Complications of HTN Flashcards
What target organs can be damaged by hypertension?
- Blood vessels –> atherosclerosis, aneurysms, aortic dissections
- CKD –> heamaturia/uraemia/proteinaemia
- Cardiac failure –> pulmonary oedema/ MI/LVH
- Stroke/TIA –> haemorrhage or infarction, seizures or vascular dementia
- Retinal damage –> haemorrhages, exudates, AVnipping, papilloedema
What complications of HTN can arise in the heart?
- increased LV mass, with or without chamber dilation –> LVH
- left atrial abnormalities
- myocardial ischaemia
- systolic and diastolic LV dysfunction (Heart failure)
- Atrial and ventricular arrhythmias
- Sudden death
What is the relationship between mortality and systolic BP?
- Mortality rises as systemic BP rises above 120 mmHg
- Mortality also rises with age bracket –> highest risk of mortality at 80-89 yrs vs lowest at 40-49 yrs
What is the background of the development of essential hypertension?
what factors are involved in the development of hypertensive heart disease?
What actually occurs in hypertensive heart disease?
- Pathophysiology of developing hypertensive disease (primary/essential) based off backgroud of–> genetics/age/sex/obesity/ salt intake/ ethnicity
- Haemodynamic factors:
- Blood pressure
- wall stress
- volume load
- arterial stiffness
- compliance
- Non-haemodynamic:
- Angiotensin II
- Aldosterone
- SNS
- Insulin resistance
- Hemorheologic –> study of flow of blood
- Hypertensive heart disease –> leads to:
- altered coronary reserve
- endothelial dysfunction
- perivascular fibrosis
- systolic and diastolic dysfunction (HF)
- LVH
- cardiac dysrhythmias
- myocardial fibrosis
What are the clinical consequences of hypertensive heart disease?
- Angina pectoris
- Asymptomatic HF or symptomatic HF
- Cardiac dysrhythmias
- Acute coronary syndromes
- MI
- sudden death
What are the pathogenic processes underlying cardiac damage from hypertension?
- neurohormonal processes:
- Activation of RAAS
- Enhanced adrenergic activity
- Increased production/reduced catabolism of biologically active molecules (Angiotensin ii, cytokines and growth factors)
- Haemodynamic processes:
- Increased peripheral resistance
- increased wall stress
- decreased coronary reserve
- Vascular processess:
- Endothelial dysfunction
- Vascular remodelling
- Decreased vascular compliance
- Increased vascular reactivity
- coronary and peripheral vascular atherosclerosis
- Myocardial
- Left ventricular remodelling
- Foetal gene expression
- Myocyte hypertrophy
- alteration in extracellular matrix
What are the common presenting symptoms of congestive heart failure?
- Dysponea /SOB at rest or on exertion
- exercise intolerance
- fatigue and weakness
- orthopnoea
- paroxysmal nocturnal dysponea
- GI complaints
What are the common signs of Congestive heart failure?
- Resting tachycardia
- third heart sound
- vascular congestion
- peripheral oedema
- hypotension
- organomegaly (e.g. liver)
- pleural effusion
- cachexia
How do you manage hypertensive heart disease?
Medication for:
LV systolic dysfunction?
LV diastolic dysfunction?
If concordant IHD OR arrythmia?
if concordant HF?
If AF?
- Effective management of high BP to regree LVH
- ACE-I or ARB for LV systolic dysfunction
- ARB’s for LV diastolic dysfunction
- Beta blockers in the presence of IHD (angina, ACS, MI) and of arrhythmias (AF)
- for IHD –> BB, nitrates, ACE-i, CCB’s
- in HF, ACE-i are first line (ARB’s valid alternative), beta blockers prolong survival, if congestive symptoms, loop diuretics or antialdosterone
- in AF –> combine anticoagulation (vitamin K antagonists, NOAC’s (apixaban, dabigatran, rivaroxaban)
For Hypertensive heart disease –> manage other cardiovascular risk factors (statins, aspirin, antidiabetics)
What is shown by the LIFE trial?
