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Complexities of Health and Illness > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Main structural components of the circulatory/cardiovascular system

A
  • heart - peripheral vascular system - haematological system (blood and components)
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2
Q

Function of the circulatory / cardiovascular system

A
  • delivers oxygen, nutrients and other requirements to the cell - removes and transports waste eg carbon dioxide to be excreted
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3
Q

Three types of circulation

A
  • pulmonary (to/from the lungs) - systemic (to/from the body tissues) - coronary (supplying blood to the heart tissue)
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4
Q

What is the main influence on coronary circulation flow

A

the pressure in the aorta

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5
Q

Valves within the heart

A
  • atrioventricular valves (open when ventricles are relaxed) * tricuspid valve * mitral valve - semilunar valves (open when ventricles are contracting) * pulmonary semilunar valve * aortic semilunar valve
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6
Q

Layers of the blood vessel from inside out

A
  • Lumen - Tunica intima (simple squamous epithelial cells) - Tunica media - Tinuca adventitia
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7
Q

Differences between the structure of veins and arteries

A
  • Veins lumens are wider - Arteriers tunica media is wider - Veins have valves - arteries closer to the heart have more elastic fibres i the tunica media - veins have more smooth muscle to assist in returning blood to the heart against gravity - some capilliaries (eg those in the lungs) are only 1 epithelial cell wide
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8
Q

Blood flow resistance is impacted by:

A
  • vessel length - vessel diameter - blood viscosity - blood turbulence
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9
Q

3 main components of blood

A
  • erythrocytes (red blood cells) - leukocytes (white blood cells) - thrombocytes (platelets)
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10
Q

The 4 stations of the conductive pathway of the heart

A
  • SA node (aka pacemaker) - located in the right atria and starts the spark - AV node - located on the back wall of the heart between the right atria and right ventricle - Bundle of HIS - located in the septum - the Pirjinke Fibres - spread the electrical charge throughout the myocardium
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11
Q

Blood flow through the entire circulatory system

A

Right atrium > right AV valve > right ventricle > pulmonary SL valve > pulmonary artery > arterioles > capillaries > venuoles > veins > pulmonary vein > left atrium > left AV valve > left ventricle > aortic SL valve > aorta > arteries > arterioles > capillaries > venuoles > veins > vena cava > right atrium

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12
Q

Layers of the heart wall from outside in

A
  • pericardium (serous pericardium, aka epicardium) * parietal layer * visceral layer - myocardium - endocardium
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13
Q

What is the serious pericardium and what does it do?

A
  • double walled membranous sac - protects the heart from infection and inflammation - anchors the heart in place - contains nociceptors and mechanoceptors which cause changes in blood pressure and heart rate - the parietal and visceral layers are separated by the fluid-filled pericardial cavity which lubricates and reduces friction as the heart beats
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14
Q

Heart sounds

A

S1 - occurs when the atrioventricular valves close, during ventricular contraction S2 - occurs when the semilunar valves close, ventricular relaxation

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15
Q

Where is it easiest to hear each of the valves?

A

• aortic valve: second intercostal space on the right-hand side of the sternum • pulmonary valve: second intercostal space on the left-hand side of the sternum • tricuspid valve: fourth intercostal space on the left-hand side of the sternum • mitral valve: fifth intercostal space in the midclavicular line (apex)

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16
Q

What are diastole and systole?

A
  • diastole - relaxation, blood fills the ventricles - systole - contraction, propels blood from the ventricles
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17
Q

What is the cardiac cycle?

A
  1. atrial systole 2. isovolumetric ventricular contraction 3. ejection 4. isovolumetric ventricular relaxation 5 passive ventricular filling
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18
Q

Main branches of the coronary arteries

A
  • left coronary artery - left anterior descending artery (aka anterior interventricular artery) - circumflex artery - right coronary artery
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19
Q

What is angiogenesis?

A

growth of new blood vessels

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20
Q

What are the 5 key phases to the cardiac action potential?

A

0 depolarisation 1 early rapid repolarisation 2 plateau phase 3 final rapid repolarisation 4 resting membrane phase

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21
Q

What do the different sections of an ECG show?

A
  • P wave - right and left atrial depolarisation - PR interval - time from the onset of atrial activation to the onset of ventricular activation (~0.12 to 0.2 seconds) - QRS complex - ventricular depolarisation - ST segment - ventricular myocardium is depolarised, ventricles are contracting - QT interval - electrical systole of the ventricles - T wave - ventricular repolarisation - TP segment - ventricular relaxation and filling
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22
Q

What is cardiovascular disease?

A

Disorders of the heart and blood vessels.

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23
Q

What is coronary heart disease (aka ischemic heart disease, coronary artery disease, heart disease)?

A

Disorders of the coronary arteries, eg. angina, myocardial infarction

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24
Q

What is arteriosclerosis?

A

chronic abnormal thickening and hardening of artery walls

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25
Q

What is atherosclerosis?

