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Year 2 Medicine @ Lancaster Uni > 2.01 - Heart conditions and CHD 🫀 > Flashcards

2.01 - Heart conditions and CHD 🫀 Flashcards

1
Q

What is starlings law of contractility?

A

The relationship between velocity of contraction and the pre-loading of cardiac muscle

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2
Q

What does a higher pre-load lead to?

A

A higher force of contraction

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3
Q

Why is the relationship between force and velocity of contraction?

A

Helps the heart to adapt its pumping strength

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4
Q

What are the features of cardiac muscle?

Structural features

A
  • Shorter length and less circular
  • Show branching
  • Contain central nuclei
  • Connected by intercalated discs
  • Discs contain desmosomes which allow propagation
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5
Q

What is the pathway of an action potential?

5 steps

A
  1. SA node - pacemaker potential
  2. AV node - Provides delay for filling
  3. AV bundle - Potential from atria to ventricles
  4. Right/Left bundle branches
  5. Purkinje fibres - Begin at apex and move upwards
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6
Q

What is the function of an ECG?

A

Allows the electrical activity of the heart to be observed

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7
Q

What does a P wave show on an ECG?

A

P = Atrial depolarisation

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8
Q

What does the presence of a P-wave prove?

A

Sinus rhythm

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9
Q

What does the PR period show?

A
  • The time between the P wave and QRS complex
  • Allows for filling
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10
Q

What does the QRS complex show?

A

Ventricular depolarisation

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11
Q

What does the ST interval show?

A
  • The period between QRS and T wave
  • Should be flat
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12
Q

What does the T wave show on an ECG?

A

Ventricular repolarisation

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13
Q

Where are the limb leads placed?

A
  • Red = Right arm
  • Yellow = Left arm
  • Black = Right Leg
  • Green = Left leg
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14
Q

Where are the chest leads placed on an ECG?

A

V1 = 4th ICS, right of sternum
V2 = 4th ICS, left of sternum
V3 = Midway between V2 and V4
V4 = 5th ICS, mid-clavicular line
V5 = 5th ICS, anterior axillary
V6 = 5th ICS, mid-axillary

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15
Q

Which leads look at the lateral aspect of the heart?

A

I, AVL, V5, V6

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16
Q

Which leads look at the inferior aspect of the heart?

A

II, III, AVF

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17
Q

Which leads look at the posterior/septal aspect of the heart?

A

V1, V2

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18
Q

Which leads look at the anterior aspect of the heart?

A

V3, V4

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19
Q

Where is the aortic valve ausculated on the chest?

A

2nd ICS on the right

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20
Q

Where is the pulmonary valve ausculated on the chest?

A

2nd ICS on the left

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21
Q

Where is the tricuspid valve auscultated on the chest?

A

4th ICS, primarily on the left

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22
Q

Where is the mitral valve auscultated on the chest?

A
  • Apex of the heart
  • 5th ICS mid-clavicular
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23
Q

What are the two main arteries that supply the heart?

A
  • LCA
  • RCA
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24
Q

What are the branches of the LCA?

A
  • LAD (AIVA)
  • LMA
  • LCxA
  • Also PIVA in 20% of people
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25
Q

What are the branches of the RCA?

A
  • RMA
  • Also PIVA in 80% of people
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26
Q

What does the RCA supply?

A
  • Right Atrium
  • Right ventricle
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27
Q

What does the RMA supply?

A

Supplies the right ventricle and the apex of the heart

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28
Q

What does the LAD (AIVA) supply?

A

Supplies the left and right ventricles and the IV septum

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29
Q

What does the LCxA supply?

A

Supplies the left atrium and left ventricle

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30
Q

What does the left marginal artery supply?

A

Supplies the left ventricle

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31
Q

What does the PIVA supply?

A

Supplies the left and right ventricle as well as the IV septum

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32
Q

Where does the majority of the drainage of the heart take place?

A

Coronary sinus

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33
Q

What are the main tributaries to the cardiac sinus?

A
  • Great cardiac vein
  • Small cardiac vein
  • Middle cardiac vein (Posterior IV vein)
  • Posterior cardaic vein
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34
Q

Where does the RCA venously drain?

