frothy sputum
Orthopnoea (ask about the number of pillows used)
Paroxysmal nocturnal dyspnoea

111
Q

Signs of pulmonary or systemic congestion include:

A

Fine basal crackles (bilateral)
Peripheral oedema (bilateral)
Dull percussion at the lung bases
Raised jugular venous pressure (JVP)
Hepatomegaly
Gallop rhythm (S3 or S4 heart sounds)
Murmur

112
Q

Signs of hypoperfusion include

A

Hypoxia
Tachypnoea and accessory muscle use
Tachycardia
Cyanosis
Cold, pale, and sweaty peripheries
Oliguria
Confusion/agitation
Syncope/pre-syncope
Narrow pulse pressure

113
Q

differential diagnosis for AHF

A

Asthma,
chronic obstructive pulmonary disease (COPD), pneumonia,
and pulmonary oedema

114
Q

Bedside investigations for AHF

A

Vital signs: may show hypoxia (often SpO2 < 90%), tachycardia, and tachypnoea. The systolic blood pressure may be normal, elevated, or reduced (hypotension is associated with cardiogenic shock and poor prognosis). The pulse pressure may be narrow (<25% of the sBP).

ECG: the ECG is rarely normal. Abnormalities (e.g. signs of ischaemia or arrhythmias) are very common in AHF and an alternative diagnosis should be considered if the ECG is completely normal.

115
Q

Laboratory investigations for AHF

A

AHF is unlikely and can be ruled out if:

BNP is less than 100 ng/litre
NT‑proBNP is less than 300 ng/litre

Arterial blood gas: often shows type 1 respiratory failure, or type 2 respiratory failure in those with pre-existing chronic lung conditions.

Baseline blood tests (FBC, U&E, coagulation, CRP): anaemia may be a contributing factor.

Cardiac troponin: to detect myocardial infarction (MI) as the underlying cause, however, troponins are often elevated in AHF patients without myocardial infarction.

Thyroid-stimulating hormone (TSH): thyroid abnormalities may precipitate AHF.

D-dimer: performed if a pulmonary embolism is suspected and Well’s score is low (if Well’s score is high proceed to imaging). Note that D-dimer can be positive in AHF in patients without a pulmonary embolism.

116
Q

Imaging for AHF

A

Chest X-ray
A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly (cardiothoracic ratio >50%) – may be difficult to assess on an AP film
D: dilated upper lobe vessels
E: effusions (i.e. pleural effusions – blunted costophrenic angles with meniscus sign)

Echocardiogram (transthoracic ultrasound scan): Biventricular systolic and diastolic function for ventricular dilation, reduced ejection fraction, ventricular hypertrophy and poor contractility
Valve disease
Ventricular wall rupture
Pericardial effusion
Intracardiac shunts: the presence of a dilated inferior vena cava with reduced respiratory variation is indicative of high venous pressure

Bedside lung ultrasound: may reveal extracardiac pathology such as pulmonary embolism or B-lines (consistent with interstitial oedema in pulmonary oedema)

117
Q

underlying causes of AHF

A

Acute coronary syndrome (ACS)
Hypertensive crisis
Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
Pulmonary embolism

118
Q

management for AHF

A

Oxygen
Loop diuretics
Nitrates
Non-invasive ventilation (NIV)
Cardiogenic shock

119
Q

Long-term management for AHF

A

Diuretic
ACE-inhibitor (ACEi) or angiotensin receptor blockers (ARB)
Beta-blocker
Aldosterone antagonist

Other specialist drugs
Ivabradine: for patients who cannot have a beta-blocker or who are on the maximum dose already, if they are in sinus rhythm with a heart rate >75
Sacubitril valsartan: for patients who decompensate on an ACEi/ARB
Hydralazine and nitrate: for patients who cannot tolerate an ACEi/ARB, or who are on the maximum dose
Digoxin: for patients with atrial fibrillation and uncontrolled tachycardia despite a beta-blocker

FCM Physiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions