Week 4 - Hypertension & Heart Failure Flashcards
Outline hypertension.
• Silent killer - few symptoms, more complications.
- Occipital headache may be the only symptom clinically (but not in all cases).
• Affects 25% of population, <35% aware.
- Very common clinically.
- Primary disease and complication (diabetes, atherosclerosis).
- Majority asymptomatic.
• Presents for the first time with complication.
- Complications very severe e.g. terminal organ failure.
- Dizziness, headache (occipital) and visual difficulties (late stage) - if symptoms present.
- Leading risk factor for MI, stroke and atherosclerosis.
• Chronic organ damage - heart, kidney, brain, eye.
- All organ damage can be explained by its damage of the blood vessels.
• BV damage:
- Macroangiopathy - atherosclerosis (medium and large arteries). Due to atherosclerosis in hypertensive patients.
- Microangiopathy - arteriolosclerosis (arterioles and capillaries).
Describe the physiology of blood pressure control.
• BP = CO x PR.
Cardiac output is affected by: • Blood volume: - Sodium, mineralcorticoids, ANP. • Cardiac factors: - HR, contractility.
Peripheral resistance is affected by: • Humoral factors: - Constrictors - angiotensin II, catecholamines, thromboxane, leukotrienes, endothelin. - Dilators - prostaglandins, kinins, NO. • Neural factors: - Constrictors - α-adrenergic. - Dilators - β-adrenergic. • Local factors: - Autoregulation. - pH, hypoxia.
Identify the grades of hypertension.
• Hypotension
- Systolic - <90 mmHg
- Diastolic - <60 mmHg
• Desired
- Systolic - 90-119 mmHg
- Diastolic - 60-79 mmHg
• Prehypertension
- Systolic - 120-139 mmHg
- Diastolic - 80-89 mmHg
• Stage 1 hypertension
- Systolic - 140-159 mmHg
- Diastolic - 90-99 mmHg
• Stage 2 hypertension
- Systolic - 160-179 mmHg
- Diastolic - 100-109 mmHg
• Hypertensive emergency
- Systolic - ≥180 mmHg
- Diastolic - ≥110 mmHg
Define hypertension.
• ‘Sustained increase in BP’
- Temporary increase in BP occurs with physical activity, stress etc.
- Hypertension is sustained - measured multiple times on different occasions.
Describe left-sided and right-sided hypertension.
Left/systemic hypertension (most common):
• Essential (primary): ~95% (increased peripheral resistance).
- Idiopathic - exact aetiology unknown. Multifactorial disorder. Commonest clinically.
• Secondary ~5% (renal, CVS, neuro and endocrine).
- Due to known cause - kidney disease, CVD, neuro and endocrine disorders → can give rise to secondary hypertension.
Pulmonary/right sided hypertension (increased BP within pulmonary circulation leading to right sided hypertension - affects right ventricle):
• Chronic - cor pulmonale - lung disorder.
- Commonest - due to lung disease.
• Acute - pulmonary embolism.
Outline left ventricular hypertrophy in systemic hypertension.
• Hypertension → ventricular hypertrophy.
Systemic hypertension → LVH. • Pathology: - Concentric hypertrophy. - >500g (350g). - >2cm thickness (1.3) - 2cm is taken as a guideline for hypertension. Normal is ~1.3cm. - LA dilation - fibrillation. - LV dilation at late stage.
• Prognosis (4 stages):
- Asymptomatic or compensated HT.
- Progressive IHD.
- Renal damage, stroke.
- Progressive CHF and SCD.
Outline right ventricular hypertrophy in pulmonary hypertension.
Pulmonary hypertension → RVH. • Pathology: - Concentric hypertrophy. - Due to pulmonary disorder (cor pulmonale). - Acute in pulmonary embolism. - RA & RV dilation - late.
• Prognosis:
- Asymptomatic - compensated.
- Hepatic congestion - nutmeg.
Explain microangiopathy.
• Thickening of small blood vessels - arteriolosclerosis.
- Commonest damage to small blood vessels is thickening of arterioles (thickening and hardening of small blood vessels - arteriolosclerosis).
2 types:
1. Protein deposition - hyaline (DM)
• Due to protein deposition, more common in diabetes but can also be seen in HT - known as hyaline arteriolosclerosis.
- Smooth muscle proliferation - hyperplastic (HTN).
• Due to smooth muscle cell proliferation usually in chronic hypertension causing thickening known as hyper plastic.
• Both can be seen in HT and kidney but can be seen in every organ. Common in kidney, retina and cerebral blood vessels.
Identify the grades of hypertensive retinopathy.
• Grade I - thickening of arterioles.
• Grade II - focal arteriolar spasms (AV nipping).