A

A form of arteriosclerosis, with soft deposits of intra-arterial fat and other variations depending on the severity of the inflammatory condition - the main cause of coronary heart disease

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26
Q

Clinical manifestations of atherosclerosis

A
  • maybe none - transient ischaemic events (stable angina - infarction with manifestations - peripheral artery obstruction leading to pain, neurovascular changes, disability
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27
Q

Risk factors for coronary artery disease

A
  • higher age - male or postmenopausal female - family history - dyslipidaema and atherosclerosis-promoting diet - hypertension - smoking - diabetes mellitus and insulin resistance - obesity - sedentary lifestyle - inflammatory factors
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28
Q

What is metabolic syndrome (syndrome x)

A
  • abdominal obesity, insulin resistance,
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29
Q

Pathophysiology of coronary heart disease

A
  • narrowing of a major coronary artery by > 50%, leading to ischaemia, especially during exercise - commonly from atherosclerosis - can also be from (less commonly) spasm, hypotension, arrhythmias, anaemia)
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30
Q

Causes of cardiovascular cardiac-type pain

A
  • myocardial ischaemia - myocardial infarction - pericarditis - heart valve disorders - cancer - sickle cell occlusion
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31
Q

Causes of non-cardiovascular cardiac type pain (chest pain)

A
  • dissecting aortic aneurysm - herpes zoster (shingles) - oesophageal reflux / spasm - pneumonia - pneumothorax - pleurisy - peptic ulceration - gallbladder disease - musculoskeletal / costochondral - pulmonary embolism
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32
Q

Clinical manifestations of stable angina pectoris

A
  • 3 - 5 minutes with no permanent damage - usually substernal, from heaviness or pressure to severe pain - may radiate to neck, lower jaw, left arm, left shoulder, occasionally to back or down right arm - likely due to lactic acid or abnormal stretching of myocardial nerve fibres - pallor or diaphoresis - dyspnoea, nausea and vomiting - Prinzmetal’s angina from coronary artery spasm is unpredictable, maybe at rest - silent ischaemia is mainly in older adults with vague symptoms of fatigue, mild dyspnoea, a feeling of unease
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33
Q

Clinical manifestations of unstable angina

A
  • pain occurs at rest and is increasing in severity / frequency - pain increasing with coronary artery spasm or unstable plaque / thrombus blockage - pain lasts 10mins or longer and radiates to neck and/or left shoulder/arm
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34
Q

What is myocardial infarction?

A
  • when ischaemia becomes infarction - irreversible cell death and tissue necrosis - numerous electrolyte and chemical changes - two types: subendocardial MI, where thrombus break up before distal necrosis occurs (usually non-STEMI) and transmural MI where the thrombus remain and distal necrosis occurs (usually STEMI, “full thickness” infarction, results in severe cardiac dysfunction if survived.
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35
Q

What is “good” cholesterol?

A
  • High density lipoproteins - transport excess cholesterol away from tissues and back to the liver for metabolism
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36
Q

What is “bad” cholesterol?

A
  • low density lipoproteins - transport cholesterol from the liver to the tissues and organs where it is used to build plasma membranes - contributes significantly to plaque deposits and coronary artery disease
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37
Q

Indications of different lipid-lowering drugs

A
  • to lower LDL-C (hypercholesterolaemia) - to lower triglyceride (hypertriglyceridaemia) - both (hyperlipidaemia)
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38
Q

Drug types to lower hypercholesterolaemia

A
  • statins - bile acid-binding resin - nicotinic acid - ezetimibe - fibrate
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39
Q

Drug types to lower hypertriglyceridaemia

A
  • fibrate - fish oil - nicotinic acid
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40
Q

Drug types to lower mixed hyperlipidaemia

A
  • guided by predominant disorder including: - statins - fibrate - nicotinic acid
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41
Q

Statins care considerations

A
  • administer at bedtime - child-bearing-age women should use condoms to avoid pregnancy - multiple drug interactions including some antbioltics and antihypertensives - avoid grapefruit juice which alters metabolism of the drug - regular ophthalmic examinations as can increase risk of cataracts
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42
Q

In relation to the specialised properties of the conduction cells of the heart cells, what is automaticity?

A

inherent ability to spontaneously initiate an electrical impulse -normally only by pacemaker cells - affected by potassium and calcium levels

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43
Q

In relation to the specialised properties of the conduction cells of the heart cells, what is conductivity?

A
  • ability of a cell to transmit an action potential along its membrane - all cardiac muscle tissue - affected by potassium and calcium levels
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44
Q

In relation to the specialised properties of the conduction cells of the heart cells, what is refractoriness?

