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Medical Studies 1 > Week 2 Cardiovascular > Flashcards

Week 2 Cardiovascular Flashcards

1
Q

define stable coronary artery disease

A

a pathological process characterised by atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or non obstructive

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2
Q

list the symptoms of angina

A

chest pain
radiating pain to left jaw
dyspnoea
sweating
fatigue
syncope
anxiety

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3
Q

explain chest pain as a symptom of angina

A

reduced blood flow to the heart muscle due to coronary artery stenosis, leading to ischemia

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4
Q

explain radiating pain to left jaw as a symptom of angina

A

referred pain due to the convergence of sensory nerve fibres in the spinal chord (commonly seen in myocardial ischemia)

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5
Q

explain dyspnoea as a symptom of angina

A

decreased oxygen supply to the heart results in inadequate pumping capacity, reducing oxygen delivery to body tissues, including the lungs

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6
Q

explain sweating as a symptom of angina

A

the body’s sympathetic response to ischemia often accompanied by an adrenaline release

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7
Q

explain fatigue as a symptom of angina

A

reduced oxygen delivery to the heart muscle, leading to reduced CO and loss of consciousness

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8
Q

explain syncope as a symptom of angina

A

severe ischemia can cause a sudden drop in CO, leading to loss of consciousness

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9
Q

explain anxiety as a symptom of angina

A

psychological and physiological reaction to chest pain and fear of cardiac events

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10
Q

Describe how a mismatch between oxygen supply and demand arises

A

-when an obstruction in the coronary artery occurs, this prevents perfusion, creating a supply demand mismatch, heart can’t receive enough oxygen, leading to ischemia and possible angina
-mild to moderate stenosis due to atherosclerosis is clinically inconsequential
-fixed vessel narrowing over a prolonged period of time can lead to pressure drop and limited vessel flow

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11
Q

what factors impact the haemodynamic significance of stenotic lesions

A

-extent of stenosis
-degree of compensatory vasodilation
-myocardial oxygen demand

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12
Q

describe how the extent of stenosis can impact stenotic lesions

A

greater stenosis, means greater narrowing of coronary artery and reduced blood flow to the heart

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13
Q

describe how the degree of compensatory vasodilation can impact stenotic lesions

A

reflects the ability of the heart to self-regulate blood flow by widening smaller vessels, compensating for reduced flow due to stenosis

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14
Q

describe how myocardial oxygen demand impacts stenotic lesions

A

determines the stress placed on the heart, with increased demand potentially exacerbating the impact of coronary artery stenosis (by increasing mismatch)

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15
Q

describe the process of anaerobic metabolism in cardiac myocytes during ishcemia and how this process can lead to the accumulation of metabolic by-products and lead to dyspnoea

A

-myocardial ischemia causes cardiomyocytes to with from oxygen dependent (aerobic) to oxygen-absent (anaerobic) metabolism
-anaerobic metabolism produces more lactic acid and lowers cellular pH, impairing cardiomyocytes function
-damaged cardiomyocytes impair myocardial relaxation and cause decreased left ventricular contractility and cardiac output
-blood backs up into LV and LA and pulmonary vessels
-increased pulmonary capillary pressures pushed fluid into alveoli
-decreased gas exchange (dyspnoea)

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16
Q

describe how myocardial ischemia can lead to stimulation of pain pathways

A

-myocardial ischemia causes cardiomyocytes to with from oxygen dependent (aerobic) to oxygen-absent (anaerobic) metabolism
-anaerobic metabolism produces metabolites that stimulates cardiac spinal afferent nerves
-myocardial visceral afferent and somatic sensory nerve fibres mix and enter spinal cord via T1-T4 nerve roots
-brain interprets increased nerve signalling as pain coming from skin T1-T4 dermatomes (referred pain)

