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Year 2 > Hypertension And Heart Failure > Flashcards

Hypertension And Heart Failure Flashcards

1
Q

What is preload?

A

Pressure in the ventricles prior to contraction. The greater the pre-load, the greater the forcefulness of heart contraction.

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2
Q

What is afterload?

A

Peripheral resistance of the body that the heart must work against to contract in systole, altered by the tone of blood vessels.

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3
Q

What is end-diastolic volume?

A

Volume of blood left in the ventricles at the end of diastole before systole. The greater the EDV, the greater the pre-load.

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4
Q

What is stroke volume?

A

Volume of blood pumped out of the left ventricles of the heart during systole.

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5
Q

What is Frank-Starling relationship?

A

Relationship between pre-load and stroke volume.
Initially, increase in pre-load will lead to more forceful contraction and increase in stroke volume. However, excess increase in pre-load overstretches the muscle fibres and results in decrease in stroke volume. It is a disproportional relationship.

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6
Q

What happens when there is an increase in end diastolic volume?

A

Causes muscle contraction and increase in stroke volume.

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7
Q

What is cardiac output?

A

Cardiac output is the amount of blood pumped out of the heart, measured by the stroke volume (ml) x the heart rate (bpm) Normal cardiac output is 5L/min.

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8
Q

What are the types of heart failure?

A

Systolic heart failure and Diastolic heart failure.

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9
Q

What is ejection fraction?

A

The stroke volume as a proportion of the total volume of blood in the ventricles. Normal ejection fraction is 55-70% and is reduced in left sided heart failure.

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10
Q

What is systolic heart failure?

A

Typically affects the left ventricles, where the pumping function of the heart is insufficient, which results in a lower ejection fraction. It has 3 main causes:

Dilated cardiomyopathy
Ischaemic heart disease due to atherosclerotic plaque
Hypertension.

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11
Q

What is dilated cardiomyopathy?

A

Dilation/increase in the size of the heart chamber, which typically occurs after an infection.

This increases pre-load and stroke volume to a point, however the greater chamber size causes the thinning and weakening of the cardiac muscles that makes it unable to pump and causes systolic heart failure.

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12
Q

How does hypertension lead to heart failure?

A

Greater peripheral resistance and afterload means that the left ventricle must pump harder to overcome these forces, which leads to hypertrophy of the overworked muscles. This results in compression of the coronary arteries and a greater oxygen demand due to a larger size. The left ventricle will have weaker contraction and this will eventually result in systolic failure.

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13
Q

What is Left sided diastolic heart failure?

A

Issue with filling of the left ventricle, however the ejection fraction is preserved. It is caused by:

Aortic stenosis
Hypertension that reduces the space in the chamber
Restrictive cardiomyopathy
Kidney RAAS signalling

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14
Q

How does aortic stenosis lead to heart failure?

A

Narrowing of the aorta means there is reduced blood flow out of the heart so the left ventricle must pump harder, and this leads to hypertrophy of the left ventricle, reducing the space in the chamber for blood to fill and causes diastolic heart failure.

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15
Q

How does hypertension lead to diastolic heart failure?

A

There is concentric hypertrophy in the left ventricle, where the new sarcomere are parallel to existing sarcomeres that reduces the space in the chamber for blood to fill.

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16
Q

How does restrictive cardiomyopathy lead to heart failure?

A

Stiffened ventricles have reduced compliance that reduces the ability of the left ventricle to stretch and fill with blood, causing diastolic heart failure.

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17
Q

How does kidney disease lead to heart failure?

A

Reduced renal perfusion activates the RAAS system to cause more fluid retention and stimulate heart contractility and stroke volume.

However, this results in an excess fluid buildup which will leak out of blood vessels into tissues and cause oedema.

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18
Q

What is a consequence of left-sided heart failure?

A

Blood backs up into the pulmonary artery, which causes pulmonary artery hypertension and results in pulmonary oedema. Excess blood in the vessels reduces the rate of gas exchange between the alveoli and makes the vessels prone to rupture.

The blood that leaks is taken up by macrophages to form haemosiderin, brown as a result of iron accumulation.

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19
Q

What are the features of pulmonary oedema?

A

Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea (intermittent SOB at night)
Crackles on auscultation.

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20
Q

How is pulmonary oedema treated?

A

Diuretics to remove the excess fluid build up from the body via urination

Oxygen supply, due to impaired gaseous exchange and ventilators support

Vasodilators such as:
—> Morphine: it reduces blood pressure by inducing vasodilation which also reduces pre-load
—>Nitrates

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21
Q

What is anarsca?

