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NSC2500 - Pharm & Physiology > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

Define Chronotropic

A

the effect on the heart rate (firing of senatorial node)

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2
Q

Define Dromotropic

A

The effect on conduction velocity (through the atrioventricular node); affects heart rate.

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3
Q

Define Inotropic

A

The effects on myocardial contractility (and thus stroke volume)

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4
Q

Define Bathmotropic

A

The effect on the degree of excitability

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5
Q

Define Lusitropic

A

The effect on the relaxation of myocardium during diastole

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6
Q

Define VasoPressor

A

Increase vascular tone, increasing systemic vascular resistance and blood pressure

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7
Q

Define Vasodilator

A
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8
Q

Briefly describe the physiology of the heart

A

A closed system of the heart and blood vessels that circulates blood to all part of the body.

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9
Q

Explain Cardiodynamics (Including cardiac output, components and stroke volume)

A

Cardiac output : Volume of blood expelled from the heart in one minute, An indicator of blood flow through peripheral tissues

Stroke Volume: Volume of blood pumped by each ventricle in one contraction.

Specific drugs can increase or decrease preload and after load affecting both stroke volume and cardiac output

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10
Q

What are three fundamental components of the heart

A

Heart, Vessels, Blood

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11
Q

What are the major functions of the heart

A

Transportation of O2 and CO2, distribution of nutrients and transport of waste, circulation of hormones.

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12
Q

Briefly describe the anatomy of the heart

A

Four chambers,
Atria (right to left): Receiving chambers, assist with filling the ventricles, blood enters under low pressure
Ventricles (Right to left): Discharging chambers, Thick-walled pumps of the heart, during contraction, blood is propelled into circulation.

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13
Q

Briefly explain the hearts chambers and circulation
(Pulmonary and systemic)

A

Heart functions as a double pump - right side works as the pulmonary circuit pump, left side works as the systemic circuit pump.
Pulmonary Circulation- Blood is pumped out of the right side through the pulmonary trench, which splits into pulmonary arteries and take oxygen-poor blood to the lungs.

Systemic Circulation- Oxygen-rich blood returned to the left side of the heart is pumped out into the aorta and circulates to all body tissues
Oxygen-poor blood returns to the right atrium via systemic veins, which empty blood into the superior or inferior vena cava.

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14
Q

What does the coronary circulatory system consist of?

A

Coronary Arteries - Branch from the aorta to supply the heart muscle with oxygenated blood
Cardiac Veins - Drain the myocardium of blood
Coronary Sinus- A large vein on the posterior of the heart; receives blood from cardiac veins

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15
Q

What are some factors affecting Stroke Volume?

A

preload - blood force that stretches the ventricle at the end of diastole
Contractibility- force of ventricular contraction
After-load- Resistance to ejection of blood, caused by opposing pressures in the aorta and systemic circulation

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16
Q

What are the two systems that regulate heart activity? And what do they include?

A
  1. Extrinsic Intervention from ANS
  2. Intrinsic conduction system (Nodal System) Senatorial (SA) node, Atrioventricular (AV) node, atrioventricular bundle (bundle of his), purkinje fibres
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17
Q

Explain the Intrinsic System and Pace Maker cells for the electrical conduction of the heart

A

Pacemaker (Auto rhythmic) cells: Smaller than contractile cells, do not contain many myofibrils, do not contribute to the contractile force of the heart

Initiate action potentials
- have unstable resting potentials called pacemaker potentials

Uses Ca++ rather than Na+ for rising phase of the action potential

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18
Q

Define Contractile Cells

A

Action potential of cardiac contractile cells (cardiomyocytes) is different to neurone and skeletal muscle

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19
Q

Explain the normal electrical activity on the heart

A

Sinoatrial (SA) node, atrioventricular (AV) node and purkinje cells display pacemaker activity.

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20
Q

Extrinsic innervation of the heart?