A
  • Small cardiac vein
  • Middle cardiac vein
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35
Q

Where does the RMA venously drain?

A
  • Small cardiac vein
  • Middle cardiac vein
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36
Q

Where does the PIVA venously drain?

A
  • Left posterior IV vein
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37
Q

Where does the LCA venously drain?

A
  • Great cardiac vein
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38
Q

Where does the LAD venously drain?

A
  • Great cardiac vein
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39
Q

Where does the LMA venously drain?

A
  • Left marginal vein
  • Great cardiac vein
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40
Q

Where does the CxA venously drain?

A
  • Great cardiac vein
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41
Q

Where can S1 heart sounds be best heard?

A

Apex of heart

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42
Q

Where can S2 heart sounds be best heard?

A

Left 2nd ICS

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43
Q

What is the defintion of athersclerosis?

A
  • Progressive disease seen by formation of sizeable plaques within arteries
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44
Q

What is the function of LDL’s?

A

Promote atherosclerosis formation (Not good)

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45
Q

What is the function of HDL’s?

A

Try to remove excess cholesterol from the blood (Good fats)

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46
Q

What can be a complication that arises from athersclerotic plaque formation?

A
  • Artery stenosis
  • Thromboembolic events
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47
Q

Is athersclerosis usually symptomatic or asymptomatic?

A

Usually asymptomatic, until cap breaks off plaque

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48
Q

What cells within a plaque can cause the cap to break off?

A

Foam cells

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49
Q

What is ACS?

A
  • Acute coronary syndrome
  • Sudden or severe reduction in blood flow through the coronary arteries
  • Often caused by clot or plaque rupture which lodges in artery
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50
Q

What is the defintion of CHD?

A
  • Coronary heart disease
  • Disease caused by occlusion of the coronary arteries which can lead to ischaemia of heart tissues
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51
Q

What is the epidemiology of CHD?

A
  • Most common cause of death in the UK
  • 2.3 million in the UK living with CHD
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52
Q

What trend is being seen in mortality/morbidity in relation to CHD?

A
  • Decreased mortality
  • Increased morbidity
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53
Q

What are the clinical features of CHD?

A
  • Angina
  • Palpitations
  • Sweating
  • Nausea
  • SOB
  • Dizziness
  • Tachycardia
  • Weakness
  • Tiredness
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54
Q

What are the main contributors to the development of CHD?

A
  • Increasing age
  • Gender (Being male)
  • Social deprivation
  • Smoking
  • Ethnicity
  • Poor nutrition
  • Lack of exercise
  • Excess alcohol
  • Physcosocial wellbeing
  • Obesity and Diabetes
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55
Q

What is the management of CHD in those with no previous cardiac events?

A
  • If QRISK > 10% = Statin
  • NICE -> 20mg Atorvastatin at night
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56
Q

What is the management of CHD in those with a history of cardiac events?

AAAA

A

A - Aspirin + 2nd antiplatlet such as clopidogrel
A - Atorvastatin - 80mg
A - Atenolol - Max tolerated dose (Or other beta blocker
A - ACEi - Max tolerated dose, Eg. Ramipril

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57
Q

What tests do the NICE guidelines recommend in those with CHD?

A

Lipids and LFT’s after 3 months

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58
Q

What is the pathophysiology surrounding CHD?

A
  • Occurs as a result of progressive artery occlusion which leads to clinically significant stenosis
  • An increase in myocardial oxygen demand leads to ischaemia
  • Develops as a result of atherosclerotic plaque formation
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59
Q

What investigations are needed to help diagnose CHD?

A
  • ECG
  • FBC
  • CRP
  • ESR
  • Angiography
  • BP
  • Exercise stress tests
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60
Q

What is the genetic impact on the development of CHD?

A
  • More likely if parents have CHD
  • Several regions of genome associated with CHD
  • Genetic predisposition is thought to exist
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61
Q

What is the definition of heart failure?