A
  • tissue is un-responsive to stimulation during initial phase of contraction, allowing for regular contraction and relaxation
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45
Q

How is cardiac output (CO) determined

A

CO = stroke volume (SV) x heart rate (HR)

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46
Q

What is stroke volume regulated by:

A
  • preload - degree of stretch of heart fibres before contraction - afterload - force ventricles must overcome to eject their blood volume - contractility - inherent capability of the cardiac muscle fibres to shorten
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47
Q

Main drug types affecting cardiac function

A
  • positive inotrophic (eg adrenaline, dobutamine) - increase force of myocardial contraction - negative inotrophic (eg propanolol) - decreases force of myocardial contraction - positive chronotrophic (eg adrenaline) - accelerate heart rate by increase rate of impulse formation in SA node - Negative Chronotropic (eg digoxin) - slows HR down by decreasing impulse formation = Positive Dromotropic (eg phenytoin) - increase conduction velocity through specialised conducting tissues Negative Dromotopic (verapamil) delays conduction velocity through specialised conducting tissues
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48
Q

What is digoxin?

A
  • Cardiac glycoside - Mechanisms of action: - Inhibits active transport of Na⁺ and K⁺ across myocardial cell membrane by interrupting the Na⁺- K⁺ pump - Alters the electrophysiological properties of cardiac tissue – decreases automaticity and increases resting membrane potential of atrial tissue and AV node. - Effects on the heart: - Increased contractile force - Decreased conduction through AV node - Decreased heart rate - Stabilises rhythm disturbances
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49
Q

Indications and pharmacokinetics of digoxin

A
  • Cardiac arrhythmias - Atrial fibrillation - Atrial flutter - Paroxysmal atrial tachycardia - Heart Failure - Available in oral or parenteral form - Rapid onset of action and rapid absorption - 30-120mins orally and 5-30mins IV - Primarily excreted unchanged in urine (don’t prescribe for patients with renal disease)
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50
Q

Potential adverse reactions of digoxin?

A
  • GI disturbances – Nausea and vomiting, diarrhoea - CNS effects – visual disturbances, confusion, nightmares, agitation and drowsiness - Cardiac arrhythmias (with digitalis toxicity) -premature ventricular beats, AV block disorders, ventricular arrhythmias
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51
Q

Digoxin toxicity

A
  • Low Therapeutic Index – therapeutic dose is very close to the toxic dose. - Digoxin induced cardiac arrhythmias caused by depression of the SA and AV node - Antidote – digoxin-specific immune antigen-binding fragment (Fab) - Pre-disposing factors indicating need to monitor for signs and symptoms of toxicity - Hypokalaemia - Hypercalcaemia - Hypomagnesaemia - Coexisting conditions – kidney disease or failure
52
Q

Digoxin care considerations

A
  • Monitor pulse for 1 full minute before administration – Withhold dose if pulse is less than 60 bpm in adult and 90bpm in infant. - Check dose and prescription carefully – digoxin has a small margin of safety and small errors can cause serious problems - Administer IV doses very slowly over at least 5 mins – to avoid cardiac arrhythmias - Avoid IM administration – can be quite painful - Avoid administering oral dose with food – delays absorption
53
Q

Indications for use of antiarrhythmic medication

A
  • Restoration of haemodynamic stability - Prevention of life-threatening arrhythmias - Prevention of sudden cardiac death - Controlling ventricular rate - Preventing thromboembolism in atrial fibrillation
54
Q

Classifaction of antiarrhythmics

A
  • Class I drugs - Block/interfere with the sodium channel - Class 1a – Disopyramide - Class 1b – Lignocaine - Class 1c - Flecainide - Class II – β adrenoceptor antagonists (eg Atenolol, metoprolol) - Class III – increase duration of the action potential and effective refractory period (eg Amiodarone and sotalol) - Class IV – calcium channel blockers (eg Verapamil) - Drugs not included under this classification include adenosine, atropine, adrenaline, digoxin
55
Q

What is amiodarone?

A
  • Mechanism of action - Prolong the effective refractory period by prolonging the action potential duration - Decrease automaticity, prolongs AV conduction and decreases automaticity of Purkinje fibres - Can block K⁺, Na⁺ and Ca⁺ channels and β receptors - Indications - Prevention and treatment of serious atrial and ventricular arrhythmias, management of acute tachyarrhythmia’s - Highly individual in its availability - Poorly absorbed – has a bioavailability of 20-86% - Onset of action varies from several days to weeks - Steady state plasma levels reached after several weeks
56
Q

Adverse reactions of amiodarone

A
  • Dizziness - Bitter taste - Headache - Flushing - Nausea & Vomiting - Constipation - Ataxia - Weight loss - Fever - Tremors - Paraesthesiae of fingers and toes - Photosensitivity and blurred vision - Blue-grey skin discolouration - Pulmonary fibrosis or pneumonitis - Cough - Allergic reaction
57
Q

