What are modifiable and non modifiable CVD risk factors
Mod: hypertension, smoking, high LDL, sedentary lifestyle, obesity, poor nutrition, excessive alcohol consumption
Non-mod: increased age, gender (male more likely before menopause), family Hx, ethnicity
Determinants of BP
BP = CO x SVR/TPR (systemic vascular resistance) CO = HR x SV
Normal regulation of blood pressure
- Short term: baroreceptors (found in carotid arteries) and endocrine. Baroreceptors reduce sensitivity with age. Baroreceptors stimulate SNS (adrenaline binds to alpha receptors in vessels = vasoconstriction) (noradrenaline binds to beta 1 receptor in heart = increase HR/contractility) or PNS activation
Long term: renal system - RAAS
What are the alpha 1/ beta 1/beta 2 located, MOA
Alpha 1: located on blood vessel - lead to vasoconstriction/dilated pupils
Beta 1: located on cardiac cells - increases rate and force of contraction. Increase contractility
Beta 2: found on smooth muscles in bronchioles and blood vessels: bronchodilation + vasodilation
What is hypertension and what are the risk factors
Hypertension: SBP>140mm/Hg or DBP > 90mmHg. Primary: no specific cause, secondary: due to specific cause
Risk factors: genetics, age, high sodium, glucose intolerance, smoking, obesity, alcoholic
Clinical manifestations of hypertension and it’s complications
Silent killer - no early symtpoms.
Later: due to damage of organs/vascular: heart disease, renal insufficiency, brain dysfunction, impaired vision, impaired mobility, vascular occlusion
Complications: organ disease in heart, brain, PVD, kidney, eyes
Pathophysiology of primary hypertension
- Genetic + environmental factors
- Leads to (1) defects in renal sodium haemostatis (poor sodium excretion —> sodium/water retention), (2) functional vasoconstriction (3) defects in vascular smooth muscle growth/structure.
- Leads to increase in CO and TPR = hypertension
Non-pharmacological management of hypertension
Lifestyle changes: dietary restriction (Na), increase K intake. Weight loss, exercise, smoking cessation, relaxation.
Pharmacological management of hypertension
- beta blockers: beta adrenergic antagonist - olol. Work against beta 1 and 2. To reduce heart rate/contractility = reduce CO and BP. Adverse: bronchospasm (block b2)
- Alpha 1 blockers: -sin. Block vasoconstriction = vasodilation = reduce TPR.
- ACE inhibitors: effect the RAAS -pril. Inhibit ACE = no conversion of Ag 2 = no release of aldosterone = no Na/h20 retention = reduced BP
- Diuretics - furosemide. Each drug Work differently ~ reduce sodium retention/absorption = decrease BP
- Angiotensin 2 blockers - blocks vasoconstriction / aldosterone = reduced fluid retention
- Calcium channel blockers - prevent Ca in cardiac cells = reduce contractility
What is coronary artery disease
Prolonged ischemia leading to chronic stable angina or acute coronary syndrome (unstable angina/NSTEMI or STEMI)
Risk factors for CAD
C-HAM-FOLDS Cocaine Hypertension Age Male Family Hx Obese Lipids Diabetes Smoking
How does CAD most likely develop
Atherosclerosis - narrowing and stiffening of the arteries that perfuse the myocardium - loss of recoil in BV
Oxygen demand vs oxygen supply
- Environment + free radicals = arterial wall injury
- Free radicals + LDL enter damaged artery wall and oxidise
- Injured arteries/oxidised LDL signal monocytes that turn into macrophages, engulf LDL and form foam cells. Foam cells signal for more monocytes/backup = Build up of foam cells - fatty streak
- Smooth muscle cells within arterial wall produce collagen to form a fibrous plaque cap. Calcium is also deposited = stiffened BV.
- Narrowing BV = reduced perfusion & Increases demand = ischemia = angina
Management of CAD
Lifestyle: smoking cessation, diet changes, exercise,
Pharmacological: statin (lipid lowering med), ace inhibitors, beta blockers, anti platelet therapy
Angioplasty, standing, bypass
What is angina and what causes the chest pain?
Angina = chest pain when myocardial O2 demand > O2 supply = ischemia
Patho:
- Atherosclerosis
- Myocardium becomes hypoxic within 10 sec of occlusions
- Anaerobic metabolism
- Lactic acid accumulation
- Lactic acid irritates myocardial nerve fibres = pain
Symptoms of angina
Usually 3-5 min with no permanent damage
Pain: heaviness/pressure can radiate to neck/jaw/left arm
SNS: pallor/diaphoresis
Dyspnoea can occur
Chronic stable angina vs unstable angina
Chronic stable angina
- cause: myocardial ischemia usually to CAD
- characteristic: episodic pain lasting 5-15min, provoked by exertion,/ relieved by GTN
Unstable angina
- cause: rupture of thickened plaque
- characteristic: new onset angina, chronic stable angina that increases frequency, duration, severity. Occurs at rest/minimal exertion. Not responsive to GTN
Goal for management of angina and it’s management
Goal: restore a balance between myocardial O2 demand and supply
Management
1. Nitrates (GTN) = metabolism and converted into nitric oxide in vessel walls —> NO causes vasodilation of peripheral blood vessels (reduces TPR = decreases preload and afterload = decreases SV = decreases CO = decreases O2 demands) + dilates coronary arteries = increase blood flow ischemic area
- ACE inhibitors, beta blockers, Ca+ channel blockers, antiplatelet/anticoagulants, statins, opioids
How CAD develops from stable to unstable/NSTEMI
- Deterioration of once stable plaque
- Rupture
- Platelet aggregation
- Thrombus
Unstable: (partial occlusion) chest pain that is new onset, occurs at rest, worsening pattern
NSTEMI: (partial occlusion) no ST elevation, severely occluded artery, partial thickness damage of heart
STEMI: (complete occlusion) ST elevation, sudden complete occlusion, full thickness damage of heart
What is an MI and it’s complications
NSTEMI/STEMI
Result of sustained ischemia causing irreversible myocardial cell death = loss of contractile function
Damage to myocardial cells release adrenaline/noradrenaline
Adrenaline: short term then reduces BP due to reduced contractility of necrotic tissue = decreased perfusion
Noradrenaline: vasoconstriction= cool/clammy/pale skin
Complications: arrhythmia, HF, cardiogenic shock, pain, diaphoresis, N/V,