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17
Q

cardiac chest pain is usually related to which dermatomes

A

C3 to T5

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18
Q

C3-C4 dermatome is relevant to

A

neck and upper shoulder pain

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19
Q

C5-T1 dermatome is relevant to

A

upper chest, shoulder and back pain

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20
Q

what is acute coronary syndrome

A

used to describe suspicion or confirmation of acute MI

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21
Q

what are the main types of acute coronary syndrome

A

-ST-elevation myocardial infarction (STEMI)
-non-St-elevation MI
-Unstable angina

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22
Q

describe how spontaneous coronary artery dissection leads to acute coronary syndrome

A

sudden tearing of the layers in a coronary artery wall, often leading to a blockage

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23
Q

describe how coronary artery spasm can lead to acute coronary syndrome

A

temporary constriction of a coronary artery, restricting blood flow to the heart

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24
Q

describe how coronary microvascular dysfunction can lead to acute coronary syndrome

A

impaired function of the small blood vessels in the heart, affecting blood supply to the heart muscle

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25
describe how MI with non obstructed coronary arteries can lead to acute coronary syndrome
a heart attack (MI) that occurs with no visible blockages in the major coronary arteries
26
describe how atherosclerosis can lead to acute coronary syndrome
progressive build up of plaque in the arteries, narrowing blood vessels and reducing blood flow
27
what is a STEMI
ST-elevated myocardial infarction; severe heart attack with ST segment elevation on the ECG, indicating complete coronary artery blockage
28
what is an NSTEMI
non-ST elevated myocardial infarction, partial heart attack with no ST segment elevation, indicating partial coronary artery blockage
29
what is stable angina
chest pain or discomfort during physical exertion. typically relieved by rest or medication
30
what is unstable angina
chest pain or discomfort caused by reduced blood flow to the heart, often a precursor to a heart attack (MI)
31
what is a patient history used to diagnose in terms of coronary conditions
used to diagnose stable angina
32
what is serum troponin used to diagnose in terms of coronary conditions
is used to diagnose unstable angina (non exertional pain without marked elevation or troponin) serum troponin elevation indicates a STEMI or NSTEMI
33
what is ECG used to diagnose in terms of coronary conditions
Is used to distinguish between STEMI (ST elevation) and NSTEMI (ST depression/T wave inversion)
34
PLOT RADIO for ACS
crushing pain radiating to left shoulder/jaw onset at rest/exertion not exacerbated
35
PLOT RADIO for stable angina
crushing pain radiating to left shoulder/jaw onset at exertion not exacerbated
36
PLOT RADIO for aortic dissection
tearing pain radiating to back/shoulder onset at rest/exertion not exacerbated
37
PLOT RADIO for pericarditis
sharp pain nil radiation onset at rest/exertion exacerbated by deep breathing
38
PLOT RADIO for Pulmonary embolism
pleuritic pain radiating to back/shoulder onset at rest/exertion exacerbated by inspiration
39
PLOT RADIO for pneumothorax
pleuritic pain nil radiation onset at rest/exertion exacerbated by inspiration
40
PLOT RADIO for pneumonia
pleuritic pain radiates to back/shoulder onset at rest/exertion exacerbated by deep breathing
41
PLOT RADIO for GORD
burning pain radiating up oesophagus onset at rest/exertion exacerbated supine or eating
42
how does claudication occur in CVD
-atherosclerotic plaques in the peripheral arteries which causes stenosis and reduced blood flow to the muscle during exercise (increased oxygen demand) -the disruption in oxygen supply leads to ischemia -lactic acid produced -leading to pain *intermittent nature refers to temporary relief when at rest
43
identify the ways that we can investigate a suspected acute coronary syndrome
ECG serum troponin Angiography
44
describe ECG use as investigation for ACS
device that measures electrical activity of the heart, can be used to identify abnormal activity (STEMI, NSTEMI)
