Cardiovascular Flashcards
Hypertension
BP = CO x SVR
When there is increased peripheral resistance, blood flow is imposed by friction between the artery walls, blood pressure increases due to blood viscosity and diameter of the arteries. 2 + readings of 140/90 = pre hypertension. Primary / idiopathic / essential HTN - due to unknown causes
Secondary HTN
Due to other organ damage such as renal
Modifiable risk factors
Diet, smoking, alcohol, lack of exercise
Non modifiable risk factors
Age, gender, family history
Pathophysiology of HTN
Genetic and environmental factors, Sympathetic nervous system stimulation, Excess adipose tissue = increased renin-angiotensin and aldosterone, insulin resistance, Na+ retention in the kidneys, Vasoconstriction - increased CO & SVR = HTN
Six classes of anti hypertensives
ACE inhibitor Angiotensin II inhibitors A blocker B blocker Ca+ channel blockers Diuretics
Three types of diuretics
Loop
Thiazides
Potassium sparing
Mechanism of action of b blocker
Inhibits the action of epinephrine on the B1 receptors of the cardiac muscle to reduce contractility and reduce SVR = reduced BP
Mechanism of action of Ca channel blockers
By inhibiting calcium ion channels it prevents calcium from entering the cardiac muscle and arteries, vasodilation can be accomplished by reducing contraction caused my Ca.
Spironolactone is
A potassium sparing diuretic, MOA inhibits NA/K exchange channel, increasing NA elimination and therefore H2O but sparing K
Amiloride
K sparing diuretic. MOA acts independent of aldosterone decreases water retention and Na in DCT
‘Prils’
ACE inhibitors - inhibits enzyme ACE to prevent conversion of angiotensin I to II
Metoprolol
B blocker - reduce the speed and force of heart contractions by blocking the effects of adrenergic (norepinephrine) receptors on the b1 receptors of the heart
Valsartan, Losartan
Angiotensin II receptor blockers. Angiotensin II causes vasoconstriction.
Furosemide
Loop diuretic, blocks reabsorption of Na, K and H2O in the loop of henle therefore increasing urine output
Atherosclerosis
Inflammatory cellular response leading to formation of fibro-fatty lesions (plaques) in the intimal layer of M&L arteries. Progressive accumulation of smooth muscle cells, lipids, and connective tissue.
IHD
Ischemic Heart Disease - narrowing of the arterioles due to atherosclerosis
AMI
Acute Myocardial Infarction - complete occlusion of a coronary artery with a thrombus. Cellular necrosis
Dyslipidemia
Abnormal level of lipid concentration in the blood, imbalance of cholesterol, triglycerides, HDL and LDL
Patho of atherosclerosis
Focal accumulation of lipids in a vessel wall due to increased plasma lipoproteins, reaction to injury, proliferation of smooth muscle cells due to endothelial injury - inflammatory response. LDL accumulates -> macrophages phagocytise to create foam cells which builds up to progress to fatty streaks. Often accumulate at branch points.
Unstable plaque
Thrombus / emboli
Atorvastatin, simvastatin and pravastatin do what
Inhibit the enzyme HMG-CoA which is responsible for cholesterol production in the liver. Grapefruit juice contraindicated because of metabolism by cytochrome p450
Spironolactone is
A potassium sparing diuretic
Clexane
Is a low molecular weight heparin
Heparin
Can be used IV for thromboembolism or SC for prevention. Heparin forms a complex with anti thrombin II to inactivate clotting factors (thrombin) 11a & Xa to prevent further clots. Does not dissolve current clots. Prevents progression of existing clots.
Warfarin
Vitamin K antagonist by inhibiting production of epoxide reductase therefore reducing coagulation factors.
Alteplase (t-PA)
Binds to plasminogen on the fibrin clot to degrade fibrin and convert to plasmin which degrades the clot.
CVD
Progressive loss of elasticity of arterial walls leads to progression of atherosclerosis and cardiovascular disease. Increasing chance of MI due to stable / unstable angina.
Unstable angina
Can be NSTEMI if myocardial injury occurs. More than 50% of the artery is occluded.
Right coronary artery supplies
Inferior of the heart
What artery is responsible for lateral MI
Left circumflex artery
What artery is occluded during anterior MI?
Left anterior descending artery
Coronary arteries arise from
Aorta, aortic semi lunar valve
Majority of blood flow to the coronary arteries occurs during
Diastole
Most abundant blood supply goes to
Left ventricle - thicker myocardium
Patho of myocardial ischemia
Coronary artery becomes temporarily blocked causing hypoxia (loss of oxygen and glucose) therefore converting to anaerobic metabolism, releasing lactic acid which releases kinins and adenosine to create chest pain. Reversible when blockage is reversed by nitrates and oxygen is supplied due to vasodilation.
Alteplase t-PA mechanism of action
Binds to plasminogen of the plaque and converts fibrin to plasmin, therefore dissolving the thrombus/embolus
Warfarin action
Inhibits expoxide reductase and depletes vitamin k from the liver therefore inhibits synthesis of clotting factors.
When do unstable angina symptoms often occur
At rest
Beta blockers should be used for which type of angina
stable angina only, not to be used with heart block (unstable angina)
Prizmental angina is
coronary spasm +/- atherosclerosis, altered CA+ channel function - treatment is a Ca+ channel blocker
