Week 4: Cardiology (2) (cardiac physiology and pathology) Flashcards
What is BP?
- Driving force to perfuse organs with blood (force per. Unit area acting on vessels)
- Not uniform throughout body
- Reported as systolic (SBP) and diastolic (DBP)
- Cyclical with the cardiac cycle
- Physiologically regulated variable- it changes
calculating Mean arterial pressure
Mean arterial pressure = CO x TPR (total perisperhal resistance)
- CO= SV and HR
MAP= SBP + (2xDPB)/3 (this is how we actually calculate)
blood pressure regulation
- Autonomic sympathetic activity
- RAAS
- Local action by autacoids e.g. bradykinin and NO- action of endothelium on vascular smooth muscle
Resistance and increased mean arterial pressure
Radius decreases and resistance increase
- Smooth muscle tone changes TPR
- Vasoconstriction increase peripheral resistance, requiring higher BP to drive blood through the systemic circulation
RAAS: renin release
Renin Release
The first stage of the RAAS is the release of the enzyme renin. Renin released from granular cells of the renal juxtaglomerular apparatus (JGA) in response to one of three factors:
- Reduced sodium delivery to the distal convoluted tubule detected by macula densa cells.
- Reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole.
- Sympathetic stimulation of the JGA via β1 adrenoreceptors.
The release of renin is inhibited by atrial natriuretic peptide (ANP), which is released by stretched atria in response to increases in blood pressure.
RAAS: Angiotensin I
Production of Angiotensin II
Angiotensinogen is a precursor protein produced in the liver and cleaved by renin to form angiotensin I.
Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE). This conversion occurs mainly in the lungs where ACE is produced by vascular endothelial cells, although ACE is also generated in smaller quantities within the renal endothelium.
RAAS: angiotensin II binding
Angiotensin II exerts its action by binding to various receptors throughout the body. It binds to one of two G-protein coupled receptors, the AT1 and AT2 receptors. Most actions occur via the AT1 receptor.
The table below outlines its effect at different points. These will be discussed in more detail below.
BNP
Brain-type natriuretic peptide (BNP) is a hormone secreted primarily by the ventricular myocardium in response to wall stress such as volume expansion and pressure overload. BNP is a marker for congestive heart failure
→ secreted in response to ventricular wall stress, therefore reduces BP by increasing natureisis (reducing preload and afterload)
hypertension and types
NICE: 140/90 mmHg= hypertension
- 90% essential/primary/idiopathic hypertension
- Second hypertension (due to other pathology)
- Pre hypertension
- Isolated systolic/diastolic hypertension
- White coat/clinic
Risk factors of hypertension
- Smoking.
- Being overweight or obese.
- Lack of physical activity.
- Too much salt in the diet.
- Too much alcohol consumption (more than 1 to 2 drinks per day)
- Stress.
- Older age.
- Genetics.
signs and symptoms of hypertension
- Usually presents asymptomatically—manage BP to reduce risk of stroke
Diagnosis of hypertension
- Screening those at risk
- Increasing public awareness of risk factors
- Appropriate lifestyle changes to limit risk- no immediate gain presence a challenge
- Reliable measurements based on clinical guidelines
- Regular monitoring and refinement of medication
- Hypertension is a silent killers
Clinical diagnosis (best practice) of hypertension
- Sitting, relaxed and arm is supported
- Both arms, >15 mmHg difference repeat measurement and use arm with higher reading
- Measurements over period of visit +/- ABPM/HBPM
- Emergency treatment required? (>180 SBP or 120 DBP + clinical signs)
- CVD risk and end organ damage should be assessed whilst waiting for hypertension confirmation
Pathophysiology of hypertension
- Elevated BP (essential/primary/idiopathic)- still not completely understood
- Leads to vascular changes
- Remodelling
- Thickening
- Hypertrophy
- Increases vasoactive substances inc ET-1, NAd, angII
- Vascular remodelling also occurs as a direct result of local salt sensitivity
- Hyperinsulinemia and hyperglycaemia lead to endothelial dysfunction and increased reactive oxygen species- NO signalling reduced.
These factors result in:
- Permanent and maintained medial hypertrophy of vasculature increasing TPR and decreasing compliance of the vessel
- End organs specifically at risk
- Renal
- Peripheral vascular disease
- Aneurysm
- Vascular dementia
- Retinal disease
- Also causes hypertensive disease- left ventricular heart failure- dilated cardiac failure
- Increased morbidity and mortality
Prehypertension
- Slippery slope (>120/60 <140/90 mmHg
- Aim (to reduce CVD risk)
- Promotion of regular exercise
- Modified diet
- Reduction in stress and increased relaxation
- Limit alcohol intake
- Discourage excessive caffeine consumption
- Smoking cessation
- Reduced dietary sodium
- These should be promoted in all patient groups
staging of hypertension
Non-pharmacological treatment of hypertension
- Weight reduction
- Moderate salt intake
- Aerobic exercise
- Smoking cessation
primary hypertension therapeutic agents
- Angiotensin converting enzyme inhibitors (ACEi)
- Angiotensin (AT1) receptor blockers (ARBs)
- Calcium channel blockers (CCBs)
- Diuretics- thiazide and thiazide-like
- Other. Agents for resistant hypertension
Physical assessment for hypertension
Look for secondary causes: Cushing’s syndrome, enlarged kidneys (PCK disease), renal bruits, radio-femoral delay (coarctation).
investigations for hypertensives
- Test for the presence of protein in the urine by sending a urine sample for estimation of the albumin: creatinine ratio and test for haematuria using a reagent strip.
- Blood sample to measure plasma glucose, electrolytes, creatinine, estimated glomerular filtration rate, serum total cholesterol and HDL cholesterol.
- Bloods may suggest secondary cause (low potassium, high Na: hyperaldosteronism
- Examine the fundi for the presence of hypertensive retinopathy.
- Arrange for a 12-lead electrocardiograph to be performed.
- Consider echocardiography if suggestion of LVH, valve disease or LVSD or diastolic dysfunction.
Hypertensive emergencies
- Crisis in an increase in BIP
- If sustained over few hour will lead to irreversible end organ damage
- Encephalopathy
- LV failure
- Aortic dissection
- Unstable angina
- Renal failure
Symptoms and signs of hypertensive emergency
- Severe chest pain
- Headache
- Nausea and vomiting
- Severe anxiety
- Seizures
Presentations of hypertensive crisis
*
- Emergency: high BP associated with a critical event: encephalopathy, pulmonary oedema, acute kidney injury, myocardial ischaemi
- Urgency: high BP without a critical illness, but may include ‘malignant hypertension’: associated with grade 3/4 hypertensive retinopathy
aim of therapy in hypertensive crisis
Aim of therapy: reduce BP to 110mmHg in 3-12 hours (emergency) or 24 hours (urgecy).