45
describe serum troponin as investigation for ACS
cardiac enzyme that is over produced during myocardial damage, indicative of MI
46
Describe angiography as investigation for ACS
imaging modality that enables visualisation of blood vessels, can allow for observation of occlusions
47
Explain the importance of early intervention in management of acute coronary syndrome
-time is directly related to the extent of MI, the earlier intervention the better the outcomes/survival rate
48
what are the interventions for ACS
thrombolysis and PCI/angioplasty
49
Describe the use of PCI/angioplasty
Percutaneous coronary intervention; a catheter with a deflated balloon at its tip is inserted into narrowed artery, balloon is inflated to compress the plaque and widen the vessel, stent is often placed to decrease risk of re-narrowing
50
describe the use of thrombolytics
-medical treatment that involves the administration of medication (thrombolytic agents) to dissolve blood clots within the body -particularly used in STEMI
51
which leads correspond to the lateral surface of the heart
I, aVL, V5, V6
52
which leads correspond to the inferior surface of the heart
II,III,aVF
53
which leads correspond to the anterior surface of the heart
V3,V4
54
which leads correspond to the septal surface of the heart
V1,V2
55
ECG findings of unstable angina
ST segment depression, T wave inversion
56
ECG findings for NSTEMI
ST segment depression, T wave inversion
57
ECG findings for STEMI
ST segment elevation
58
how do troponin levels change for various ACS
unstable angina has normal troponin NSTEMI and STEMi can have a rise/fall in troponin
59
Whats a TIMI score
tool used to assess the risk of adverse outcomes in patients with UA or (NSTEMI) in the next 14 days
60
list the criteria in TIMI score | America
age risk factors ASA (aspirin) prior stenosis angina ST-depression cardiac markers (each worth one point)
61
how is age assessed in TIMI
individuals over the age of 65 are at high risk
62
how are risk factors assessed for TIMI
presence of at least three additional risk factors for CAD (HTN,diabetes,smoking,hyperlipidaemia,hypercholesterolaemia,FHx,obesity)
63
how is ASA use assessed in TIMI
use of aspirin in last seven days
64
how is prior stenosis assessed in TIMI
checking for the presence of severe angina in last 24 hours
65
how is ST depression assessed in TIMI
presence of ST segment deviation on ECG
66
how are cardiac markers assessed in TIMI
checking for elevated levels of cardiac markers (troponin)
67
describe the primary management of an ACS
-admit to hospital -12 lead ECG (diagnose STEMI vs NSTEMI/UA) -reperfusion (<90m means angioplasty, <30m means thrombolytics) -administer MONA -echocardiogram, chest x ray, cardiac enzyme test -discharge
68
list the secondary management of ACS
dual anti platelet therapy statins ACE inhibitors Beta-blockers lifestyle changes cardiologist referral TASS (thrombolytics, asprin, stool softeners and sedatives)
69
how many MI's are repeat events
30%
70
describe dual anti-platelet therapy for secondary ACS management
medical treatment involving the use of two antiplatelet medications, administer for at least 12 months post MI
71
describe statins use for secondary ACS management
drug used to lower cholesterol, stabilise plaque and reduce inflammation, administered post MI irrespective of initial baseline cholesterol
72
describe ACE inhibitor use for secondary ACS management
anti-hypertensive agents that reduce BP post MI
73
describe beta blocker use for secondary ACS management
negative inotropic effect, reduces workload on heart post MI
74
describe lifestyle change implementation for secondary ACS management
smoking and alcohol cessation healthy diets exercise
75
describe cardiologist referral for secondary ACS management
consistent monitoring of symptoms, bloods and lipids over time
76
whats MONA
morphine, oxygen, nitroglycerin, aspirin
77
whats TASS
thrombolytics, anticoagulants, stool softeners, sedatives
78
location of the precordial leads
V1 Fourth intercostal space, right of sternum V2 Fourth intercostal space, left of sternum V3 Halfway between V2 and V4 V4 Fifth intercostal space, midclavicular line V5 Fifth intercostal space, anterior axillary line V6 Fifth intercostal space, midaxillary line *all on left expect V1
79
how many types of myocardial infarction is there
5 types SIDPC | sudden/imbalance/death/PCI/CABG