A

Branches from both the sympathetic and parasympathetic ANS divisions regulate heart rate and force contraction

Stimulated by the sympathetic cardioacceleratory centre (Noradrenaline and adrenaline B1 adrenoreceptor)
Heart is inhibited by the parasympathetic cardioinhibitory center (Acetylcholine - Muscarininc M2 receptor)

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21
Q

Explain the extrinsic alteration of cardiac pacemaker activity from the sympathetic activity

A

NA and Ad increase channel activity
Binds to B1 adrenergic receptor which activate cAMP and increase channel open time
Causes more rapid pacemaker potentials. Increased chronotropic effects (increased HR), increased dromotropic effects ( increased conduction of APs), increased inotropic effects (increased contractility)

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22
Q

Explain the extrinsic alteration of cardiac pacemaker activity from the parasympathetic activity

A

ACh binds to M2 Muscarinic receptors
Increases K+ permeability and decreases Ca2+ permeability = hyperpolarising then membrane
Longer threshold = slower rate of action potential
decreased chronotropic effects (decreased HR), decreased dromotropic effects (decreased conduction of APs), Decreased inotropic effects (Decreased contractility)

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23
Q

Define secondary hypertension

A

Has identifiable cause, renal artery constriction, narrowing of aorta, pheochromocytoma, bushings Diases, primary aldosteronism, hyper/hypothyroidism

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24
Q

Define primary hypertension

A

Essential, idiopathic
risk factor - hyperlipidemia, diabetes, genetics and family history, diet, stress

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25
Q

What are the main classes hypertensive drugs?

A

Diuretics, sympatholytic agents, vasodilators, angiotensin antagonists

26
Q

How do diuretics work work for hypertension?

A
27
Q

How do adnrenorector blockers work for hypertension?

A
28
Q

What is hypertension?

A

Is the most common condition of the cardiovascular system
Exact causes are unclear but influenced by genes, family hx, diet, alcohol intake.
Increases incidence of runway failure, ischaemic heart disease, cardiac failure, and stroke

29
Q

What is Malignant hypertension?

A

Hypertensive emergency
Blood pressure is at least 190 systolic over 110-120 diastolic
Develops quickly

30
Q

What is the normal regulation of blood pressure and how are these things maintained?

A

Arterial blood pressure (BP) is directly proportionate to the product of cardiac output (CO) and peripheral vascular resistance.
Maintained: Arterioles, post capillary, heart, kidney.

31
Q

How do hypertensive drugs lower blood pressure?

A
  1. Dilating arteriolar resistance vessels; reduced peripheral vascular resistance (after load)
  2. Dilating venous capacitance vessels, reduced venous return to heart (preload) lead to reduced cardiac output
  3. Education of cardiac contractility and heart rate; lower heart rate and stroke volume gives reduced cardiac output
  4. Depletion of body sodium and reduction in plasma volume
32
Q

What is ishaemic heart disease?

A

A condition where there is an imbalance between myocardial oxygen supply and demand results in hypoxia.

33
Q

What is the balance of oxygen and supply and demand in ischaemic heart failure?

A

The oxygen demand goes up but the supply goes down, often caused by atherosclerosis

34
Q

Are symptomatic intervention for ischaemic heart disease and the drugs involved

A

Reduce O2 demand and or improve coronary flow
Nitrates, Ca2+ Channel Blockers, B-blockers.

35
Q

What are the different types of angina?

A

Stable, Unstable, Vasospastic,
Acute coronary syndrome

36
Q

What is the importance of oxygen supply and demand of the different types of angina?

A

With insufficient oxygen to support cardiac oxidate metabolism (reduced oxygen supply/demand ratio) the myocardium becomes hypoxic.

37
Q

What is the symptomatic treatment for angina?

A

Symptomatic: Beta Blockers (reduce HR and contractility therefore reduction in cardiac workload), Nitrates (Vasodilation to reduce preload & after load), Ca++ channel blockers.

38
Q

Explain the development and progression of plaques in terms of atherosclerosis

A

Plaque is caused by the accumulation of lipid-laden, macrophages within the arterial wall.
Development:
1. Endothelial cell injury
2. Migration of inflammatory cells
3. SMC proliferation and lipid deposition
4. Gradual development of the atheromatous plaque with lipid/necrotic core.

39
Q

What are the different sources of lipoproteins?

A

2 Sources: Dietary (gut) & de novo synthesis (liver)

40
Q

What are the approaches used to treat/prevent thrombus formation ?

A

Treatments: Dietary changes to reduce cholesterol and lipids, cessation of smoking, control o blood pressure, control of diabetes, exercise, Drugs to reduce plasma cholesterol (Aspirin)
prevent: Myocardial infarction, Other atherosclerotic disorders (stroke, peripheral vascular disease), re-infarction.