Care considerations for amioderone

A
  • Dose should be titrated to the lowest amount needed to achieve control of arrhythmia – decrease risk of severe adverse effects - Continually monitor cardiac rhythm when initiating or changing dose – detect potentially serious adverse effects and to evaluate effectiveness - Administer parenteral form only if oral is not suitable – consider changing to oral dose as soon as possible – decrease potential for adverse effects - Dose may be reduced in people with renal or hepatic dysfunction – reduced dose needed to ensure therapeutic effects without increased risk of toxic effects
58
Q

Divisions of the nervous system

A
59
Q

Functions of the Autonomic Nervous System

A
  • Regulates internal viscera
  • heart, blood vessels, digestive organs, kidneys and reproductive organs
  • Assists in maintaining homeostasis
  • No conscious control
  • Parasympathetic (PNS) and Sympathetic (SNS) branches
60
Q

What is acetylcholine (ACh)

A
  • A neurotransmitter
  • Released by cholinergic neurons
  • Deactivated naturally by acetylcholinesterase
  • Drugs that mimic ACh – muscarinic receptor agonists
  • Drugs that are anti- ACh – muscarinic receptor antagonists
  • Involved in neurotransmission in much of the SNS and PNS
  • Lacks tissue selectivity (widespread effect)
61
Q

What is atropine?

A
  • a Muscarinic Receptor Antagonist (Anticholinergic, Parasympatholytic)
  • Wide range of effects due to widespread distribution of muscarinic receptors in the body
  • Non-selective
  • Therefore extensive adverse reactions
  • Readily absorbed after oral or parenteral administration (ocular, ET tube)
  • 50% of the drug is bound to plasma proteins and crosses the placental and blood-brain barrier
  • Metabolism – primarily liver

Excretion ~ via urine

62
Q

Nursing considerations for atropine

A
  • Provide comfort measures – to help the person tolerate the drug effects
  • Sugarless lozenges to suck and frequent mouth care – alleviate problems associated with dry mouth
  • Control of lighting – to alleviate photophobia
  • Small and frequent meals – to alleviate GI discomfort
  • Bowel program including a high-fibre diet – to alleviate constipation
  • Safety precautions (side rails, assist ambulation, advice to avoid driving and operating hazardous machinery) – to prevent injury with possible CNS side effects
  • Analgesics – for relief if headaches occur
  • Voiding before medication – if urinary retention is a problem
  • Encourage fluid intake and monitor heat exposure – the ability to sweat will be reduced
63
Q

Clinical uses of atropine

A
  • Prior to surgery: Premedication to prevent excessive salivation and respiratory tract secretions.
  • Anticholinesterase poisoning
  • Treat bradycardia during resuscitation
  • Asystole
  • Relaxation of the pupil of the eye (mydriasis)
64
Q

What does the sympathetic nervous system do?

A

Regulates heart, secretory glands and vascular and non-vascular smooth muscle

65
Q

What are catecholamines, and what are the three naturally occurring catecholamines?

A

Catecholamines are hormones made by your adrenal glands, which are located on top of your kidneys. Your adrenal glands send catecholamines into your blood when you’re physically or emotionally stressed

  • dopamine
  • adrenaline
  • noradrenaline
66
Q

What are adrenergic nerves?

A

Nerves that contain noradrenaline or adrenaline.

67
Q

What are adrenoceptors?

A

Receptors that are stimulated by endogenous catecholamines

  • Adrenaline
  • Noradrenaline

There are many subtypes:

  • Alpha (α) – divided into α₁ α₂
  • Beta (β) – divided into β₁ β₂ β₃

With these subtypes having different effects on various parts of the body

Development of agonist and antagonist drugs depending on their targeted use

68
Q

Major effects of different subtypes of adrenoceptors

A
  • α₁
  • vasoconstriction of peripheral blood vessels
  • dilation of pupils
  • increased contractility of the heart (inotropic effect)
  • α₂
  • inhibition of transmitter release
  • aggregation of platelets
  • contraction of smooth muscle
  • β₁
  • increased heart rate (chronotropic effect)
  • increased contractility of the heart (inotropic effect)
  • β₂
  • relaxation of uterus
  • glycogenolysis
  • dilation of bronchial smooth muscle
69
Q

Types of adrenergic drugs

A
  • Direct-acting adrenoceptor agonists (sympathomimetic)
  • Mimic effects of noradrenaline (NA) or adrenaline
  • Directly stimulate alpha and beta adrenoceptors
  • Mixed acting adrenoceptor agonists
  • Release NA indirectly and also directly activate adrenoceptors
  • Indirect-acting adrenoceptor agonists
  • Facilitate release of NA from or block uptake of NA into nerve terminals
  • Adrenoceptor antagonists (sympatholytic)
  • Block the action of the sympathetic nervous system
70
Q

What do direct-acting adrenoceptor agonist drugs do?