80
describe type one MI
Mi due to plaque disruption, fissure, erosion, rupture, dissection
81
describe type two MI
Mi due to oxygen supply/demand mismatch; respiratory failure, emboli
82
describe type three Mi
ischemia without biomarkers available, sudden cardiac death
83
describe type four Mi
associated with PCI; during operation or stent thrombosis
84
describe type five MI
myocardial infarction associated with cardiac surgery (CABG)
85
list the non atherosclerotic conditions that can cause MI
artery dissection coronary artery spasm myocarditis embolism
86
describe artery dissection
tear in the coronary artery wall leading to reduced blood flow to the heart
87
describe coronary artery spasm
sudden, temporary constriction of a coronary artery, reducing blood flow
88
describe myocarditis
inflammation of the heart muscle, which can lead to MI
89
describe embolism
blockage of a coronary artery by a non-atherosclerotic embolus, often originating from an external source
90
list the causes of type 2 MI
anaemia coronary artery spasm hypotension hypoxia
91
how does anaemia lead to MI
a low red blood cell count can reduce the oxygen carrying capacity of the blood (lowered Hb levels), leading to ischaemia and possible MI
92
how does coronary artery spasm lead to MI
sudden temporary vasoconstriction of a CA, reducing blood flow to the heart
93
how does hypotension lead to MI
low BP can result in inadequate blood flow to the coronary arteries, causing oxygen deprivation to the heart
94
how does hypoxia lead to MI
insufficient oxygen in the blood, often due to respiratory problems or lung disease, can lead to oxygen deprivation to the heart
95
list the causes of coronary artery spasm
smoking, drugs and endothelial dysfunction
96
symptoms of coronary artery spasm
chest pain dyspnoea tachycardia palpitations syncope jaw/shoulder pain
97
list modifiable risk factors for atherosclerosis
smoking, physical inactivity, diet
98
how is smoking linked to atherosclerosis
tobacco use damages blood vessels and promotes inflammation, accelerating atherosclerosis formation
99
how is physical inactivity linked to the atherosclerosis
a sedentary lifestyle can increase the risk of atherosclerosis due to increased weight gain and reduced cardiovascular fitness
100
how is diet linked to atherosclerosis
poor dietary choices high in saturated fats can contribute to plaque build up in arteries
101
list the non modifiable risk factors for atherosclerosis
age family history biological sex
102
how is age linked to atherosclerosis
atherosclerosis risk increases with age as arterial damage accumulates over time
103
how is family history linked to atherosclerosis
family history of atherosclerosis and related conditions can increase susceptibility
104
how is biological sex linked to atherosclerosis
men tend to have higher risk of atherosclerosis compared to premenopausal women; however, the risk even outs post menopause
105
Describe the role of hyperlipidaemia and hyopercholesterolaemia in the development of atherosclerosis
-when LDL's are high, they can infiltrate artery walls -LDL's become oxidised-->inflammation -WBC's recruited, which phagocytose LDL's-->foam cells -foam cells contribute to atherosclerotic plaques -as plaques grow-->harden and narrow arteries -stenosis restricts blood flow
106
Outline how fibre intake reduces coronary heart disease risk
-GI action: soluble fibre such as beta-glucans and pectin, bind to cholesterol in the digestive tract and help eliminate it from the body, lowering LDL cholesterol -Sugar absorption:fibre slows down the absorption off sugar, promoting stable blood sugar levels and reducing diabetic risk
107
how do plant sterols and stanols work
Plant sterols and stanols compete with cholesterol for absorption in the intestines. They reduce the amount of cholesterol absorbed into the bloodstream.
108
list the benefits of plant sterols and stanols
reduced LDL levels no side effects convenient
109
describe reduced LDL levels as a benefit of plant sterols and stanols
-primary benefit, consuming foods with these compounds can significantly lower LDL levels
110
describe no side effects as a benefit of plant sterols and stanols
-unlike cholesterol lowering medications, plant sterols and stanols are generally-well tolerated and have no significant risks
111
describe convenience as a benefit of plant sterols and stanols