A

Severe generalised oedema of the body due to heart failure which develops over weeks and causes weight increase, ascites and pleural effusion.

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22
Q

What is the cause of right sided heart failure?

A

Right sided heart failure is also known as congestive heart failure, becauase blood will back up to the body and lead to oedema. It can occur due to:

Progression of left sided heart failure, where fluid will back up into the lungs and pulmonary artery
Arterial/ventricular septal defect
Chronic lung disease
Pulmonary embolism

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23
Q

What are causes of right sided heart failure unrelated to left-sided heart failure?

A

Atrial/ventricular septal defect, where high pressure blood from the Ieft moves to the right and results in pulmonary artery hypertension, concentric hypertrophy of the right side of the heart that causes ischaemia and reduced blood volume.

Lung disease creates state of hypoxia so the pulmonary artery compensates to take up more oxygenated blood via constriction, leading to right sided heart failure. This is cor pulmonale.

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24
Q

What does ascites indicate?

A

Fluid buildup in the peritoneal space due to oedema as a result of heart failure.

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25
Q

What is the consequence of right-sided heart failure?

A

Raised JVP
Fluid back up into the organs such as the spleen and liver, causing liver cirrhosis and oedema
Abdominal ascites
Pitting oedema

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26
Q

How is heart failure investigated?

A

Chest X-ray
Levels of pro-BNP
Echocardiogram

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27
Q

Why is BNP raised in heart failure?

A

Ventricles release BNP when overstretched due to volume overload, when there is issues with the pump function of the heart on the left side to act locally . The greater the levels of BNP, the lower the ejection fraction.

28
Q

When is ANP released?

A

ANP is released by the atria due to high blood pressure and volume. It acts systemically to inhibit the RAAS system and sympathetic activation in order to prevent cardiac hypertrophy.

29
Q

What is the pharmacological treatment of heart failure?

A

ABCDE

ACE inhibitors,
Beta blockers to reduce sympathetic system overactivation
Calcium channel inhibitors
Diuretics, typically loop and thiazide in combination to reduce AKI associated kidney damage.

30
Q

Where is angiotensinogen produced?

A

Liver

31
Q

Where is aldosterone released?

A

Adrenal gland, which acts on the alpha intercalated cells in the DCT to increase salt and water reabsorption.

32
Q

Which drugs can be used to reduce aldosterone levels?

A

Spironolactone is a non-selective competitive aldosterone antagonist for the aldosterone dependent Na+/K+ exchanger on the collecting duct which reduces Na+ and H20 reabsorption with a K+ sparing effect. It also antagonises androgen receptors and leads to gynaecomastia in men

Epelerone is a selective aldosterone and mineralcorticoid antagonist with no effects of gynaecomastia.

33
Q

How can beta blockers treat heart failure?

A

Reduces sympathetic nervous system activation, increasing diastolic coronary blood flow and decreasing myocardial oxygen demands.

34
Q

What is an ISA beta blocker?

A

Beta blockers with intrinsic sympathomimetic activity, that can be competitive agonists and antagonists. They lower peripheral resistance and minimise the effects of bradycardia because they maintain cardiac output and heart rate at rest.

35
Q

What is a Non-ISA beta blocker?

A

Antagonists of the beta-adrenergic receptors however, they result in bradycardia.

36
Q

What is a selective beta blocker?

A

Beta blockers which only antagonist B1 adrenergic receptors.

37
Q

What is a non-selective beta-blocker?

A

Beta blockers which antagonist both beta-1 and beta-2 adrenergic receptors.

38
Q

What is inotropy?

A

Force of contraction.

39
Q

What is chronotropy?

A

Rate of contraction.

40
Q

What is the beta-1 receptor?

A

Present in cardiac myocytes, SA and AV node and juxtaglomerular apparatus to result in increased blood pressure and cardiac output.

41
Q

What is the beta-2 receptor?

A

Present in the:
Uterus which reduces labour contractions.
Pancreas islet cells to increase insulin release.
Adipose tissue to increase lipolysis.
Ciliary body to increase aqueous humour production.

42
Q

When should beta blockers be avoided?

A

Non-selective beta blockers should be avoided in asthmatic patients.

43
Q

What is hypertension increase risk for?

A

Stroke and Coronary Artery Disease.

44
Q

What is hypertension?

A

Blood pressure over 140/90 measured on two consecutive readings at different occasions. The home blood pressure recordings or average blood pressure measured must be 135/85mmHg.