- Losartan prevents more cardiovascular morbidity and death compared to atenolol in hypertensive patients with LVH (by reduction in stroke risk)
- remember prolonged HTN promotes LVH, eventually leading to HF, increased O2 demand which results in angina, hypertrophy of heart muscle can disrupt conduction pathways –> predisposed to AF and ischaemic stroke
- also predisposed to intracerebral haemorrhage or retinopathy.
Define stroke
- A rapidly developing focal neurological deficit lasting longer than 24 hrs or causing death, which is attributable to a vascular cause
How does the risk of stroke alter with SBP?
How does increasing age affect this?
how does stroke mortality change with quality of HTN control?
- at ages 40-69 yrs each difference of 20 mmHg usual SBP –> associated with 2x increase in stroke death rate (either ischaemic or haemorrhagic)
- also two fold difference in death rate from IHD and other vascular causes
- Risk of mortality increased with age bracket, double risk at 80-89 vs 40-49 yrs.
Risk of mortality from stroke decreases with well controlled hypertension, untreated HTN ~ 3x more likely to die with Odds ratio of around 3.5, under 140 mmHg OR around 1.3.
What are the two main classifications of ischaemic stroke?
What are their clinical features? on neuroimaging?
what are their supporting features?
- Large artery atherosclerosis or cardioembolism (heart pumps embolism to block major cerebral artery)
- clinical features = cortical impairment, cerebellar or brainstem signs
- neuroimaging = stenosis or occlusion of a major brain artery, cortical/subcortical infarct >1.5cm
- supporting features = carotid artery stenosis > 50%, history of TIA, same territory PVD OR hisotry of TIA in different territories, known source of cardioembolus
- Small vessel occlusion (lacunar infarct) –> lacunar syndrome (motor/sensory involvement of –> 2 arm/face/leg/ataxic hemiparesis)
- neuroimaging = subcortical or brainstem infarct >1.5cm
- supporting features = history of HTN or diabetes
Management of ischaemic stroke?
- Early intervention –> Thrombolysis! (tPA, alteplase) or mechanical thromboectomy
- Early tx –> aspirin, anticoagulants (clopidogrel)
- long term prevention –> Antiplatelet therapy (Clopidogrel, aspirin), anticoagulant therapy (warfarin/ NOAC)
- Revascularisatio –> carotid endoarterectomy or angioplasty/stents
- Anti hypertensives and statins
- Rehabilitation
What are the 4 types of brain bleeds?
How common are haemorrhagic strokes?
What are the types of haemorrhagic stroke?
- Haemorrhagic strokes occur in around 10% stroke patients and includes:
- Extradural/ epidural - liner skull vault fracture tearing middle meningeal artery - characteristic picture of head injury with bried unconciousness, followed by lucid interval, then lower GCS again
- subdural - rupture of intracerebral bridging veins, often following head injury- common in elderly and on anticoagulants.
- subarachnoid - 5%, dramatic onset, sudden severe headache, vomiting and papilloedema
- intracerebral and cerebellar - approx 10% strokes - higher mortality than ischaemic stroke - associated with more severe headaches/coma
- large haematoma may act as a space occupying lesion, cause raised ICP and brain displacement/herniation
- Hypertensive disease –> associated with rupture of microaneurysms, can also have arteriorvenous malformations, aneurysms, dural venous thrombosis, coagulopathies and anticoagulants and thrombolysis can cause haemorrhage.
- CT imaging - may reveal intraparenchymal, intraventricular or subarachnoid blood
What are the most common related diseases assocaited with ESRD?
- Glomerulonephritis
- Hypertension
- Diabetes
- 50% of diabetic patients and 25% of hypertensive patients end up with ESRD
How does ethnicity relate to the need for renal replacement therapy?
- South asian populations and black populations have the greatest need for renal replacement therapy, these populations are at greatest risk for development of diabetes and hypertension.
How does risk of IHD relate to BP?
- Risk of IHD increases with increasing SBP and microalbuminuria
- patients presenting with microalbuminuria are at greater risk of cardiovasacular disease
How do you classify chronic kidney disease?
