Week 5: Cardiovascular 1 - Hypertension, Coronary Artery Disease, Heart Failure Flashcards
What is Mean Arterial Pressure?
Mean arterial pressure = (stroke volume x heart rate) x systemic vascular resistance
* Stroke volume x heart rate = Cardiac output
What is stroke volume?
Stroke volume is the amount of blood pumped from the left ventricle per beat
What is heart rate?
Heart rate is the speed at which the heart beats (typically measured per minute)
What is systemic vascular resistance?
Systemic vascular resistance is the resistance applied to the blood by the vessel walls
- Diameter is a key factor
How the body response to normal fluctuations
- Baroreceptor reflex
Baroreceptor contain in carotid artery - send message to brain stem - brain stem activates either sympathetic or parasympathetic NS to either increase or reduce MAP respectively by stimulating the SA node
The baroreceptor reflex effect and pathway
- Increase MAP - increase parasympathetic tone which decreases HR which occurs through the neurotransmitter of PNS is acetylcholine that binds to muscarinic acetylcholine receptors at SA node
- Decrease MAP - increase sympathetic tone which increases HR and SV which occurs through the neurotransmitter of SNS noradrenaline that binds to beta-adrenoreceptors at SA node and cardiomyocyte
How the body responds to normal fluctuations
- RAAS
Renin-angiotensin-aldosterone system (RAAS)
- Draw pathway
- Pathway acts to increase SV, increase and increase SVR which increases MAP
Factors contributing to primary hypertension
Genetics Age Diet (Na+ intake) Baroreceptor reset Lifestyle (stressors and increase sympathetic tone)
Goals of anti hypertensives
- Reduce MAP
- Reduce incidence of micro vascular complications
- Reduce incidence of macro vascular complications
- Avoid adverse drug reactions
Factors contributing to the decision to start anti hypertensive therapy
- Not solely based on systolic and diastolic pressure
- Premised upon patient’s absolute cardiovascular risk
- Warranted if pressure is persistently > 160/100mmHg
Anti hypertensive - ACE inhibitors
- Examples
- MOA
- Adverse effects
- Practice points
Examples
- Ramipril
- Perindopril
- Lisinopril
- Enalapril
MOA
- Inhibit angiotensin converting enzyme which prevents conversion of angiotensin I to angiotensin II
Adverse effects
- Hypotension
- Hyperkalaemia
- Persistent dry cough
Practice points
- Very effective and often primary selection
- Involved in Triple Whammy interaction
- Not to be used in combination with ARB
Anti hypertensives - Angiotensin receptor blockers (ARB)
- Example
- MOA
- Adverse effects
- Practice points
Examples
- Candesartan
- Telmisartan
- Olmesartan
- Irbesartan
MOA
- Antagonise the angiotensin type 1 receptor thereby preventing angiotensin II from binding and initiating downstream effects
Adverse effect
- Hypotension
- Hyperkalemia
Practice points
- Often used to replace ACE inhibitor when they are not tolerated
- Involved in Triple Whammy interaction
- Not to be used with ACE inhibitors
Anti hypertensives - Calcium channel blockers
- Why use calcium channel blockers
- What are the two types of calcium channel blockers
Calcium has an effect on the muscle contractility of all muscles including cardiac muscle and arteriole smooth muscle
Two types of calcium channel blockers are
- Dihydropyridine calcium channel blockers
- Non-dihydropyridine calcium channel blockers
Anti hypertensives - Dihydropyridine calcium channel blockers
- Examples
- MOA
- Adverse effects
- Practice points
Examples
- Amlodipine
- Felodipine
- Lercanidipine
- Nifedipine
MOA
- Inhibits influx of calcium into only arteriole smooth muscle (decreases vasoconstriction)
Adverse effects
- Vasodilatory effects (headache, dizziness, hypotension and peripheral edema)
Practice points
- Selective calcium channel blocker
- Narrow range of indications (mainly just hypertension)