A
  • When cardiac output is inadequate for the metabolic requirements of the body.
  • Can be systolic, diastolic, LVF, RVF, AHF/CHF, HOHF, LOHF
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62
Q

What is the epidemiology around heart failure?

A
  • Between 1% - 3% of general population
  • Roughly 10% are elderly patients
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63
Q

What clinical signs are associated with HF?

A
  • Cyanosis
  • Oedema
  • Narrow pulse pressure
  • Reduced BP
  • RV heave
  • Displaced apex beat
  • Valvular diseases
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64
Q

What cardiac conditions can lead to the development of HF?

A
  • Reduced contractility
  • Increased afterload
  • Increased preload
  • Restricted filling
  • Arrhythmias
  • Persistent high output states
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65
Q

What is acute HF classified as?

A

A medical emergency

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66
Q

How is acute HF managed pharmacologically?

A
  1. Diuretics
  2. ACEi
  3. Beta blockers
  4. Spironolactone
  5. Digoxin
  6. Vasodilators
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67
Q

What is the pathophysiological process that leads to HF development?

A
  • HF -> Drop in MAP
  • This leads to an increase in sympathetic tone
  • SNS -> vasoconstriction and adrenaline release
  • Eventually leads to a maintained high CO
  • This overtime leads to increased myocyte damage which starts the process again
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68
Q

What investigations are needed when diagnosing HF?

A
  • ECG
  • FBC
  • U&E
  • Chest XR
  • Echocardiography
  • BNP (B-type natiuretic peptide)
69
Q

Is there a genetic component to the development of HF?

A
  • Congestive heart failure can be passed on between generations of the same family
  • HTN, Diabetes etc. all contribute and these conditions are hereditary.
70
Q

Define Angina

A
  • Symptomatic, reversible cardiac ischaemia
  • Often produced due to exertion
71
Q

What are the different types of angina?

A

Stable - On exertion
Unstable - At rest, longer, more painful
Variant - Unpredictable, often at night
Decubtis Angina - Occurs when lying down

72
Q

What is the epidemiology surrounding angina?

A
  • Prevalence increases with age
  • Increased incidence in men
  • 3% of men in the US
73
Q

What are the clinical features relating to angina?

A
  • Heavy/tight retrosternal pain
  • Pain occurs with stress, cold weather, exercise etc
  • Pain relieved by resting or within 5 mins by GTN spray
74
Q

What is the most common cause of angina?

A
  • An atheroma caused by CHD (Build of cholesterol that leads to partial occulusion)
75
Q

What are some other causes of angina?

A
  • Anaemia
  • Aortic stenosis
  • Coronary artery spasm
  • Arteritis
  • Tachyarrythmias
76
Q

What are the non-pharmacological management options for angina?

A
  • Address lifetsyle factors such as smoking and excess alcohol intake
77
Q

What is the first line management of angina that should be given as soon as possible?

A
  • GTN spray
  • Given sublingual 1-2 sprays
  • Form of a nitrate
78
Q

What are other pharmacological options for the treatment of angina other than GTN spray?

A
  • Beta blockers
  • CCB’s
  • Anti-anginal medications (Nitrates)
79
Q

What is the mechanism of action of GTN spray?

A
  • Relaxes smooth muscle cells in the vessel wall
  • Causes vasodilation
80
Q

What surgical interventions are available for those with angina?

A
  • Stent
  • CABG (Coronary artery bypass graft)
81
Q

What is the pathological process that leads to the development of angina?

A
  • Stenosis of artery which causes temporary cardiac ischaemia as muscle can’t get enough oxygen
  • Stenosis caused by atheroma
82
Q

What signs would be seen on an ECG that could indicate the presence of angina?

A
  • ST depression
  • Wave inversions
83
Q

What investigations should be undertaken in the diagnosis of angina?

A
  • ECG
  • Angiography
  • FBC
  • Exercise ECG
84
Q

Is there a genetic component to the development of angina?

A
  • Not an inherited condition
  • Higher chance if there is a strong family history as this can lead to more likely cardiac diseases
85
Q

What is a myocardial infarction?

