Hypertension Flashcards

1
Q

Cardiac Output

A

Amount of blood pumped by each ventricle in one minute

product of heart rate (HR) and stroke volume (SV)

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2
Q

CO is affected by

A

venous return, peripheral vascular tone and neurohumoral factors

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3
Q

Generating max heart rate

A

estimated by taking the maximal value of 220 bpm and subtracting the individual’s age.

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4
Q

ANS regulation of HR

A

◉Sympathetic nervous system (SNS)noradrenaline/norepinephrine (+ve inotrope)
◉Parasympathetic nervous system (PNS) acetylcholine and opposes the SNS - dominates slows HR and causes vagal tone (-ve inotrope)

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5
Q

what happens if the vagus nerve is cut?

A

the heart would lose its tone, increasing the heart rate by 25 beats per minute.

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6
Q

Example of a sympathetic reflex

A

Atrial (Bainbridge) reflex - initiated by >blood in aria
causes stimulation of SA node
Stimulates baroreceptors in atria > SNS stimulation

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7
Q

Chemical reg of HR

A

◉Catecholamines
va β1-adrenoceptors on SA nodal cells.

Adrenaline/NA open Na+Ca ion chemical or ligand gated channels
>rate of depolarisation < period of repolarisation
Massive incr of A/NA + SNS stimulation = arrhythmias
◉ Thyroid Hormones
> thyroxin, thyroid hormone > HR>contractility
longer duration than catecholamines
may trigger tachycardia
◉ calcium ions
>ca> HR and contractility
hypercalcemia - short QT interval (depol to repol +vent systole) and wide T wave
very high>cardiac arrest

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8
Q

Stroke volume

A

EDV - ESV

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9
Q

EDV

A

end diastolic volume

amount of blood collected in a ventricle during diastole

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10
Q

ESV

A

amount of blood remaining in a ventricle after contraction

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11
Q

Factors affecting SV (3)

A

Preload
Contractility
Afterload

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12
Q

Frank- starling law of the heart

A

ability of the heart to change its force of contraction and therefore stroke volume (preload critical) in response to changes in venous return

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13
Q

Stroke volume is affected by

A

Slow heart rate + exercise = > venous return to heart >SV

Blood loss+rapid heartrate =< stroke volume

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14
Q

Classes of Hypertension

A

Primary/idiopathic/essential hypertension 90-95% (Complex interaction of genes, environmental factors and lifestyle)
Secondary hypertension 5-10% ( identifiable cause - kidney, pregnancy, sleep apnea, renovascular, endocrine, obesity etc)

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15
Q

Causes linked to Primary hypertension

A
Age 
Obesity
Physical activity
Smoking
Alcohol consumption
Genetic predisposition
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16
Q

Causes linked to Secondary hypertension (ROPE)

A

Renal disease - Renal artery stenosis, renal parenchymal disease
Cardiovascular disease
Hormonal- aldosteronism, thyroid, pheochromocytoma
Neurological - Quadriplegia, Dysautonomia
Pregnancy
Obstructive sleep apnoea

17
Q

What causes prolonged smooth muscle contraction- thickening of arterial vessel wall leading to increased HR (4)

A

◉RAAS
◉Autonomic system dysregulation - > symp >HR>Co>BP
HR,CO >BP
Stress >symp activity
◉Genetics - defects in renal Na hemostasis, vascular smooth muscle growth and structure
◉Endothelial dysfunction - imbalance between vasodilator and vasoconstrictor molecules. Pro thrombotic, Pro inflammatory and pro constrictive phenotypes

18
Q

Baroreceptors

A

Negative feedback systems control
Located in carotid sinus and aortic arch
>arterial pressure> walls expand> firing frequency of action potentials by baroreceptors
< arterial pressure

19
Q

Vasodilator molecules

A

Prostacyclins
NO
Bradykinin
Atrial Natriuretic peptide(ANP)

20
Q

Vasoconstrictor Molecules

A
Raise BP
Angiotensin 2
Thromboxane
Endothelin
Catecholamines
21
Q

Primary Hyperaldosteronism (Conn’s syndrome) desc. and causes (4)

A

Too much aldosterone production, renin

22
Q

Secondary Hyperaldosteronism(3)

A

Excessive renin > more aldosterone by RAAS
When BP in kidneys is lower than rest of body
◉Renal artery stenosis
◉Heart Failure
◉Renal artery obstruction

23
Q

Investigating Hyperaldosteronism

A

◉Renin: Aldosterone ratio
◉Investigate Aldosteronism effects - HBP,Hypokalaemia,Alkalosis
◉Imaging - CT/MRI, renal doppler ultrasound, CT angio/MRA - renal stenosis/obstruction

24
Q

Management of Hyperaldosteronism

A

◉Aldosterone agonists - Eplerenone, Spironolactone
◉Surgical removal
percutaneous renal artery ◉angioplasty via femoral artery

25
Q

Diagnosis criteria for HTN

A
140/90 - Stage 1
160/90 - Stage 2
180/120 - Stage 3
135/85 - AMBP stage 1
150/95 AMBP Stage 2

Old < 80yo - 140/90
80+ yo 150/90

in Diabetes 130/80