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Medical Studies 1 > Week 4 Cardiovascular > Flashcards

Week 4 Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

what are the triggers for inflammatory heart disease

A

-pathogens, damaged cells and irritants

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2
Q

outline the mechanism of inflammatory heart disease

A
  1. Triggering Event:
    • Infection (e.g., bacteria, viruses)
    • Autoimmunity
    • Toxins/Drugs
  2. Immune System Activation
    • Immune cells (macrophages, T-cells) respond to infection or damage.
    • Cytokines amplify inflammation.
  3. Chronic Activation Against Self-Antigens:
    -Molecular mimicry: Immune system mistakes heart tissue for foreign antigens.
    • Leads to autoimmunity (e.g., Rheumatic heart disease).
  4. Inflammation and Damage:
    -Inflammation and fluid accumulation around the heart.
  5. Outcome:
    • Persistent inflammation → fibrosis, impaired heart function, heart failure.
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3
Q

define pericarditis

A

inflammation of the fibrous sac surrounding the pericardium

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4
Q

define myocarditis

A

inflammation of the heart muscle (cardiac myocytes)

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5
Q

define endocarditis

A

inflammation of the inner layer of the heart (endocardium); involves heart valves

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6
Q

what are lesions present in endocarditis called

A

vegetations (include mass of platelets, fibrin, organisms, inflammatory cells)

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7
Q

endocarditis effects which parts of the heart

A

can impact: IV septum, chordae tendinae, cardiac devices, valves

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8
Q

is endocarditis infective or non infective

A

can be both

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9
Q

causes of myocarditis

A

-virus
-other infections
-immune conditions
-drugs/toxins
-vaccination
-physical trauma

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10
Q

investigation features of myocarditis

A

-ECG changes
-raised cardiac enzyme levels
-inflammatory markers

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11
Q

findings for pericarditis

A

-sharp chest pain, postural
-ST elevation
-Pericardial rub
-pericardial effusion

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12
Q

list the types of pericardial effusion

A

serous
serosanguineous
chylous

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13
Q

what causes serous pericardial effusion

A

CCF. low albumin

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14
Q

what causes serosanguineous pericardial effusion

A

blunt chest trauma
malignancy
ruptured MI
aortic dissection

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15
Q

what causes chylous pericardial effusion

A

mediastinal lymphatic obstruction

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16
Q

Outline the pathophysiology of RHD

A

-Exposure to Streptococcus A
-Left untreated–>Infection due to autoimmune responses in areas of the body–> ARF
-Recurrences of ARF
–>RHD

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17
Q

how does RHD cause dyspnoea

A

back flow or reduced forward flow of blood due to valve dysfunction leads to reduced oxygen supply, resulting in breathlessness

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18
Q

how does RHD cause chest pain

A

obstructed blood flow and increased pressure in the heart chambers can cause chest pain

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19
Q

how does RHD cause fatigue

A

inefficient pumping due to valve lesions requires the heart to work harder, leading to fatigue

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20
Q

how does RHD causes palpitations

A

irregular blood flow and turbulence can cause palpitations, especially in regurgitant valves

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21
Q

what are immune complexes

A

-molecules formed by the binding of multiple antigens to antibodies
-unchecked IC’s can lead to inflammation via complement and neutrophil action

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22
Q

How do immune complexes form in infective endocarditis

A

in IE, the body produces antibodies against bacteria, forming immune complexes that can circulate in the blood and deposit in tissues.

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23
Q

when are immune complexes removed from the circulation

A

when Ag=Ab (if Ab smaller than it won’t be removed)

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24
Q

what symptoms are present upon exposure to strep A

A

sore throat, skin sores

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25
Q

how long do symptoms after exposure to strep A last

A

10 days to 6 weeks

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26
Q

what are the symptoms of ARF

A

acute fever

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27
Q

how long do the symptoms of ARF last

A

5-15 years

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28
Q

what are the symptoms of RHD

A

complications to cardiac functions

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29
Q

how long do the symptoms of RHD last

A

until death

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30
Q

major diagnostic criteria for RHD

jones

A

chorea
carditis
arthritis
subcutaneous nodules
erythema marginatum

CCASE

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31
Q

minor diagnostic criteria for RHD

jones

A

fever
raised inflammatory markers
arthralgia
ECG (PR segment prolongation)
previous RF

frapp

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32
Q

what are erythema marginatum

A

Pink or red rings with clear centers, usually not itchy. (bulls eye)

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33
Q

what is chorea

A

Involuntary, jerky movements, often associated with neurological disorders

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34
Q

consequences of native RHD with MVR

A

heart failure
Afib
stroke
infective endocarditis
pregnancy issues

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35
Q

consequences of RHD with MVR only

A

acute surgical complications

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36
Q

consequences of native RHD only

A

acute valvulitis

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37
Q

what is native RHD

A

RHD that affects the patient’s own original heart valves

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38
Q

list the causes of endocarditis

A

S.aureus (31%)
Coagulase-negative staph (11%)
viridian group strep (17%)
Strep bovis (6%)
other Strep (6%)
Enterococcus species (10%)
others (fungi, yeast,HACEK) (19%)

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39
Q

what are the complications of endocarditis

A

uncontrolled infection
emboli
HF
mycotic aneurisms

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40
Q

what are mycotic aneurysm

A

infectious organisms, typically bacteria from the heart valve infection, spread through the bloodstream and infect the arterial wall.

