Cardio - Hypertension Flashcards
What are the causes of hypertension?
Hypertension is classified as either primary (also known as essential or idiopathic), or secondary. Essential hypertension constitutes approximately 90% of cases. Primary (essential) hypertension is high blood pressure that is multi-factorial and doesn’t have one distinct cause.
What are some of the secondary causes of hypertension?
- Renal - 80% of secondary causes - Diabetic nephropathy, Renovascular disease, Glomerulonephritides, Polycystic kidney disease
- Congenital - Coarctation of the aorta
- Endocrine - Phaeochromocytoma, Acromegaly, Cushing’s syndrome/disease, Conn’s syndrome, Hyperthyroidism
- Drugs - Steroids, NSAIDs, Ciclosporin, MAOIs
- Toxins - MDMA
Cocaine, Serotonin syndrome - Pregnancy-related - Pregnancy-induced hypertension, Pre-eclampsia
- Causes on the ICU - Inadequate sedation, anxiety, pain
Hypoxia, hypercapnia, hypothermia
Vasoactive medications
Fluid overload
Increased ICP
What is the normal axis for left ventricular depolarization in an adult?
– 30 to +90 degrees
What is a ‘strain pattern’, and why is it important?
● ST segment depression and asymmetrical negative T waves in the lateral precordial leads
● Patients with this pattern have an increased risk of cardiovascular morbidity and mortality
With respect to left ventricular hypertrophy (LVH), what are the Sokolow– Lyon criteria?
LVH should be suspected if the combined amplitude of the R wave in V5 or V6 plus the
S wave in V or V2 is >35 mm, or if the R wave in aVL is ≥ mm
What is malignant hypertension?
Malignant hypertension is a hypertensive emergency most commonly seen in untreated essential hypertension, but also occurs in RAS or phaeochromocytoma.
It is severe hypertension associated with retinopathy, papilloedema, encephalopathy, microangiopathic haemolytic anaemia and nephropathy.
The pathological hallmark is arteriolar fibrinoid necrosis. There is arterial myointimal proliferation, platelet and fibrin deposition, MAHA and abnormal vascular autoregulation producing widespread endothelial injury and vasoconstriction.
End-organ ischaemia results and there is a compensatory activation of the RAA system, which worsens the hypertension and a vicious cycle ensues. The profound hypertension triggers natriuresis, and the resulting intravascular depletion may be unmasked as the blood pressure is brought under control.
Define hypertension
Hypertension is defined as a systolic BP >140 mmHg or a diastolic BP >90 mmHg.
The British Hypertension Society grades hypertension based on severity:
Grade 1 140/90 – 159/99 mmHg
Grade 2 160/100 – 179/109 mmHg
Grade 3 ≥180/110 mmHg
What is the management of malignant hypertension?
Patients with malignant hypertension should be managed in a high-dependency environment. An ABCDE approach should be used and abnormalities treated as they are found. Short-acting drugs are preferred: intravenous beta-blockers
(e.g. labetalol, esmolol), GTN and SNP are the agents of choice. Specific management
goals are:
1 Diastolic BP should be lowered to 100–105 mmHg over a period of 2–6 hours
– There should not be more than a 25% reduction in MAP (compensatory autoregulatory changes mean that organ dysfunction is a potential risk if BP is lowered more quickly than this)
2 Further gradual reductions should be made over the ensuing 24 hours
What is posterior reversible encephalopathy syndrome (PRES)?
PRES is associated with an abrupt increase in blood pressure, and is most commonly seen in association with renal disease, pre-eclampsia and some drugs, e.g. ciclosporin. It is a syndrome of headache, confusion, seizures and visual disturbance. It is characterised radiologically by oedematous lesions within the parietal and occipital lobes, seen as diffuse hyperintense lesions in the white matter on T2-weighted MRI. Rapid control of the hypertension will reverse the changes.
What is Aortic Stenosis?
- Narrowing of the aortic valve
- caused by degenerative disease rheumatic disease and valve thrombosis
Describe the pathophysiology of LV failure in the context of AS?
- Progressive narrowing of Aortic valve area
- Inc in pressure gradient across AV
- INcreased LV afterload and pressure
- Compensatory LV hypertrophy to maintain CO
- Eventual exhaustion of LV’s ability to compensate
What is the definition of severe Aortic Stenosis?
- often defined by echo
- Valve area les than 1cm (2.5-4.5)
- Peak velocity >4m/s (<2.5)
- Mean gradient >40mmHg (<5mmHg)
How is blood pressure determined?
BP = CO x HR
CO
- HR and contractility - determined by cardiac tissue and CVS
- Preload - managed by kidneys and CNS
Vascular resistance
- Arterial/venous vasodilatation - effected by vascular smooth muscle and RAAS
How would you manage a critically unwell patient with severe AS?
- Maintaining adequate diastolic blood pressure is vital to perfusing the hypertrophied LV
- Optimize preload - Cautious fluid bolus, Avoid venodilators and diuretics in these patients as they can cause acute decompensation
- Avoid Tachycardia as it impairs diastolic filling time
- Support Contractility - with classic low flow, low gradient AS
- Treat reversible causes
What is the difference between the Pacemaker potential and the Ventricular potential?
Pacemaker potential is the action potential conducted in the SA and AV node:
- Phase 0 - influx ca2+ causing membrane to go from -40mV to +20mV
- Phase 3 - Repolarisation phase, which occurs as K+ channels open and Ca2+ channels close
- Phase 4 - A steady influx of Na+/K+ (funny current) which gradually depolarises the cell.
Sympathetic stimulation increases the funny current, increasing the rate of depolarisation.
Parasympathetic stimulation increases K+ permeability, hyperpolarising the cell and flattens the gradient of phase 4.
Ventricular Action Potential
Phase 0: Depolarisation
At the threshold potential, voltage-gated fast-Na+ channels open briefly, causing depolarisation. The membrane potential peaks at 30mV.
Phase 1: Partial Repolarisation
The closure of Na+ channels results in K+ fleeing the cell down its electrochemical gradient, causing a slight drop in voltage called partial repolarisation.
Phase 2: Plateau
L-type Ca2+ channels open, causing a slow inward Ca2+ current which maintains depolarisation and facilitates muscle contraction.
Phase 3: Repolarisation
Membrane permeability normalises, and outward potassium current returns the membrane potential to normal.
Phase 4: Resting Potential
Membrane potential returns to its resting -85mV.