A
  • Also known as a heart attack
  • Occurs when there is occlusion of coronary arteries which leads to necrosis of myocardial tissues
86
Q

What are the two types of MI that can occur?

A
  • NSTEMI - No ST elevation seen
  • STEMI - ST elevation seen
87
Q

What is the epidemiology surrounding MI’s?

A
  • 7/10 survive due to recent advancements in care and prevention
  • 100,000 admissions a year
  • Chance increases with age
88
Q

What are some some clinical signs seen in a MI?

A
  • Palpitations
  • Sweating
  • Pallor
  • Central, crushing chest pain that radiates
  • Tachy/Brady
  • Hypo/Hyper
  • Extra hear sounds
89
Q

What are some emotional triggers that can cause a MI?

A
  • Distress
  • Anxiety
  • Fear
90
Q

What is the aetiology of a MI?

A
  • Usually a manifestation of CHD
  • Occurs due to plaque disruption
90
Q

What is a condition that can mimic a MI?

A
  • Takotsubo Cardiomyopathy
  • Also known as broken heart syndrome
  • Left ventricle changes shape causing reduced blood flow
91
Q

What are some risk factors for the occurence of a MI?

A
  • Smoking
  • HTN
  • Diabetes
  • Hyperlipidaemia
  • Male sex
  • Sedentary lifestyle
  • Poor nutrition
  • Obesity
92
Q

What managment principle should be followed immediately if a MI is suspected?

A

MONA

93
Q

What is the M in MONA?

A
  • Morphine
  • Used for pain relief
94
Q

What is the O in MONA?

A
  • Oxygen
  • Given at a low flow rate initially but can be turned up accordingly
95
Q

What is the N in MONA?

A
  • Nitrates given in the form of GTN spray
  • Helps to cause vasodilation
96
Q

What is the A in MONA?

A
  • Aspirin
  • A blood-thinning medication to try and reduce atheroma size in the occluded vessel
97
Q

What are the surgical management options for somebody if they have had a MI?

A
  • Stent in the occluded vessel
  • CABG
98
Q

What is the pathological process surrounding a MI?

A
  • Caused by the total occlusion of an artery
  • Either caused by emboli, clots or a plaque
  • This leads in stenosis of the artery
  • Which can cause ischaemia or infarction
99
Q

What occurs in minimal stenosis of a coronary artery?

A
  • Unstable Angina
100
Q

What occurs in the severe occlusion of a coronary artery?

A
  • NSTEMI
101
Q

What occurs in the total occlusion of a coronary artery?

A
  • STEMI
102
Q

What is the most important investigation when an MI is suspected?

A
  • An ECG
103
Q

What ECG changes can be seen in a STEMI?

A
  • ST elevation
  • T waves
  • Newly present LBBB
104
Q

What ECG changes can be seen in a NSTEMI?

A
  • ST depression
  • T wave inversion
105
Q

What blood test is able to show whether a MI had occured?

A
  • Troponin
106
Q

When is troponin found in the blood?

A
  • It is a protein found in muscle
  • Released when this muscle is broken down or becomes ischaemic or infarcted
107
Q

What is measured in a troponin blood test

A
  • Troponin T
  • Troponin I
108
Q

What other investigations are important in the diagnosis of an MI?

A
  • CXR
  • FBC
  • CRP
  • U&E
109
Q

What is the genetic contribution to the occurence of an MI?

A
  • A predisposition to HTN/Obesity will increase risk
  • Strong family history of ACS can be indicative of a higher chance in subsequent generations
110
Q

What is the relationship between CHD and HF?

A
  • CHD can cause muscle weakness due to increased demand which can’t be delivered
  • This causes muscle weakness meaning the heart can no longer pump efficiently to meet the demands of the body
  • This is essentially heart failure
111
Q

What is long term management protocol for a STEMI?

A

BRATS

112
Q

What is the B in BRATS?

A
  • Bisoprolol
  • Beta blocker
  • Reduces renin release (Stops RAAS)
113
Q

What is the R in BRATS?

A
  • Ramipril
  • ACEi
  • Stops the conversion of angiotensinogen in angiotensin I
114
Q

What is the A in BRATS?