Anti hypertensive - Non-dihydropyridine calcium channel blocker
- Example
- MOA
- Adverse effects
- Practice points
Examples
- Diltiazem
- Verapamil
MOA
- Inhibits influx of calcium into both arteriole smooth muscle (decrease vasoconstriction) and cardiac muscle (decrease chronotropy/inotrophy)
Adverse effects
- Vasodilatory effects (arterial smooth muscle), constipation, bradycardia
Practice points
- Non selective calcium channel blocker
- Broad range of indications (beyond hypertension)
- Serious interaction with beta blockers
Anti hypertensive - Thiazide diuretics
- Example
- MOA
- Adverse effects
- Practice points
Example
- Hydrochlorothiazide
MOA
- Inhibit the reabsorption of Na+ and Cl- within distal convoluted tubule (where sodium goes water follows therefore decrease SV)
Adverse effects
- At low doses, very well tolerated
- Electrolyte disturbances
Practice points
- Often taken within a fixed dose combination
Effects of adrenaline and noradrenaline on the body
Adrenaline and noradrenaline bind to adrenoreceptors (SNS)
- Alpha receptors include alpha 1 recepture in vasculature and alpha 2 receptor in brain
- Beta receptors include beta 1 receptor in heart (increase HR and contractile force), beta 2 receptors in lungs (bronchodilation) and beta 3 receptors in the bladder
Anti hypertensives - beta blockers
- Examples
- MOA
- Adverse effects
- Practice points
Examples
- Atenolol
- Bisoprolol
- Metoprolol
- Carvedilol
MOA
- Selectively antagonise Beta 1 adrenoreceptors in heart therefore preventing (nor)adrenaline from binding and initiating downstream effects (decreases HR and SV)
Adverse effects
- Bradycardia
- Bronchospasm
- Mask hypoglycemia
Practice point
- Weak anti hypertensive, more useful beyond hypertension
- Very serious interaction with non-dihydropyridine CaCB
Other conditions that use anti hypertensives to manage
Stable angina
Post-myocardial infarction
Heart failure (HFrEF)
Additional application of anti hypertensives in stable angina
- Definition
- Treatment of acute episodes
- Treatment to prevent acute episodes
Stable angina
Definition
- Retrosternal chest discomfort that lasts 10 min or less and subsides with rest
- Occurs when myocardial oxygen demand exceeds supply, which is usually restricted by atherosclerotic obstruction
- Commonly triggered by physical activity or emotional stress
Treatment of acute episodes
- Short acting nitrates such as GTN
Treatment to prevent acute episodes
- Beta blockers
- Non dihydropyridine calcium channel blockers
- Long acting nitrates
Nitrates
- Examples
- MOA
- Adverse effects
- Practice points
Examples
- Glyceryl trinitrate
- Isosorbide mono nitrate
MOA
- Produce vasodilation and venodilation which decreases venous return and subsequently decreases preload (reduces SV)
- Reduces oxygen demand of myocardial tissue
Adverse effects
- Vasodilatory effects (headache, dizziness, hypotension and peripheral edema)
Practice points
- Can be either short acting (s/l spray) or long acting (patch)
- Nitrate tolerance develops if there is no nitrate free period per 24 hrs
- Serious interaction with PDE-5 inhibitors
Additional application of anti hypertensives in Post myocardial infarction
Beyond scope of this course
Most patients benefit from long term combination therapy of ACE inhibitor to decrease cardiovascular mortality post MI and beta blockers to decrease myocardial O2 requirements
Additional application of anti hypertensives in Heart failure (HFrEF)
Beyond scope of unit
Most patients benefit from long term combination therapy including ACE inhibitor, beta blocker and loop diuretic
Loop Diuretics
- Example
- MOA
- Adverse effects
- Practice points
Example
- Furosemide
MOA
- Inhibit the reabsorption of Na+ and Cl- within ascending limb of loop of Henle (very potent diuretic)
Adverse effects
- Electrolyte disturbances
- Dehydration
- Hypotension
Practice points
- Need to be mindful of diuresis and impact upon adherance