A
  • Mimic the effects of sympathetic stimulation
  • Increase cardiac output
  • Vasoconstriction of arterioles and veins
  • Regulation of body temperature
  • Bronchial dilation
71
Q

Examples of direct-acting adrenoceptor agonist natural catecholamines and synthetic catecholamines

A
  • Natural Catecholamines
  • Adrenaline
  • noradrenaline
  • dopamine
  • Synthetic catecholamines
  • Dobutamine
  • Isoprenaline
72
Q

Effects of noradrenaline

A
  • High affinity for α-adrenoceptors (contained in the blood vessels of skin and mucous membranes) – produces vasoconstriction.
  • Vessels in kidneys and other visceral organs – also contain α-adrenoceptors so there is a reduction of blood flow
  • No change in heart rate or cardiac output.
  • Both systolic and diastolic pressure is increased
  • Effect is dose dependant
73
Q

Adverse reactions of Noradrenaline

A
  • Dizziness
  • Pallor
  • Tremor
  • Insomnia
  • Headache
  • Palpitations
  • Infrequently – hypertension and bradycardia
74
Q

Types of mixed-acting adrenoceptor agonists

A
  • Ephedrine – prototypical
  • Pseudoephedrine – oral and nasal decongestant.
  • Action on α-adrenoceptors in vascular smooth muscle result in vasoconstriction of dilated nasal blood vessels which relieves congestion.
  • Adverse effects – CNS stimulation (excitability, insomnia, tremor)
75
Q

Examples of indirect-acting adrenoceptor agonists

A
  • Trigger release of NA and adrenaline from storage sites in adrenal medulla and sympathetic neurons – which then activate α and ß-adrenoceptors (eg amphetamine)
  • Others block uptake of NA into sympathetic neurons (eg cocaine)
76
Q

What do adrenoceptor antagonists do?

A
  • Compete with catecholamines for binding at α-adrenoceptors

ÒInhibit sympathetic stimulation (sympatholytic)

  • α₁ -adrenoceptor selective antagonists – prazosin
  • Non-selective α₁ and α₂ adrenoceptor antagonists – phentolamine
  • Non selective α1 and ß-adrenoceptor antagonists – labetalol
77
Q

Examples of ß-adrenoceptor antagonists

A
  • ß-blockers
  • ß1-selective blockers (cardioselective blockers) - eg Atenolol, metoprolol
  • Non-selective ß-adrenoceptor antagonists affect both ß1 and ß2, eg Labetalol, propranolol
  • Contraindicated in patients with asthma due to inhibition of bronchodilation.
78
Q

Indications for ß-adrenoceptor antagonists

A
  • Angina pectoris
  • Hypertension
  • Tremors
  • Tachycardia
  • Prevent or treat cardiac arrhythmias
  • Myocardial infarction
  • Vascular headaches
79
Q

Pharmacokinetics of ß-adrenoceptor antagonists

A
  • Metabolised in liver or excreted unchanged by the kidney
  • Different agents might be more appropriate for people with renal or hepatic impairment
  • Metoprolol – metabolised by liver more suitable for people with kidney disease
  • Atenolol – predominately cleared by the kidney so more suitable for people with hepatic disease.
80
Q

Risks of ß-adrenoceptor antagonists

A
  • Abrupt Withdrawal can lead to rebound phenomenon
  • Exacerbated hypertension, angina or ventricular arrhythmias
  • May precipitate an MI
  • Other symptoms can be sweating, rebound hypertension, tremors, tachycardia or respiratory distress
  • Dosage should be halved every 3-4 days over 8-14 days
  • Avoid vigorous exercise during this time
81
Q

Nursing considerations for ß-adrenoceptor antagonists

A
  • Powerful drugs (often with multiple adverse reactions and contraindications)
  • Follow directions closely/educated patient
  • What to do if fasting/having surgery
  • What to do in case of illness
  • What to do if considering commencing complementary medications
  • Continuously monitor any individual receiving an intravenous form of these drugs
  • Titrated to patient vital signs
  • For adverse reactions (sympathetic blockade)
82
Q

What is the ejection fraction?

A

The percentage of blood that has filled the ventricle and that is then ejected with ventricular contraction. This is normally between 55 - 75%

Ejection fraction = stroke volume / end-diastolic volume

83
Q

What is preload, and what influences it?

A

Preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole.

It is influenced by venous return to the ventricle.

84
Q

What is afterload (aka left ventricular afterload)?

A

The resistance to the ejection of blood from the left ventricle.

  • Aortic diastolic pressure indicates afterload. Lower aortic pressure = decreased afterload = more rapid and easier contractility.
85
Q

What 3 major factors determine the force of myocardial contraction?

A
  • changes in the stretching of the ventricular myocardium caused by changes in ventricular filling volume (preload)
  • alterations in the sympathetic activation of the ventricles
  • adequacy of myocardial oxygen supply.
86
Q

Which organs receive unusual blood supply and why?

