HTN Flashcards
Discuss the macrociruclatory pathophysiology of HTN and target-organ damage
Uninterrupted by treatment continued vasoconstriction in chronic HTN leads to a number of deleterious consequences that culminate in TOD.
Macrocirculatory- the central components of the cardiovascular system are most affected ( heart and large blood vessels) - increase in afterload results in increasing impedance to forward flow from the heart which in turn necessitates increased contractile force to maintain aortic valve opening and the duration of EF. THis contraction against increased force increases the intraventricular wall tension which together with ongoing stimulation from SNS and RAS trigger cardiac myocyte hypertrophy and myocardail fibrosis. Initially this leads to increase in LV mass and an increase in contractility. Howevere when progressive the net effect is is LV stiffening and impaired diastolic function with an increease in LV filling pressure and diminished flow from the left atrium to LV.
If an acute rise in after load occurs a sudden abrupt decrease in SV occurs leading to flash APO.
IF more gradial or chronic a subacute rise in afterload leads to increased wall tension with compression of the subendocardail micorvasculature and mycordial ishcameia. Over time this leads to wall thinning and dilatation
Discuss the microcirculatory pathophysiology of HTN and TOD
The initial beneficial effect of vascular remodeling gradually gives way to critical luminal narrowing and the potenional for regional ischaemia from occlusion or loss of vessel wall integrity with leakage or rupture
Small vessel ischaemai episodes many of which are silent are the primary cause of chronic TOD including progressive white matter (multi infarct) disease of the brain and hypertensive nephropathy. Cerebral microbleeds seen on MRI are relatively new class of subclinical brain injury assoicated with chronic HTN and portend more rapid cognitive decline in older adutls
Discuss hypertensive emergency pathophys
Results from endotherlial injury triggered by an abrupt rise in vasuclar pressure which overwhelms autoregulatory mechanisms. A subsequent drop in NO mediated vascualr smooth msucle relaxation and excess relaease of endothelin further increase SVR which functionally maintains BP at severely elevated levels.
Unchecked wall tension ensures and termianal arterioles dilate and eventually rupture leading to proinflammatory hypercoaguable states with firbin deposition and diffuse ischaemia.
Rising pressure in the proximal capillary beds causes fluid leakgage and tissue oedema which produces acute TOD alonf with microangiopathic haemolytic anaemia and other signs of small vessel injury
Discuss PRESS
Has a neruological syndrome that is similar to that of htn encephaloapthy albiet with less global features and more region specific features .
Also associated with increased vascular permeability secondary to endothelial damage with vasogenic oedema.
PRES is characterized by a constellationos symptoms related to posterior circulation. including visual changes headache, altered mental status and seizures.
MRI is IX of choice
Full recovery once causative factor is removed- HTN is the most common condition associated with PRES alhtough it may alsp be seen with kidney disease, malignancies, cytotoxic therapy and autoimmune disease.
List HTN emergencies by Organ system
Heart
- Acute heart failure
- ACS
Brain
- CVA – ischaemia
- Spont intracranial haemorrhage
- HTN encephalopathy
Kidney
-AKI
Vascular
- aortic dissection
Other
- eclampsia
- Acute hypertensive retinopathy
Discuss IX of hypertensive emergency
Depends on presenting complaints
In almost all cases labs looking at worsening renal function, microangiopathic haemolytic anaemia are needed.
if Chest pain or SOB present, chest x-ray and cardiac biomarkers are warrented.
CTA if suspected dissection
Discuss hypertensive retinopathy
When present signifies underlying TOD and is strongly assoicated with an enhanced risk of stroke in patients with HTN.
Lesions seen include cotton wool spots, copper or silver wiring of the arteiroles, AV nicking
Grade 0- normal
Grade 1- minimal arterial narrowing
Grade 2- obvious arterial narrowing with focal irregularities
Grade 3 - arterial narrowing with retinal haemorrhages and/or exudate
Grade 4- grade 3 + disc swelling
Discuss mx of htn emergencies
Patient with true hypertensive emergency benefit from predicatably controlled effects of parenteral agent by titrated IV bolus or by adjustable infusion.
Labetalol and GTN are the most common medications used in the states but nil clear study showing one drug superior to others
GTN 5-200mic/min
Labetaolol 20-80mg q10min or infusion 1-2mg/min
Consider hydralazine 5-20mg q 30min –direct acting smooth muscle relaxant
Optimal treatment of a HTN emergency involves therapy that is directed toward the precipitant of specific TOD and consequences of elevated BP rather than the BP itself. JNC7 reccomends a reduction in MAP by 20-25% within the first hour and a pressure of160/100 by the 2-6 hour mark
The 20-25% goal comes from an understanding of cerebral autoregulation which maintains pressure between maps of 60-160 – this is reset in chornic hypertension and the lower limit sits approximatly 25% below the baseline MAP. Lowering more than this raises concern for impaired cerebral perfusion. HTN emergency patient normally will have a marked rise above there baseline BP giving a buffer to management.
