Heart Failure and Hypertension Flashcards
what two things is blood pressure determined by?
- cardiac output
2. peripheral resistance
How does angiotensin II increase blood pressure?
- causes vasoconstriction
- promotes vascular hypertrophy
- stimulates aldosterone release → sodium and water retention
What is poiseulle’s law?
resistance is inversely proportional to the fourth power of the radius
- What is primary/essential hypertension?
- What are the two potential causes of primary hypertension?
- Why are current treatments for primary hypertension not ideal?
- hypertension that does not have a particular cause
- genetic predisposition
salt and water intake - underlying cause is not known/understood, therefore we are not treating the underlying cause
- What happens in the early phase of primary hypertension?
- What drives the chronic phase of primary hypertension?
- In the chronic phase of primary hypertension, is blood volume and cardiac output normal or raised?
- What changes in endothelial function occur in the chronic phase of primary hypertension?
- increased blood volume and cardiac output
- irreversible tissue changes - thickening of walls of resistance vessels (leading to reduction in lumen diameters)
increased vascular tone - normal
- endothelium produces less NO; smooth muscle is less sensitive to NO
- What is secondary hypertension?
2. What are often the causes of secondary hypertension?
- Hypertension with an identifiable cause
2. Renal or endocrine causes
- How does renal artery stenosis lead to secondary hypertension?
- How does chronic renal disease lead to secondary hypertension?
- What is Conn’s Syndrome?
- What is Phaeochromocytoma?
- How does Coarction of the aorta cause secondary hypertension?
- poor perfusion of the kidney, means that it produces a lot of renin
- increase in BP in attempt to restore GFR
- overproduction of aldosterone due to adrenal tumour/adrenal hyperplasia
- adrenal medullary tumours which produce catecholamines
- alpha mediated vasoconstriction
- beta mediated cardiac stimulation - kidneys are hypoperfused.
What changes occur in the heart due to hypertension (2)
- accelerated coronary atheroma formation
- concentric left ventricular hypertrophy (due to increased afterload)
- increased metabolic demands on heart
- compression of cardiac vessels
What changes can occur in the aorta due to hypertension (3)
- atheroma
- aneurism
- dissecting aneurism
- intima is stripped away from the media, creating a false lumen
Name 4 hypertensive retinopathic changes
- AV nipping
- Hard Exudates
- Flame Haemorrhage
- Papilloedema
- What is accelerated hypertension?
- What retinal change indicates accelerated hypertension?
- What causes accelerated hypertension?
- recent significant increase over baseline BP that is associated with target organ damage
- Papilloedema
- loss of autoregulation in the brain, leading to dilation of cerebral arteries
- What is acute heart failure?
- What is chronic heart faiure?
- What is heart failure usually initiated by?
- What are people with heart failure at risk of?
- patient experiences sudden onset of symptoms or rapid worsening of symptoms of existing heart failure
- symptoms of heart failure are ongoing and long term
- initial cardiac insult, such as MI
- sudden death, usually from rhythm disturbance
Name the two types of fluid accumulation that can occur in acute heart failure
Pulmonary oedema
Ansarca - systemic oedema, which usually affects peripheries
- Why does pulmonary oedema occur in heart failure?
- What are the CXR findings in pulmonary oedema
- How does a patient with pulmonary oedema present?
- increase in end diastolic pressure so that it exceeds oncotic pressure in the pulmonary vessels
- enlarged heart (>1/2 size of thorax)
curly B lines - Breathlessnes, orthopnea, PND, pink frothy sputum
Name 2 physiological consequences of LV failure, and how these can worsen the problem
- decreased renal perfusion → RAAS activation → Water retention → increased preload
- Decreased BP → sympathetic activation → vasoconstriction → increased afterload
How does heart failure result in ansarca?
fall in cardiac output → fall in renal perfusion → RAAS activation → increase ADH and aldosterone → Na and H2O retention
- What is the law of laplace?
- What does wall tension represent?
- How does ventricular dilation lead to worsening heart failure?
- wall tension = (pressure inside the chamber x radius of chamber) / thickness of wall
- the amount of work the heart has to do, even before it starts to contract
- dilaition of the ventricles causes the radius of the ventricles, therefore, wall tension increases. Increased tension increases the work of the heart
- How does skeletal muscle change in heart failure?
2. How does ventilation change in heart failure?
- switch from slow twitch aerobic fibres to fast twitch anaerobic fibres
- increased
- Why is diamorphine given to those with acute pulmonary oedema?
- Which diuretic is given in acute pulmonary oedema?
- What are the most beneficial treatments of acute pulmonary oedema?
- What drug is given for inotropic support?
- relief of anxiety; possible role as vasodilator
- IV furosemide
- treatments that reduce hydrostatic pressure in the pulmonary capilaries - IV nitrate
- dobutamine (Beta 1 agonist)
How is ansarca managed?
- bed rest
daily weighing
diuretics
inotropic support
- How are diuretics used to treat ansarca?
2. how are diuretics administered and why?
- add thiazide diuretic
change the loop diuretic if already on diuretic - intravenous infusion to bypass the oedematous gut
What is the triple therapy for management of chronic heart failure
- ACE inhibitors/AngII blockers - reduced vasoconstriction and aldosterone production
- Aldosterone Antagonist (spironolactone) - reduces water retention
- beta blockers - positive inotropic effects and sympathetic blockade
- What is the “ACE Escape Phenomenon”?
2. Name 1 advantage that ACE inhibitors have over Angiotensin II receptor antagonists
- Other enzymes that convert Ang I to Ang II are not blocked by ACE inhibitors, therefore Ang II can still be produced.
- 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