A
  • Lungs. In addition to receiving oxygenated blood through the bronchial arteries (which provide nutrient-rich blood to most respiratory tissues), the lungs also receive deoxygenated blood from the pulmonary artery and, after gas exchange, oxygenated blood is drained from the lungs in the pulmonary vein.
  • Liver. In addition to receiving oxygenated blood through the hepatic artery (which provides nutrient-rich blood), an additional supply of blood enters through the hepatic portal vein — this blood contains the substances that have been absorbed from the digestive system.
  • Brain. The cerebral arterial circle contains anastomoses (connections) of arteries with arteries, which ensures that alternative routes are available for blood to enter the brain.
87
Q

Key drug groups affecting vascular function with examples

A

◆ Aldosterone receptor antagonists eg: eplerenone, spironolactone
◆ Angiotensin-converting enzyme (ACE) inhibitors eg: captopril, enalapril, fosinopril, lisinopril, perindopril, quinapril, ramipril, trandolapril
◆ Angiotensin-receptor (AT1) antagonists (also called angiotensin-receptor blockers [ARBs]) eg: candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan, valsartan
◆ Calcium channel blockers eg: amlodipine, clevidipine, diltiazem, felodipine, lercanidipine, nifedipine, nimodipine, verapamil
◆ Centrally acting adrenergic inhibitors eg: clonidine, methyldopa, moxonidine
◆ Drugs for peripheral vascular disease eg: cilostazol, pentoxifylline (oxpentifylline), oxerutins (hydroxyethylrutosides)
◆ Nitrates eg: glyceryl trinitrate
◆ Potassium channel activators eg: diazoxide, minoxidil, nicorandil

88
Q

What are the main drug groups of direct-acting vasodilators and indirect-acting vasodilators?

A

1 Direct-acting vasodilators:

✛ nitrates
✛ calcium channel blockers
✛ potassium channel activators.

2 Indirect-acting vasodilators:

✛ centrally acting adrenergic inhibitors
✛ angiotensin-converting enzyme (ACE) inhibitors
✛ angiotensin (AT1) receptor antagonists (also called angiotensin-receptor blockers, or ARBs)
✛ aldosterone receptor antagonists.

89
Q

What is an ideal antianginal drug / what does it do (there are currently no ideal antianginal drugs)?

A

◆ establishes a balance between coronary blood flow and the metabolic demands of the heart
◆ has a local rather than a systemic effect, acting directly on coronary vessels to promote coronary vasodilation with little or no effect on other organ systems
◆ promotes oxygen extraction by the heart
◆ is effective when taken orally and has a sustained action
◆ is devoid of tolerance.

90
Q

What routes is Glyceryl trinitrate (GTN) available in?

A
  • sublingual tablet
  • sublingual spray
  • transdermal patch
  • IV infusion
91
Q

What are the indications for glyceryl trinitrate (GTN)?

A

◆ prevent or treat stable angina
◆ treat unstable angina and heart failure associated with acute myocardial infarction.

92
Q

What are the potential adverse reactions of glyceryl trinitrate (GTN)?

A

◆ headache, dizziness, orthostatic hypotension, palpitations
◆ nausea or vomiting
◆ agitation, facial flushing, dry mouth, rash and blurred vision.

93
Q

What are the contraindications of glyceryl trinitrate (GTN)?

A

◆ cardiomyopathy, hypotension, hypovolaemia
◆ aortic or mitral stenosis
◆ severe anaemia
◆ raised intracranial pressure and glaucoma
◆ concurrent use of sildenafil.

94
Q

What do calcium channel blockers do?

A
  • block the inward movement of calcium through the slow channels of the cell membranes of cardiac and smooth muscle cells.
  • decrease the force of myocardial contraction
  • decrease automaticity on the SA node
  • decrease conduction in the AV junction (negative dromotropic effect)
  • decrease heart rate (negative chronotropic effect)
  • dilates coronary arteries, lowering coronary resistance and improving blood flow and oxygen delivery
  • inhibit contraction of smooth muscle in the peripheral arterioles

Used to treat:

  • angina
  • supraventricular tachydysrhythmias (verapamil)
  • hypertension
  • cerebral vasospasm after subarachnoid haemorrhage (nimodipine)
95
Q

Types of calcium channel blockers?

A

◆ phenylalkylamine type (verapamil)
◆ benzothiazepine type (diltiazem)
◆ dihydropyridine type (amlodipine, clevidipine, felodipine, nifedipine, nimodipine and lercanidipine).

96
Q

Potential adverse reactions to calcium channel blockers?

A
  • headache

nausea

  • hypotension
  • dizziness
  • skin flushing or rash
  • oedema of the ankles and feet
  • dry mouth
  • tachycardia
  • gingival hyperplasia (rarely, for some types of calcium channel blockers)
97
Q

Contraindications of calcium channel blockers?

A
  • severe bradycardia
  • congestive heart failure
  • hypotension
  • acute myocardial infarction
  • liver or kidney impairment.
98
Q

Primary effects of nitrates?