Discuss the management of HTN emergency in ACS and acuts heart failure
In ACS complicated by HTN the primary goal (beyond expeditious reperfusion) is a decrease in cardiac work and improved coronary arter perfusion each of which can be dramatically effected by changes in afterload.
Similarly in AHF reduction in SBR can reduce imedence tofoward flow enable more effected contractions
Nitric oxide donars such as GTN can be highly beneficial in both circumstances as they produce small vessel dilation which yeilds a dose dependent decrease in overall vascular resistance.
Rapid reduction in MAP has been associated with profound symptom resolution from both increased coronary artery supply and reduced subendocardial o2 demand. THis may require gtn infusion much higher than usual up to 250mic/min. – Dont use GTN in patient who have used sidenaphil (phosphodiesterase-5 inhibitors) within the preceeding 48 horus.
ACE inhibitors are also well tolerated and effected for heart failure. Enalapril can be given as a bolus or infusion (0.625-1.25mg/dose up to 2.5mg in 30 minutes) – this is due to long acting nature of enalaprilate
Labetalol and other b blockers with -ve inotropy should be avoided in the early phase of treated of heart failure with htn
Discuss HTN management in aortic dissection
Unlike with other hypertensive emergencies BP control to a specific target (>110) is essentail because it decrease ongoing injury and reduces the likelihood of perioperatiev adverse events
The immediate goal is to reduce the intimal shear forces by driving down the pressure that results from LV ejection while avoiding a reflex tachycardia.
To this end B-blocakde is always given initially such as esmolol 0.5-1 mg/kg (50-300 mic/kg/min) prior to administration of vasodilators such as sodium nitroprussid, nicardipine or clevidinpine
Labetal with both alpha and beta blocking affects can be used as a monotherapy especially as an infusion.
Discuss HTN management in acute ischaemic stoke.
Avoid extreme high and low or sudden change in BP
Optimal range appears to be between 120-200mmhg
Guidelines from AHA/ASA recommend reduction of BP under 185 and maintenance of BP under 180 in those with ischaemic stroke and who are going to be lysed
If not going to be lysed nil indication for reduction in BP unless sytolic >220 and even in such cases the goals are modet 15% reduction in the 1st 24 hours
Two larege studies SCAST (scandinavian candesartan acute stroke trial) and CATIS (china antihypertensive trial in acute ishcaemic stroke) showed nil benefit in Bp reduction in the 1st 24 hours of treatment.
For those who need lowering of the BP labetalol or nicardipine are the agents of choice with nicardipine maybe showing superioty due to longer duration of action and less BP variablility. Nicardipine infusion 5-15mg/kg
Do not use NO donors are they can increase ICP
Discuss HTN management in spont intracranail haemorrhage
HTN is strongly associated with spont ICH and ongoing HTN is associated with haematoma expansion, vasogenic oedema and rebleeding.
Several systematic reviews and multicentre trials have shown improved outcomes with BP reduction to 140/150. IN contrast with ischaemic stroke there is little evidence to suggest adverse outcomes with hypotension.
When high elevation are present systolic >200 or MAP >150 aim for a systolic of 140 as per ASA/AHA if more modest hypertension lower targets are indicated (BP160/90 or MAP 110mg/hg)
INTERACT 2 a studiy in BP reduction in Acute cerebral haemorrorage show a correlation between imrpoved functional outcome at 90 days and intensive antihypertensive therapy aiming for a BP of 140 at 1 hour. In those who achieved BP reduction of 20mm/hg in the 1st hour had a 35% less likley chance of poor outcomes.
ATACH2 is the other trial
Labetalol and nicardipine again are the agents of choice
Discuss HTN management in hypertensive encephaloapthy
Unlike acute stroke syndromws in which HTN may be reactive rather than caustivie a direct assoication exists between the degree of HTN and neurological symptos. Aim of therapy is to reduce systolic BP into the range in which autoregulation can cope
Once alternaitve have been ruled a reduction in MAP of 30-40% should be achieved - MAP targets should not be thrown out by aiming for symptoms resolution is a good messure.
The agent of choice is again labetalol and nicardipine as they evenly reduce resistance in all vascular beds in different systems evenally.
NO donors and hydralazine have a differential effect on the cerebral and systemic cirucaltion resulting ina realtive increase in cerebral BP and a shunt effect to the periphery which can ead to a decrase in cerebral blood flow and risk ishcaemia to watershed areas.
Discuss sympathetic crisis managmenet
`Hyperadrenergic states can result from endogenous sources of catecholamine excess ie: phae but a more commonly trigger by the intake of exogenous substances that interfere with norepi metabolism such as cocaine, meth. The result is cardiostimulatory and vasopressor that present with htn and tachycardia.
Administration of benzo may be sufficient to treat these patient subset.
When BP is persistently elevated or TOD is present phentolamine a reversible pure alpha blocker is indicated. Can use GTN and is indicated if chest pain due to vasospasm.
Be careful of not using isolated b-blockade leading to unopposed alpha action and increasing HTN. If used should always be paired with vasodilator. IV labetalol is susceptible to these affects as has a alpha beta ratio of 1:7 and should be avoided