• Grade III - haemorrhages (flame shape), exudates cotton wool (ischaemia), hardy waxy (lipid deposit).
• Grade IV - papilloedema.
- Oedema of optic disc.
Outline benign nephrosclerosis.
• “Grain/leather kidney”
- Damage in kidney due to chronic hypertension.
• Due to microangiopathy, microinfarcts (glomerular scarring) in cortex of kidney (small kidney).
Chronic HT - shrunken, small kidney with plenty of minute scars/depressions. Known as grain/leather kidney. Due to microangiopathy/microinfarcts in cortex of kidney leading to small irregular pitted kidney.
Describe malignant hypertension - kidney.
- Acute emergency in HT. Sudden, severe increase in BP causing microscopic haemorrhages and organ failure - rapidly progressive.
- Terminal complication of many types of hypertension.
- Rapidly rising BP - results in rapidly increasing BP.
- > 200/120 mmHg.
• Arteriole necrosis and pin point haemorrhages.
- Severe HT of short duration - instead of causing thickening - necrosis - death of small arterioles - leads to pinpoint haemorrhages. (Severe increase in BP - breakdown of small blood vessels - many parts of body e.g. kidney → leads to acute renal failure and high mortality).
- Renal failure.
- High mortality.
- Very high BP leading to acute necrosis and rupture of arterioles (necrotising arteriolitis) causing pinpoint haemorrhages.
- Flea bitten kidney - pathological description.
Outline hypertensive intracranial haemorrhage.
- Subarachnoid haemorrhage + intracerebral haemorrhage (stroke).
- Special nature of cerebral blood vessels - less collagen/support.
- Hypertensive haemorrhages.
- Intracranial blood vessels are very specialised in the sense that they have very little collagen. In the case of increased BP, the commonest site of blood vessel rupture is in the brain (cerebral blood vessels) - either externally in the subarachnoid space or internally within the brain (intracerebral haemorrhage).
Outline heart failure.
• Congestive cardiac/heart failure (CCF/CHF).
- Congestion - fluid retention on venous side.
• Failure to maintain adequate circulation due to decreased cardiac output - “failure as a pump”
- Heart not pumping → ischaemia on arterial side, retention on venous side.
• End result of - IHD, HT, valve disorders etc. - many types (depending on mechanism involved).
Describe the different types of heart failure.
• Systolic failure - IHD, HTN.
- Systolic failure common in IHD, HTN where portion of cardiac muscle is dead/fibrotic → heart unable to contract sufficiently.
• Diastolic failure - hypertrophy, fibrosis.
- Diastolic failure when heart unable to relax properly due to hypertrophy, fibrosis.
• Right sided (pulmonary) failure.
- Right sided - when right ventricle fails, commonly due to pulmonary hypertension. Increased pulmonary HT - disorders of the lung (cor pulmonale).
• Left sided (systemic) failure.
- Left sided - systemic failure, left ventricle fails.
• High output - increased demand - anaemia, hyperthyroidism etc.
- High output failure - heart is normal - trying to function but the demand has increased too much e.g. severe anaemia (heart fails to meet massive increase in demand), hyperthyroidism (excess metabolism).
Identify the symptoms of heart failure.
Symptoms (3 main categories):
• Forward failure - failure to maintain output - ischaemia.
- Ischaemia on arterial side.
• Backward failure - failure to relax (need increased filling pressure).
- Failure to relax ventricles, results in increased filling pressure required to maintain cardiac output.
• Congestive failure - fluid retention (L/R). Increased venous pres.
- Result of forward and backward - fluid retention - due to increased venous pressure.
- Depends on side affected. Left side failure - usually pulmonary oedema. Right side failure - systemic oedema (retention in systemic veins).
Outline the physiological mechanisms operating to maintain heart function in case of heart failure.
Frank-Starling mechanism:
• More stretch - more contraction → ischaemia increase.
- More stretch leads to more contraction but later on leads to severe ischaemia because more contraction needs more oxygen (already compromised oxygen supply in ischaemic heart disease).
- Initially maintained by increasing contraction but gradually heart loses sufficient oxygen → ischaemic damage.
Neuro-humoral activation (hormones and nerves to maintain the circulation during heart failure):
• Vasoconstrictors - norepinephrine.
- When the heart is not functioning well, there is stimulation of epinephrine, norepinephrine and sympathetic nervous system causing peripheral vasoconstriction → pushing blood more to maintain BP.
• Renin-Angiotensin system - fluid retention.
- Results in fluid retention and increased BP.
• Atrial Natriuretic Peptide - diuresis (opp).
- Released from heart → causes diuresis - opposite mechanism of RAAS.
Compensatory hypertrophy of heart (in response to heart failure):
• Pressure overload hypertrophy
- Concentric, thick wall, normal volume.