45
Q

What are the readings for pre-hypertension?

A

120-139 mmHg for systolic blood pressure.
80-89 for diastolic blood pressure.

46
Q

What is stage 1 hypertension?

A

Either:
Systolic blood pressure is 140-160 mmHg
OR
Diastolic blood pressure is 90-100 mmHg

The HBPM recording must be 135/85mmHg.

47
Q

What is Stage 2 hypertension?

A

Systolic blood pressure is greater than 160mmHg
Or
Diastolic blood pressure is greater than 100mHg.

The HBPM recording must be 150/95mmHg.

48
Q

What is primary hypertension?

A

Also known as essential hypertension, is the most common type of hypertension linked to modifiable risk factors such as smoking, age, alcohol, obesity, low activity, poor diet and genetics.

49
Q

What is the mechanism of primary hypertension?

A

Early stages will show higher cardiac output and blood volume. There is decreased renal sodium excretion which increases plasma volume and systolic blood pressure. This lowers renin release and causes peripheral arteriole vasoconstriction, leading to a greater peripheral resistance and diastolic blood pressure.

50
Q

How does hypertension affect the heart?

A

Causes endothelial damage which drives formation of atheroma which results in left ventricular hypertrophy.
Hypertension weakens the walls of vessels and drives aneurysm formation.
Causes aortic dissection.

51
Q

How does hypertension affect the kidneys?

A

Causes small vessel damage and reduces the GFR
Drive atheroma formation in the large vessels.
It causes the kidneys to shrink because there is parenchyma loss

52
Q

How does hypertension affect the eyes?

A

Hypertension can lead to retinopathy, where the small blood vessels of the eye are damaged. Long-term, it can lead to glaucoma, with dot haemorrhages and occlusion for retinal arteries.

53
Q

How does hypertension affect the brain?

A

Hypertension is a major cause of brain damage via haemorrhage, due to the formation of Charco-Bouchard aneurysm. It can lead to thrombosis in the small internal carotid arteries due to atheroma formation.

54
Q

What are dihydropiridines?

A

Calcium channel blockers which can cause ankle swelling, oedema and tachycardia,that can be reduced with use of beta blockers.

55
Q

What is secondary hypertension?

A

Less common cause of hypertension that is due to a secondary disease such as:
Renal disease. E.g polycystic disease
Phaemochromocytoma
Primary aldosteronism
Cushing’s syndrome due to high cortisol promoting salt retention.

56
Q

What are the signs for secondary hypertension?

A

Poor blood pressure control despite prescribing multiple anti-hypertensives
Patient is young without obvious underlying pathology.
Sudden onset of hypertension

57
Q

Which medications can cause secondary hypertension?

A

Cocaine increases sympathetic activation
Oestrogen containing contraceptives, because oestrogen upregulates angiotensinogen
Monoamine oxidase inhibitors used to treat depression, which increase availability of sympathetic neurotransmitters.

58
Q

How can thyroid pathology lead to hypertension?

A

Hyperthyroidism results in increased cardiac output, causing hypertension.

Hypothyroidism results in renal retention.

59
Q

What is aorta coarctation?

A

Narrowing of the aorta.

60
Q

What is accelerate hypertension?

A

Recent significant increase in baseline blood pressure which is acute and results in organ damage. There is a greater risk of this in smokers, people with secondary hypertension and men.

61
Q

What is the consequence of accelerate hypertension?

A

Damages small blood vessels and causes fibrinoid necrosis, with RBC fragmentation occurring in a condition called micro-angiopathic haemolytic anaemia.

62
Q

What is hypertensive urgency?

A

Hypertension with the absence of end organ disease, caused by inconsistency with medication compliance.

63
Q

What is hypertensive emergency?

A

Elevated blood pressure, that results in acute end organ stage disease.

64
Q

What is Conn’s syndrome?

A

Adrenal tumour that produces aldosterone which can lead to secondary hypertension.

65
Q

Why does papillary oedema occur?

A

Optic nerve swells up as a result of hypertension.

66
Q

How does hypertension affect the aorta?

A

May lead to an atheroma, aneurysm or dissection.
-> Aortic dissection is when there is a tear to the tunica intimate that allows blood to rush in and build up in pressure, rupturing the entire aorta and result in an aneurysm.

67
Q

What is concentric left ventricular hypertrophy?

A

Individual cell hypertrophy of the myocyte occurs which can lead to fibrosis of the left ventricle.

Year 2 (247 decks)

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