A
  • Decreased systolic blood pressure
  • decreased ventricular volume
  • increased heart rate
  • increased coronary blood flow
  • decreased coronary vessel resistance
  • decreased coronary spasm
  • increased collateral blood flow
99
Q

Primary effects of β-blockers?

A
  • Decreased systolic blood pressure
  • increased ventricular volume
  • decreased heart rate
  • decreased myocardial contractility
  • increased coronary blood flow
  • increased coronary vessel resistance
  • increased coronary spasm
100
Q

Primary effects of calcium channel blockers?

A
  • Decreased systolic blood pressure
  • decreased ventricular volume
  • variable impact on heart rate
  • decreased myocardial contractility
  • increased coronary blood flow
  • decreased coronary vessel resistance
  • decreased coronary spasm
  • decreased collateral blood flow
101
Q

Main potassium channel activators?

A
  • nicorandil
  • diazoxide
  • minoxidil
102
Q

What is the pathophysiology of the acute coronary syndromes?

A
103
Q

What do STEMI and NSTEMI stand for?

A

STEMI - ST elevation myocardial infarction

NSTEMI - non-ST elevation myocardial infarction

104
Q

Main factors contributing to myocardial ishcaemia?

A
  • Impacted coronary perfusion
  • atherosclerosis
  • thrombosis
  • vasospasm
  • poor perfusion pressure
  • Impacted myocardial workload
  • rapid heart rate
  • increased preload, afterload or contractility
  • increased metabolic demands (eg hyperthyroidism)
  • Impacted blood oxygen content
  • reduced atmospheric oxygen pressure
  • impaired gas exchange
  • low red blood cells and haemoglobin content
105
Q

What are the characteristics of metabolic syndrome or syndrome X?

A

■ abdominal obesity
■ abnormal blood lipids (low hDL, high triglycerides)

■ hypertension
■ elevated fasting blood glucose

■ clotting tendency
■ Inflammatory factors

106
Q

Clinical manifestations of angina?

A
  • Chest pain: substernal or precordial (across the chest wall); may radiate to neck, arms, shoulders or jaw.
  • Quality: tight, squeezing, constricting or heavy sensation; may also be described as burning, aching, choking, dull or constant.
  • Associated manifestations: dyspnoea, pallor, tachycardia, anxiety and fear.
  • Atypical manifestations: indigestion, nausea, vomiting, upper back pain.
  • Precipitating factors: exercise or activity, strong emotion, stress, cold, heavy meal.
  • Relieving factors: rest, position change; glyceryl trinitrate.
107
Q

Manifestations of acute myocardial infarction (AMI)?

A

■ chest pain: substernal or precordial (across the entire chest wall); may radiate to neck, jaw, shoulder(s) or left arm
Dyspnoea, shortness of breath

■ Nausea and vomiting
■ anxiety, sense of impending doom Diaphoresis
■ tachypnoea, tachycardia
■ cool, mottled skin; diminished peripheral pulses

■ hypotension or hypertension

■ palpitations, arrhythmias Signs of left heart failure
■ Decreased level of consciousness

108
Q

Key drug groups affecting cardiac function

A

◆ Antidysrhythmic drugs: adenosine, amiodarone, disopyramide, flecainide, lidocaine (lignocaine), sotalol
◆ Cardiac glycoside: digoxin
◆ Neprilysin/angiotensin (AT1) receptor inhibitor: sacubitril/valsartan
◆ Phosphodiesterase inhibitor: milrinone
◆ Selective If channel inhibitor: ivabradine

109
Q

What are the 5 phases of depolarisation/repolarisation?

A

◆ Phase 0 - depolarisation (the upstroke) of the action potential. Within a few milliseconds, the sodium channels close and are unavailable for initiation of another action potential until repolarisation has occurred.
◆ In phase 1 a partial repolarisation occurs due to inactivation of the sodium current.
◆ Phase 2 is the plateau phase that is prominent in ventricular muscle and results from a slow inward current of calcium ions via L-type voltage-sensitive calcium channels and a small outward flow of potassium ions. Calcium ion entry into the cell is essential for the excitation-contraction coupling mechanism.
◆ Phase 3 results from rapid potassium ion efflux from the cell via voltage-gated potassium channels. As more potassium leaves the cell and less calcium enters during this phase, the membrane potential reverts to −90 mV.
◆ After repolarisation phase 4, a resting period ensues during which the cell membrane actively transports sodium ions out and potassium ions in, against their concentration gradients.

110
Q

Most common forms of dysrhythmia?

A

Bradydysrhythmias

  • Atrioventricular block
  • Sick sinus syndrome

Atrial tachydysrhythmias

  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardia

Ventricular tachydysrhythmias

  • Premature ventricular ectopics
  • Ventricular tachycardia
  • Torsades de pointes
111
Q

What do class 1a antidysrhythmic drugs (eg disopyramide) do?

