Hypertension Flashcards
Cardiac Output
Amount of blood pumped by each ventricle in one minute
product of heart rate (HR) and stroke volume (SV)
CO is affected by
venous return, peripheral vascular tone and neurohumoral factors
Generating max heart rate
estimated by taking the maximal value of 220 bpm and subtracting the individual’s age.
ANS regulation of HR
◉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)
what happens if the vagus nerve is cut?
the heart would lose its tone, increasing the heart rate by 25 beats per minute.
Example of a sympathetic reflex
Atrial (Bainbridge) reflex - initiated by >blood in aria
causes stimulation of SA node
Stimulates baroreceptors in atria > SNS stimulation
Chemical reg of HR
◉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
Stroke volume
EDV - ESV
EDV
end diastolic volume
amount of blood collected in a ventricle during diastole
ESV
amount of blood remaining in a ventricle after contraction
Factors affecting SV (3)
Preload
Contractility
Afterload
Frank- starling law of the heart
ability of the heart to change its force of contraction and therefore stroke volume (preload critical) in response to changes in venous return
Stroke volume is affected by
Slow heart rate + exercise = > venous return to heart >SV
Blood loss+rapid heartrate =< stroke volume
Classes of Hypertension
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)
Causes linked to Primary hypertension
Age Obesity Physical activity Smoking Alcohol consumption Genetic predisposition
Causes linked to Secondary hypertension (ROPE)
Renal disease - Renal artery stenosis, renal parenchymal disease
Cardiovascular disease
Hormonal- aldosteronism, thyroid, pheochromocytoma
Neurological - Quadriplegia, Dysautonomia
Pregnancy
Obstructive sleep apnoea
What causes prolonged smooth muscle contraction- thickening of arterial vessel wall leading to increased HR (4)
◉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
Baroreceptors
Negative feedback systems control
Located in carotid sinus and aortic arch
>arterial pressure> walls expand> firing frequency of action potentials by baroreceptors
< arterial pressure
Vasodilator molecules
Prostacyclins
NO
Bradykinin
Atrial Natriuretic peptide(ANP)
Vasoconstrictor Molecules
Raise BP Angiotensin 2 Thromboxane Endothelin Catecholamines
Primary Hyperaldosteronism (Conn’s syndrome) desc. and causes (4)
Too much aldosterone production, renin
Secondary Hyperaldosteronism(3)
Excessive renin > more aldosterone by RAAS
When BP in kidneys is lower than rest of body
◉Renal artery stenosis
◉Heart Failure
◉Renal artery obstruction
Investigating Hyperaldosteronism
◉Renin: Aldosterone ratio
◉Investigate Aldosteronism effects - HBP,Hypokalaemia,Alkalosis
◉Imaging - CT/MRI, renal doppler ultrasound, CT angio/MRA - renal stenosis/obstruction
Management of Hyperaldosteronism
◉Aldosterone agonists - Eplerenone, Spironolactone
◉Surgical removal
percutaneous renal artery ◉angioplasty via femoral artery
