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HYMS Block 13 > Heart Failure and Hypertension > Flashcards

Heart Failure and Hypertension Flashcards

1
Q

what two things is blood pressure determined by?

A
  1. cardiac output

2. peripheral resistance

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2
Q

How does angiotensin II increase blood pressure?

A
  1. causes vasoconstriction
  2. promotes vascular hypertrophy
  3. stimulates aldosterone release → sodium and water retention
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3
Q

What is poiseulle’s law?

A

resistance is inversely proportional to the fourth power of the radius

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4
Q
  1. What is primary/essential hypertension?
  2. What are the two potential causes of primary hypertension?
  3. Why are current treatments for primary hypertension not ideal?
A
  1. hypertension that does not have a particular cause
  2. genetic predisposition
    salt and water intake
  3. underlying cause is not known/understood, therefore we are not treating the underlying cause
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5
Q
  1. What happens in the early phase of primary hypertension?
  2. What drives the chronic phase of primary hypertension?
  3. In the chronic phase of primary hypertension, is blood volume and cardiac output normal or raised?
  4. What changes in endothelial function occur in the chronic phase of primary hypertension?
A
  1. increased blood volume and cardiac output
  2. irreversible tissue changes - thickening of walls of resistance vessels (leading to reduction in lumen diameters)
    increased vascular tone
  3. normal
  4. endothelium produces less NO; smooth muscle is less sensitive to NO
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6
Q
  1. What is secondary hypertension?

2. What are often the causes of secondary hypertension?

A
  1. Hypertension with an identifiable cause

2. Renal or endocrine causes

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7
Q
  1. How does renal artery stenosis lead to secondary hypertension?
  2. How does chronic renal disease lead to secondary hypertension?
  3. What is Conn’s Syndrome?
  4. What is Phaeochromocytoma?
  5. How does Coarction of the aorta cause secondary hypertension?
A
  1. poor perfusion of the kidney, means that it produces a lot of renin
  2. increase in BP in attempt to restore GFR
  3. overproduction of aldosterone due to adrenal tumour/adrenal hyperplasia
  4. adrenal medullary tumours which produce catecholamines
    - alpha mediated vasoconstriction
    - beta mediated cardiac stimulation
  5. kidneys are hypoperfused.
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8
Q

What changes occur in the heart due to hypertension (2)

A
  1. accelerated coronary atheroma formation
  2. concentric left ventricular hypertrophy (due to increased afterload)
    - increased metabolic demands on heart
    - compression of cardiac vessels
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9
Q

What changes can occur in the aorta due to hypertension (3)

A
  1. atheroma
  2. aneurism
  3. dissecting aneurism
    - intima is stripped away from the media, creating a false lumen
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10
Q

Name 4 hypertensive retinopathic changes

A
  1. AV nipping
  2. Hard Exudates
  3. Flame Haemorrhage
  4. Papilloedema
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11
Q
  1. What is accelerated hypertension?
  2. What retinal change indicates accelerated hypertension?
  3. What causes accelerated hypertension?
A
  1. recent significant increase over baseline BP that is associated with target organ damage
  2. Papilloedema
  3. loss of autoregulation in the brain, leading to dilation of cerebral arteries
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12
Q
  1. What is acute heart failure?
  2. What is chronic heart faiure?
  3. What is heart failure usually initiated by?
  4. What are people with heart failure at risk of?
A
  1. patient experiences sudden onset of symptoms or rapid worsening of symptoms of existing heart failure
  2. symptoms of heart failure are ongoing and long term
  3. initial cardiac insult, such as MI
  4. sudden death, usually from rhythm disturbance
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13
Q

Name the two types of fluid accumulation that can occur in acute heart failure

A

Pulmonary oedema

Ansarca - systemic oedema, which usually affects peripheries

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14
Q
  1. Why does pulmonary oedema occur in heart failure?
  2. What are the CXR findings in pulmonary oedema
  3. How does a patient with pulmonary oedema present?
A
  1. increase in end diastolic pressure so that it exceeds oncotic pressure in the pulmonary vessels
  2. enlarged heart (>1/2 size of thorax)
    curly B lines
  3. Breathlessnes, orthopnea, PND, pink frothy sputum
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15
Q

Name 2 physiological consequences of LV failure, and how these can worsen the problem

A
  1. decreased renal perfusion → RAAS activation → Water retention → increased preload
  2. Decreased BP → sympathetic activation → vasoconstriction → increased afterload
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16
Q

How does heart failure result in ansarca?

A

fall in cardiac output → fall in renal perfusion → RAAS activation → increase ADH and aldosterone → Na and H2O retention

17
Q
  1. What is the law of laplace?
  2. What does wall tension represent?
  3. How does ventricular dilation lead to worsening heart failure?
A
  1. wall tension = (pressure inside the chamber x radius of chamber) / thickness of wall
  2. the amount of work the heart has to do, even before it starts to contract
  3. dilaition of the ventricles causes the radius of the ventricles, therefore, wall tension increases. Increased tension increases the work of the heart
18
Q
  1. How does skeletal muscle change in heart failure?

2. How does ventilation change in heart failure?

A
  1. switch from slow twitch aerobic fibres to fast twitch anaerobic fibres
  2. increased
19
Q
  1. Why is diamorphine given to those with acute pulmonary oedema?
  2. Which diuretic is given in acute pulmonary oedema?
  3. What are the most beneficial treatments of acute pulmonary oedema?
  4. What drug is given for inotropic support?
A
  1. relief of anxiety; possible role as vasodilator
  2. IV furosemide
  3. treatments that reduce hydrostatic pressure in the pulmonary capilaries - IV nitrate
  4. dobutamine (Beta 1 agonist)
20
Q

How is ansarca managed?

A
  1. bed rest
    daily weighing
    diuretics
    inotropic support
21
Q
  1. How are diuretics used to treat ansarca?

2. how are diuretics administered and why?

A
  1. add thiazide diuretic
    change the loop diuretic if already on diuretic
  2. intravenous infusion to bypass the oedematous gut
22
Q

What is the triple therapy for management of chronic heart failure

A
  1. ACE inhibitors/AngII blockers - reduced vasoconstriction and aldosterone production
  2. Aldosterone Antagonist (spironolactone) - reduces water retention
  3. beta blockers - positive inotropic effects and sympathetic blockade
23
Q
  1. What is the “ACE Escape Phenomenon”?

2. Name 1 advantage that ACE inhibitors have over Angiotensin II receptor antagonists

A
  1. Other enzymes that convert Ang I to Ang II are not blocked by ACE inhibitors, therefore Ang II can still be produced.
  2. ACE also breaks down kinins, which are involved in vasodilation. ACE inhibitors prevent the breakdown of kinins, therefore mediate vasodilation. AngII antagonists don’t have this positive effect

HYMS Block 13 (4 decks)

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