A
  • Aspirin
  • Blood thinner
  • Helps to reduce platelet aggregation and reduce plaque formation
115
Q

What is the T BRATS?

A
  • Ticagrelor
  • Anti-platelet
  • Given alongside aspirin
  • Prevents platelet aggregation (Binds to P2Y12)
116
Q

What is the S in BRATS?

A
  • Statin
  • Helps to reduce the levels of cholesterol in the blood
  • This helps to prevent future cardiac events and strokes
117
Q

What is the long term management protocol for a NSTEMI?

A

BATMAN

118
Q

What is the B in BATMAN?

A
  • Bisoprolol
  • Beta blocker
  • Reduces renin release (Stops RAAS)
119
Q

What is the A in BATMAN?

A
  • Aspirin
  • Blood thinner
  • Helps to reduce platelet aggregation and reduce plaque formation
120
Q

What is the T in BATMAN?

A

Ticagrelor
- Anti-platelet
- Given alongside aspirin
- Prevents platelet aggregation (Binds to P2Y12)

121
Q

What is the M in BATMAN?

A
  • Morphine
  • Opioid analgesic
  • Used for pain relief
122
Q

What is the A in BATMAN?

A
  • Anti-thrombotic agent
123
Q

What is the N in BATMAN?

A
  • Nitrates
  • In the form of GTN spray
  • Relaxes smooth muscle in vessels
  • Causes vasodilation
124
Q

What is the aim of stable angina treatment?

A
  • Relieve chest pain and discomfort
  • Prevent further exacerbations
125
Q

What is the first line management for stable angina?

A
  • GTN spray 1-2 sprays as required
  • Form of a nitrate
126
Q

What are the side effects of GTN spray?

A
  • Headaches
  • Hypotension
  • Generalised warmth
  • Light-headedness
127
Q

What are the contraindications of GTN spray?

A
  • Aortic/Mitral stenosis
  • Hypotension
  • Hypovolaemia
128
Q

What is an example of second/third line management option for angina?

A
  • Longer acting nitrates
  • Example: Isosorbide mononitrate
  • Help to control symptoms
129
Q

What is the NICE recommened second line treatment for stable angina?

A
  • Beta blockers
  • Calcium channel blockers
130
Q

What is the mechanism of action of beta blockers?

A
  • Block the mechansim of normal cardiac function by blocking beta receptors
131
Q

What are the effects of beta blockers?

4 down, 1 up

A
  • Decreased contraction speed
  • Decreased heart rate
  • Increased cardiac effciency
  • Decreased cardiac hypertrophy
  • Decreased renin excretion
132
Q

What are the adverse effects of beta blockers?

A
  • Bronchospasm
  • Hypotension
  • Bradycardia
  • Peripheral vasoconstriction
  • Unstable heart failure
133
Q

What are the contraindications of beta blockers?

A
  • Severe peripheral disease
  • Hypotension
  • Bradycardia
  • AV block
  • Asthma
134
Q

When should there be caution in the prescription of beta blockers?

A
  • COPD
  • Diabetes
135
Q

What is the mechanism of action of calcium channel blockers?

A
  • Blocks L-type calcium channels in smooth muscle cells which helps to inititae vasodilation
136
Q

Where do CCB’s act?

A
  • Heart
  • Vasculature
  • Other places
137
Q

What are the three types of CCB?

A
  1. Phenylalkylamine
  2. Benzothiazapine
  3. Dihydropyridine
138
Q

How do phenylalkylamines work?

A
  • Act selectively on the heart
  • Should NOT be used with a BB
  • Example: Verapamil
139
Q

How do benzothiazipines work?

A
  • Work on both the heart and blood vessels
  • Caution with a BB
  • Example: Diltiazem
140
Q

How do dihydropyridines work?

A
  • Work selectively on blood vessels
  • Fine to give alongside a BB
  • Example: Amlodopine
141
Q

Why should beta blockers and calcium channel blockers not be given concurrently?

A
  • Can cause fatal cardiac events
  • Severe heart block
  • Bradyarrhytmias
142
Q

What are the anatomical features of cardiac muscle?

