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Nursing Science 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

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1
Q

Hypertension

A

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

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2
Q

Secondary HTN

A

Due to other organ damage such as renal

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3
Q

Modifiable risk factors

A

Diet, smoking, alcohol, lack of exercise

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4
Q

Non modifiable risk factors

A

Age, gender, family history

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5
Q

Pathophysiology of HTN

A 
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
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6
Q

Six classes of anti hypertensives

A 
ACE inhibitor
Angiotensin II inhibitors  
A blocker
B blocker 
Ca+ channel blockers
Diuretics
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7
Q

Three types of diuretics

A

Loop
Thiazides
Potassium sparing

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8
Q

Mechanism of action of b blocker

A

Inhibits the action of epinephrine on the B1 receptors of the cardiac muscle to reduce contractility and reduce SVR = reduced BP

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9
Q

Mechanism of action of Ca channel blockers

A

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.

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10
Q

Spironolactone is

A

A potassium sparing diuretic, MOA inhibits NA/K exchange channel, increasing NA elimination and therefore H2O but sparing K

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11
Q

Amiloride

A

K sparing diuretic. MOA acts independent of aldosterone decreases water retention and Na in DCT

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12
Q

‘Prils’

A

ACE inhibitors - inhibits enzyme ACE to prevent conversion of angiotensin I to II

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13
Q

Metoprolol

A

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

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14
Q

Valsartan, Losartan

A

Angiotensin II receptor blockers. Angiotensin II causes vasoconstriction.

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15
Q

Furosemide

A

Loop diuretic, blocks reabsorption of Na, K and H2O in the loop of henle therefore increasing urine output

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16
Q

Atherosclerosis

A

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.

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17
Q

IHD

A

Ischemic Heart Disease - narrowing of the arterioles due to atherosclerosis

18
Q

AMI

A

Acute Myocardial Infarction - complete occlusion of a coronary artery with a thrombus. Cellular necrosis

19
Q

Dyslipidemia

A

Abnormal level of lipid concentration in the blood, imbalance of cholesterol, triglycerides, HDL and LDL

20
Q

Patho of atherosclerosis

A

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.

21
Q

Unstable plaque

A

Thrombus / emboli

22
Q

Atorvastatin, simvastatin and pravastatin do what

A

Inhibit the enzyme HMG-CoA which is responsible for cholesterol production in the liver. Grapefruit juice contraindicated because of metabolism by cytochrome p450

23
Q

Spironolactone is

A

A potassium sparing diuretic

24
Q

Clexane

A

Is a low molecular weight heparin

25
Q

Heparin

A

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.

26
Q

Warfarin

A

Vitamin K antagonist by inhibiting production of epoxide reductase therefore reducing coagulation factors.

27
Q

Alteplase (t-PA)

A

Binds to plasminogen on the fibrin clot to degrade fibrin and convert to plasmin which degrades the clot.

28
Q

CVD

A

Progressive loss of elasticity of arterial walls leads to progression of atherosclerosis and cardiovascular disease. Increasing chance of MI due to stable / unstable angina.

29
Q

Unstable angina

A

Can be NSTEMI if myocardial injury occurs. More than 50% of the artery is occluded.

30
Q

Right coronary artery supplies

A

Inferior of the heart

31
Q

What artery is responsible for lateral MI

A

Left circumflex artery

32
Q

What artery is occluded during anterior MI?

A

Left anterior descending artery

33
Q

Coronary arteries arise from

A

Aorta, aortic semi lunar valve

34
Q

Majority of blood flow to the coronary arteries occurs during

A

Diastole

35
Q

Most abundant blood supply goes to

A

Left ventricle - thicker myocardium

36
Q

Patho of myocardial ischemia

A

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.

37
Q

Alteplase t-PA mechanism of action

A

Binds to plasminogen of the plaque and converts fibrin to plasmin, therefore dissolving the thrombus/embolus

38
Q

Warfarin action

A

Inhibits expoxide reductase and depletes vitamin k from the liver therefore inhibits synthesis of clotting factors.

39
Q

When do unstable angina symptoms often occur

A

At rest

40
Q

Beta blockers should be used for which type of angina

A

stable angina only, not to be used with heart block (unstable angina)

41
Q

Prizmental angina is

A

coronary spasm +/- atherosclerosis, altered CA+ channel function - treatment is a Ca+ channel blocker

Nursing Science 2 (11 decks)

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