41
Q

What are the effects of acute myocardial infarction?

A

Cardiopulmonary effects: Systolic/diastolic dysfunction, Decreased cardiac output, tachycardia, arrhythmias, dyspnoea, pulmonary congestion/oedema.

42
Q

What are the causes of ischaemic stroke ?

A

Occurs when an artery supplying the brain is occluded leading to decreased blood flow to this affected area. Generally categorised by embolism or thrombolism

43
Q

What are the treatment options for ischaemic stroke?

A
44
Q

What are the goals of pharmacotherapy with myocardial infarction?

A

Maycardial infarction: The most important goal of drug therapy early in a cute myocardial infarction is to improve the oxygen supply.demand ratio for the heart.
2 strategies to improve the supply/demand ratio:
1. Restoring normal coronary blood flow
2. Decreasing myocardial oxygen consumption.
Long Term - Most patients will be placed on long-term anti-platelet therapy, or treated with beta blocker to reduce cardiac remodelling and reduce mortality.

45
Q

What is a myocardium infarction?

A

is the irreversible damage of myocardial tissue by prolonged ischaemia and hypoxia.

46
Q

What is Atherosclerosis?

A

Is a form of arteriosclerosis characterised by thickening and hardening of the vessel wall.

47
Q

What is a critical tool for the diagnosis of myocardial ischaemia?

A

ECG, in the ST segment the T will be abnormal

48
Q

What are the prophylactic interventions for disease?

A

Slower development of ischaemia
Lipid lowering drugs, anticoagulants, fibrinolytic, anti-platelet.

49
Q

Define Stable Angina

A

Caused by reduction of coronary perfusion due to obstruction by atherosclerosis.

50
Q

Define Unstable Angina

A

caused by transient thrombosis, usually in response to atherosclerotic plaque rupture.

51
Q

Define Vasospastic Angina

A

results from coronary, vasospasm, temporary reducing coronary blood flow and oxygen supply thereby decreasing the oxygen supply/demand ratio.

52
Q

Define Acute Coronary Syndrome

A

an emergency that commonly results from rupture of an atherosclerotic plaque and partial or complete thrombosis culminating in vascular occlusion. Necrosis of the cardiac muscle may ensure MI.

53
Q

What is the combination therapy for angina?

A

Nitrates alone, Beta blockers or CCBs alone, Combined nitrate and Beta blockers or CCB.

54
Q

What are the pharmacotherapy goals for ischaemic stroke?

A

Ischaemic stroke:
Divided into stroke-specific treatment and stroke prevention (prophylaxis)
Primary options- tissue plasminogen activator (tPA) (IV t-PA approved drug for treating ischaemic stroke is altephase or activease) and anti platelet agents (only approved oral anti platelet agent is Aspirin).
Long term - Antihypertnesives may include diuretics and or ACE inhibitors, lipid-lowering agents such as statins and fibrates.

55
Q

Define thrombosis and its role in clotting/coagulation?

A

Thrombosis is the counterpart to haemostasis, which involves a blood clot formation within intact vessels.

56
Q

Define embolism and its role in clotting/coagulation

A

An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site in distant from its point of origin. Emboli lodge in vessels too small to permit further passage causing either a partial occlusion or full occlusion. Depending on where they originated emboli can lodge anywhere in the vascular tree, clinical outcomes are dependent on whether the emboli lodges in the pulmonary or systemic circulations.

57
Q

What are the types of lipid lowering medications and their medications (Particularly ‘Statins’ )

A
58
Q

What are the approaches used to treat/prevent thrombus formation (particularly aspirin)

A

Inhibition of platelet function and inhibiting blood coagulation.

59
Q

Briefly explain the coagulation cascade

A

The coagulation cascade is an amplifying series of enzymatic conversions, each step proteolytically cleaves an inactive proenzymes into an activated enzyme, culminating in thrombin formation.Thrombin is the most important coagulation factor.
At the end of the cascade, thrombin converts fibrinogen into fibrin monomers that polymerise into an insoluble gel.

60
Q

Briefly explain Virchow’s triad in thrombosis

A

Three primary abnormalities lead to thrombus formation;
1. Endothelial injury
2. Stasis or turbulent blood flow
3. Hypercoagulability of the blood

NSC2500 - Pharm & Physiology (9 decks)

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