fortified foods, such as markantes, spreads and certain dairy products provide a convenient way to incorporate plant sterols and stanols into daily diet without supplements
112
Outline the links between dietary sodium, salt and hypertension
consuming high levels of dietary sodium can lead to increased BP as sodium attract water within the nephron, causing the body to retain more fluid which increases fluid retention
113
Outline DASH diet
-Fruits and vegetables which have essential nutrients + lower BP -Whole grains (brown rice, oats) which provide sustained energy and additional fibre to diet
114
Outline mediterranean diet
-plant based foods:rich in fruits, veg,whole grain, legumes which provide essential vitamins, minerals, fibres and antioxidants -healthy fats: olive oil (high in monounsaturated fats) and fatty fish (omega acids) aid heart health -moderate dairy (yoghurt and cheese) provide source of calcium and protein with less fat
115
Outline Australian dietary guidelines
emphasize the importance of a balanced diet that includes a variety of nutritious foods, while limiting unhealthy fats, added sugars, and salt. They also highlight the importance of physical activity, breastfeeding, and safe food practices.
116
what is peripheral arterial disease
atherosclerotic affection of the peripheral arterial tree
117
what are the signs/symptoms of peripheral arterial disease
claudication HTN arcus cornealis tar staining
118
identify the pathology of asymptomatic PAD
atherosclerotic plaque-->arterial stenosis--> collateral blood supply--> asymptomatic PAD
119
identify the pathology of symptomatic PAD
atherosclerotic plaque-->arterial stenosis-->reduced peripheral perfusion-->peripheral arterial ischemia-->claudication and other symptoms
120
what is cerebrovascular atherosclerosis
atherosclerosis of the arteries that supply the brain
121
symptoms and signs of cerebrovascular atherosclerosis
unilateral weakness confusion unilateral vision loss hemi-negligence dysphasia dizziness/syncope
122
explain the mechanism of production of calf pain during walking
atherosclerotic plaque formation-->arterial stenosis-->collateral blood supply-->further stenosis-->reduced peripheral perfusion (increased O2 demand)-->insufficient person-->ischemia-->build up of metabolites-->intermittent claudication
123
List the pharmacological options for PAD/cerebrovascular atherosclerosis
Dual antiplatelet therapy Statin therapy ACE inhibitor
124
how does dual anti platelet therapy work for PAD/cerebrovascular atherosclerosis
reduces the risk of blood clot formation in narrowed arteries, important in preventing thrombotic complications
125
how does stain therapy work for PAD/cerebrovascular atherosclerosis
lowers LDL cholesterol levels, managing a key risk factor for atherosclerotic progression in PAD
126
how does ACE inhibitor work for PAD/cerebrovascular atherosclerosis
helps control BP and reduces the risk of cardiovascular complications in patients with PAD
127
list the non pharmacological options for PAD/cerebrovascular atherosclerosis treatment
smoking cessation dietary modifications regular exercise
128
how does smoking cessation aid PAD/cerebrovascular atherosclerosis
vital for PAD management, quitting smoking reduces the risk of disease progression and improves blood flow by eliminating a major contributor to arterial damage
129
how does dietary modification aid PAD/cerebrovascular atherosclerosis
a heart-healthy diet lowers cholesterol and blood pressure, reducing the risk of PAD complications and helps maintain overall vascular health
130
how does regular exercise aid PAD/cerebrovascular atherosclerosis
chances walking distance and alleviated claudication symptoms by improving muscle oxygenation, overall CV health and arterial function
131
ECG for UA
-can be normal -can have ST depression -can have T wave inversion
132
ECG for NSTEMI
-has ST depression -can have T wave inversion
133
ECG for STEMI
-St elevation -can have T wave inversion
134
what leads do you look at for ECG axis assessment
lead 1 and Lead aVF
135
positive lead 1 and positive lead aVF =
normal axis
136
positive lead 1 and negative lead aVF =
left axis deviation
137
negative lead 1 and positive lead aVF =
right axis deviation
138
negative lead 1 and negative lead aVF =
extreme axis

Medical Studies 1 (15 decks)

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