A
  • Striated appearance
  • Branched cells
  • Single nucleus
  • Intercalated discs
143
Q

What are the functional features of cardiac muscle?

A
  • Automaticity
  • Rhythmicity
  • Excitation-contraction coupling
  • Long refractory period
144
Q

What are the metabolic features of cardiac muscle?

A
  • Rich blood supply
  • High mitochondrial density
  • Aerobic metabolism
145
Q

What is the main pharmacological management strategy for chest pain?

A

SLEW

146
Q

What is the S in SLEW?

A
  • Smoking cessation
147
Q

What is the L in SLEW?

A
  • Low fat diet (Low fat, low unsaturated fat)
148
Q

What is the E in SLEW?

A
  • Exercise
  • Reduces cholesterol, reduce BP
149
Q

What is the W in SLEW?

A
  • Weight loss
150
Q

What is the seen on an ECG trace showing AFib?

A
  • Irregular and rapid
  • Typically around 150 BPM
  • No p waves present
  • Irregular R-R intervals
  • Finrillatory waves
151
Q

What is the seen on an ECG trace showing ventricular tachycardia?

A
  • Unusual QRS shape resembling an S
  • Rapid heart rate
  • Wide QRS complexes
  • Electrical impulses orginate in ventricles
152
Q

What is the seen on an ECG trace showing VFib?

A
  • Lacks normal electrical activity (Rapid and erratic)
  • No effective cardiac output
  • Loss of consciousness
  • Absence of pulse
153
Q

What is the seen on an ECG trace showing atrial flutter?

A
  • When atria beat regularly but too fast
  • Atria contract out of time with the ventricles
  • Typically tachy with heart rates seen to be around 150-180 BPM
  • Saw-tooth pattern between complexes
154
Q

What is the seen on an ECG trace showing sinus tachycardia?

A
  • P waves are present
  • Heart rate faster than normal
  • Common response to execise or stress
  • Concerning at rest
  • Regular R-R intervals
155
Q

What is the seen on an ECG trace showing sinus bradycardia?

A
  • P waves are present
  • Heart rate slower than usual
  • Usually lower than 60 BPM
  • Oftern occurs at rest in athletes
156
Q

What are the two ways to calculate rate from an ECG?

A
  • 300/Big squares
  • Rhythm strip (10sec) x 6
157
Q

What are the values of large and small squares on an ECG trace?

A
  • Large square = 0.2 seconds
  • Small square = 0.04 seconds
158
Q

Which two leads should be checked first when reading an ECG?

A
  • aVR and II
159
Q

What are the three layers of the heart wall?

A
  • Endocardium
  • Myocardium
  • Epicardium
160
Q

What is the function of the endocardium?

A
  • Innermost layer of wall
  • Lines cavities and valves of the heart
  • Simple squamous epithelium
  • Regulates contractions
  • Aids in embryological development
161
Q

What is function of the myocardium?

A
  • Composed of cardiac muscle which is involuntary striated cardiac muscle
  • Responsible for contraction of the heart
162
Q

What is the function of the epidcardium?

A
  • Outermost layer of the heart
  • Formed by visceral layer of pericardium
  • Connective tissue and fat
  • Lubricating fluid into pericardial cavity
  • Lined by simple squamous epithelial cells
163
Q

What are the two main layers of the pericardium?

A
  • Fibrous (Outer)
  • Serous (Inner)
164
Q

What are the functions of the pericardium?

A
  • Fixes the heart in position
  • Prevents overfilling
  • Lubrication
  • Protection from infection
165
Q

What is the nerve responsible for innervating the pericardium?

A
  • Phrenic nerve (C3-C5)
166
Q

What are the features of the fibrous pericardium?

A
  • Made of tough connective tissue and is non-distensible
  • Rigid structure
  • Can contribute to tamponade
167
Q

What are the two layers of the serous pericardium?

A
  • Outer parietal layer (Lines fibrous layer)
  • Internal visceral layer (Forms epicardium)

Year 2 Medicine @ Lancaster Uni (15 decks)

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