- Based off of eGFR - greater than or equal to 90 ml/min/1.73m2 indicates there may be kidney damage but still a normal GFR
- dropping below 90 to 60 - indicates mild GFR
- dropping below 60-45 indicates mild-moderate GFR
- below 45-30 = moderate GFR
- 30-15 severe GFR
- Below 15 - indicates kidney failure or need for dialysis
What are the haemodynamic abnormalities in chronic kidney disease?
How does this contribute to elevated blood pressure?
- Related to equation for mean BP = CO x total SVR
-
SVR changes: Increased vasoconstriction
- CKD leads to increased RAAS due to reduced blood flow in peritubular capillaries down sclerosed glomeruli (reduced Na+ at macular densa, release Renin at JGA)
- leads to renin release –> elevated ATii —> vasoconstriction –> increased SVR
- less functioning glomeruli means remaining glomeruli need to increase GFR –> remember ATii vasoconstricts efferent arteriole
- but endothelial dysfunction too –> impaired NO production, oxidative stress and elevated endothelin levels –> endothelin vasoconstricts AA, plus NA from SNS –> reduced GFR
- all detrimental to the kidney in the long term –> leads to vasoconstrictor effect on the glomeruli within the nephron
-
Cardiac output changes: Increased Cardiac output
- increased CO and increased intravascular volume
- increased intravascular volume by Na+ retention (Due to increase in RAAS) and decrease in GFR due to less functioning glomeruli (less excreted)
- Increase in extracellular fluid volume –> increase in perfusion peripheral tissues and increased vasoconstriction.
- increase in renal nerve activity –> RAAS increases sympathetic outflow, as does increased Na+
- overactivity of SNS –> increased CO, vasoconstriction, more renin release
How does untreated CKD lead to nephrosclerosis?
How can we prevent deterioration of eGFR in CKD with RAAS blockade?
Which is the better method?
In untreated CKD –> constriction of the efferent arteriole and dilation of the afferent arteriole in attempt to increase GFR –> hyperfiltration leads to damage within the microvasculature of glomerulus –> nephrosclerosis
With RAAS blockade: ACE i
Beneficial in reducing early signs of kidney disease (macroalbuminuria). ACEi reduce breakdown of bradykinin, dilates efferent arteriole, more congestion within bowman capsule
In ARB:
Only blocking ATii effect, some efferent arteriole dilation but not as much as bradykinin still broken down, therefore less dilation, less congestion.
Reduce deterioration of eGFR with RAAS blockade but more so with ARB.
What are the benefits of blocking the RAAS?
- both in diabetic nephrosclerosis and hypertensive nephrosclerosis, RAAS blockage prevents renal deterioration
- prevent macroalbuminuria, end stage renal disease
- hence why guidelines have changed and the use of ARB reduces progression of renal disease in diabetics
- use of ARB reduces progression of renal disease in diabetics more than CCB’s
Define hypertensive retinopathy
Hypertensive retinopathy =
retinal vascular damage caused by hypertension.
Arteriolar constriction
arteriovenous nicking
vascular wall changes
flame shaped haemorrhages
cotton wool spots
yellow hard exudates
optic disk edema
What are the different classifications of hypertensive retinopathy?
- Mild= grades 1-2)
- focal arteriolar narrowing or generalised
- arteriovenous nicking (small arteriole corrses small venule resulting in compression of vein with bulging either side)
- arteriolar wall opacity
- Moderate - grade 3
- mild retinopathy PLUS one or more of:
- retinal haemorrhages
- microanuerysm
- cotton wool spots
- hard exudates
- mild retinopathy PLUS one or more of:
- Malignant - grade 4
- moderate retinopathy AND optic disc swelling and macular oedema (papilloedema)
Describe the images shown:
A
B
C
D
- A = generalised narrowing of the arterioles
- B = generalised narrowing PLUS focal constriction, arteriolar sclerosis with widening or the reflex stripe
- C = above PLUS haemorrhages and exudates
- D = PLUS oedema of disc - papilloedema