A
  • sodium channel blocker

↓ rate of depolarisation

↓ AV conduction

↓ contractility

↑ action potential duration

↑ effective refractory period

112
Q

What do class 1b antidysrhythmic drugs (eg lidocaine) do?

A
  • sodium channel blocker

↓ rate of depolarisation

↓ action potential duration

↑ effective refractory period

113
Q

What do class 1c antidysrhythmic drugs (eg flecainide) do?

A
  • sodium channel blocker

↓ rate of depolarisation

↓ AV conduction

↓ contractility

114
Q

What do Class IV antidysrhythmic drugs (eg verapamil, diltiazem) do?

A
  • Calcium channel blockers

↓ action potential duration

↓ AV conduction

↓ contractility

115
Q

What do Class III antidysrhythmic drugs (eg amiodarone, sotalol) do?

A
  • potassium channel blockers

↑ action potential duration

↑ effective refractory period

↓ AV conduction

↓ Contractility (sotalol)

116
Q

What do Class II antidysrhythmic drugs (β-adrenoceptor antagonists) do?

A

↓ AV conduction

↓ contractility

117
Q

Key drug groups affecting vascular smooth muscle?

A

◆ Aldosterone receptor antagonists: eplerenone, spironolactone
◆ Angiotensin-converting enzyme (ACE) inhibitors: captopril, enalapril, fosinopril, lisinopril, perindopril, quinapril, ramipril, trandolapril
◆ Angiotensin-receptor (AT1) antagonists (also called angiotensin-receptor blockers [ARBs]): candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan, valsartan
◆ Calcium channel blockers: amlodipine, clevidipine, diltiazem, felodipine, lercanidipine, nifedipine, nimodipine, verapamil
◆ Centrally acting adrenergic inhibitors: clonidine, methyldopa, moxonidine
◆ Drugs for peripheral vascular disease: cilostazol, pentoxifylline (oxpentifylline), oxerutins (hydroxyethylrutosides)
◆ Nitrates: glyceryl trinitrate
◆ Potassium channel activators: diazoxide, minoxidil, nicorandil

118
Q

Three main direct-acting vasodilators

A

✛ nitrates
✛ calcium channel blockers
✛ potassium channel activators.

119
Q

4 main indirect-acting vasodilators

A

✛ centrally acting adrenergic inhibitors
✛ angiotensin-converting enzyme (ACE) inhibitors
✛ angiotensin (AT1) receptor antagonists (also called angiotensin-receptor blockers, or ARBs)
✛ aldosterone receptor antagonists.

120
Q

Key drug groups for lipid-lowering drugs

A

◆ Bile acid-binding resins: colestyramine (cholestyramine), colestipol
◆ Fibrates: fenofibrate, gemfibrozil
◆ HMG-CoA reductase inhibitors (commonly known as statins): atorvastatin (DM 22.1), fluvastatin, pravastatin, rosuvastatin, simvastatin
◆ PCSK9 inhibitors: alirocumab, evolocumab (DM 22.2)
◆ Additional drugs: ezetimibe, nicotinic acid

121
Q

Indications for Atorvastatin

A

treatment of hypercholesterolaemia and mixed hyperlipidaemia

122
Q

Contraindications for atorvastatin

A

◆ where there is a condition of preexisting liver disease
◆ in women of childbearing age unless adequate contraceptive cover is assured (Pregnancy Safety Category D)
◆ in people with severe intercurrent illness (infection, trauma).

123
Q

Common adverse reactions for atorvastatin

A 
◆ GIT discomfort, headaches, insomnia and dizziness
◆ an elevation of hepatic transaminase levels within the first few weeks of treatment (dose-related, start at lower end of the dosage range).
◆ development of myopathy, which can progress to rhabdomyolysis and renal failure. The latter is more likely when the statins are combined with inhibitors of CYP3A4, but an increased incidence has also been observed in combination with the fibrate class of lipid-lowering drugs and nicotinic acid.
124
Q

Most common fetal/paediatric congenital heart diseases?

A
  • ventricular septal defect
  • atrial septal defect
  • patent ductus arteriosus (bypass of pulmonary circulation in utero doesn’t close after birth)
  • Tetralogy of Fallot - overriding aorta, pulmonary stenosis, right ventricular hypertrophy, ventricular septal defect
125
Q

Common noninvasive cardiac diagnostic testing procedures used to diagnose coronary heart disease

A
  • transthoracic echocardiography
  • stress testing (exercise, pharmacological, and nuclear)
  • multidetector computed tomography
  • coronary artery calcium scoring (with electron beam computed tomography
  • or computed tomographic angiography)
  • cardiac magnetic resonance imaging
126
Q

Drugs used for pharmaceutical stress-testing.

A
  • Adenosine
  • Dipyridamole
  • Dobutamine
  • Regadenoson

Complexities of Health and Illness (5 decks)

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