- Due to increased BP → concentric thickening of LV wall maintaining the normal chamber volume.
• Volume overload hypertrophy
- Dilation of chamber, wall thick/thin.
- Excess fluid blood volume → dilation of ventricles leading to increased chamber volume and the wall may be thick/thin.
Describe the RAAS compensatory mechanism.
Renin → Angiotensin → Aldosterone → increased BP and increased fluid retention.
- Kidneys have renin releasing endocrine cells at juxtaglomerular apparatus.
- Between afferent and efferent arterioles there are specialised cells of DCT which recognise amount of blood going in and the filtrate going out. When there is decreased BP or decreased glomerular flow → releases renin.
- Renin activates angiotensinogen by breaking it to release angiotensin I.
- Angiotensin converting enzyme (ACE) of endothelium activates angiotensin I to angiotensin II.
- Angiotensin II → vasoconstriction.
- Aldosterone → fluid retention.
- Results in increased BP.
Describe neurohormonal mechanisms in heart failure.
- Any inciting event → baroreceptors in heart stimulate the vasomotor centre in brain → increased sympathetic nervous system activity.
- Also links to RAAS
- Together, neural-humoral mechansims cause increased BP (decreased renal flow, increased aldosterone, sodium reabsorption and H2O reabsorption - trying to maintain circulatory volume and pressure).
Explain the progression of CHF.
- Cardiac failure - gradually worsening of the situation due to continuing damage (e.g. as a result of ischaemia or hypertension) and the compensatory mechanisms gradually breaking down.
- Typically patient presents with gradually decreasing cardiac function with acute exacerbations compensated by the compensatory mechanisms (e.g. neuro-humoral mechanisms) but ultimately leading to gradual cardiac failure and death.
Explain the pathophysiology of clinical features.
• Low cardiac output and tissue perfusion (ischaemia, less oxygen supply).
- SOB, weakness, anxiety (feeling rotten).
• Venous congestion
- Systemic → oedema, effusions (RVF).
When it affects right side of heart causes systemic oedema, abdominal discomfort, hepatosplenomegaly, ascites (features of systemic congestion).
- Pulmonary → pulmonary oedema (LVF).
Left sided failure - pulmonary oedema. LVF always gives rise to secondary RVF as well because only one circulation with one pump. Whether it is right or left, ultimately gives rise to combined failure.
• Acute Heart Failure:
- Myocardial infarction → sudden.
Sudden failure due to massive MI.
• Chronic Heart Failure:
- Ischaemia, valvular disorders, hypertension etc.
Most commonly due to the above.
Identify the signs of CHF on CXR.
- Cardiomegaly - left sided enlargement in hypertension. Right sided enlargement in cor pulmonale.
- Left sided enlargement - boot shaped heart.
- Left sided enlargement gives rise to pulmonary oedema.
- Kerley B Lines - interstitial oedema.
- Heart failure cells - haemosiderin in macrophages.
Describe the brown induration of the lung in LVF.
- Increased pulmonary pressure leads to breakage of the capillaries → release of RBCs within the alveoli → RBCs are broken down by macrophages → macrophages retain the haemosiderin in the alveoli.
- Chronic microscopic haemorrhages in the alveoli results in the whole lung appearing as brownish induration.
Describe the liver congestion in RVF.
- In the case of right sided heart failure, the congestion occurs in the systemic side - liver, spleen, pedal (systemic) oedema. These things lead to hepatosplenomegaly.
- One of the important features seen in liver is congestion of the central areas of hepatic lobules around the central vein → leads to appearance of nutmeg liver (secondary to pulmonary disorders).
- Cardiac sclerosis - nutmeg liver.
Summary heart failure.
• Cardiac failure is decreased output, deficient circulation, venous retention.
- Pump failure leading to decreased oxygenation (decreased arterial circulation) and retention of blood in venous side.
• End stage of several different heart disorders.
• IHD and HT, common in elderly.
- End stage of several heart disorders - IHD and HT most common.
• Difficult to diagnose, manage → poor prognosis.
- Difficult to diagnose and manage because the compensatory mechanisms are maintaining the normal physiology for some time. Gradually they become worse and all patients carry a poor prognosis later.
• Right/left, sys/dias, forward/backward, high output.
- Note the difference between each.
• Venous congestion, fluid retention, (venous) hypertension (is the end result).
- Left sided - HTN, IHD - pulmonary oedema.
Retention of fluid, venous pressure increases in the lungs.
- Right sided - COPD, Cor pulmonale, systemic fluid retention.
Due to lung disease, retention is in the systemic side.
• Compensatory mechanisms:
- Adrenergic stim. Renin, Angiotensin and Aldosterone, ANP etc.