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41
Q

Outline a basic approach to managing infective endocarditis

A

-antibiotics (broad–>specific)
-heart failure management eg diuresis
-surgery is used in 50% of cases

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42
Q

Explain the pathogenesis of infective endocarditis

A

-introduction of pathogen: bacteria or fungi enters bloodstream
-bloodstream circulation:pathogens circulate in bloodstream and may adhere to damaged or abnormal heart valves, which provide site of attachment due to turbulent blood flow or structural abnormalities/ pathogens can also adhere to platelets from NBTE
-vegetation formation: adhered pathogens trigger immune réponse leading to thrombotic vegetations formation
-emboli and secondary infections: fragments of vegetations can break off and travel to organs causing secondary infection/infarction

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43
Q

clinical signs of infective endocarditis

A

Janeway lesions
osler nodes
Roth spots
septic:spleen, kidney, lung, vertebra ,arthritis
-abscess, stroke, seizures
-synovitis
-glomerulonephritis

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44
Q

what is abscess

A

A localized collection of pus, often causing pain and swelling.

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45
Q

major criteria for infective endocarditis

DUKES

A

-microbiological evidence of endocarditis
-positive echo showing vegetation and associated valve damage

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46
Q

minor criteria for infective endocarditis

DUKES

A

F - Fever
E - Elevated CRP
V - Valve abnormalities
E - Endovascular phenomena (e.g., splinter hemorrhages)
R - Roth spots (retinal hemorrhages with pale centers)
V - Vascular phenomena (e.g., Janeway lesions, splinter hemorrhages)
I - Immunological phenomena (e.g., Osler’s nodes, glomerulonephritis)
A - Atypical bloods (positive blood cultures, anemia)

FEVER VIA

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47
Q

what are Roth spots

A

retinal hemorrhages with pale centers

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48
Q

location of the SA node

A

border between the superior vena cava and right atrium

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49
Q

location of the atrioventricular node

A

border between the right atrium and right ventricle

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50
Q

location of the bundle of HIS

A

within the right atrium, distal to the AV node near the tricuspid valve

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51
Q

location of bundle branches

A

subendocardial, along the IV septum towards the apex

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52
Q

location of purkinje fibres

A

lateral extensions of the left and right bundle branches

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53
Q

explain the cardiac conduction system process

A

-resting membrane potential of -70m/v
-slow influx of Na+ depolarises the membrane
-T-type Ca2+ channels open, further depolarising the membrane
-L-type Ca2+ channels open, further depolarising the membrane
-membrane potential exceeds threshold, action potential occurs
-K+ channels open, efflux of K+ initiates hyper polarisation

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54
Q

features of the conduction system of heart

A

-SA node can generate 60-100 Ap’s per minute
-AV/HIS are stimulates by SA node
-cardiomyocytes require greater Ca influx and release to conduct excitation-contraction compared to SA nodal cells

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55
Q

Outline how the electrical, signal spreads though the myocardium

A

-depolarisation begins at SA node
-SA node depolarisation reaches AV node
-depolarisation is transported fast by His-purkinje system to cardiomyocytes of ventricles
-depolarisation spreads apex-base

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56
Q

function of SA node

A

Primary pacemaker of the heart, initiating the electrical impulse that causes atrial contraction.

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57
Q

function of AV node

A

Delays the electrical impulse, allowing time for the ventricles to fill with blood before they contract.

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58
Q

function of bundle of HIS

A

ransmits impulses from the AV node to the ventricles.

59
Q

function of bundle branches

A

Conduct impulses to the respective ventricles

60
Q

function of purkinje fibres

A

Distribute the electrical impulse to the ventricular myocardium, causing ventricular contraction.

61
Q

Describe the process of excitation-contraction coupling in cardiac muscle.

A

Action Potential: Electrical signal spreads through the heart muscle.
Calcium Influx: Signal opens channels; Ca²⁺ enters the cell.
Calcium Release: More Ca²⁺ released from the sarcoplasmic reticulum (SR).
Contraction: Ca²⁺ binds to troponin, causing muscle fibers to contract.
Relaxation: Ca²⁺ is pumped back into the SR, and the muscle relaxes.
Refractory Period: Ensures the heart relaxes before the next contraction.

62
Q

How is the action potential generation modified by the autonomic NS

A

-without control, SA node would fire 100-110 Ap’s per minute
-symp—>increases HR
-parasymp–> decreases HR

63
Q

how does parasympathetic stimulation impact HR

A

-increases K+ currents and causes hyper polarisation, which slows depolarisation and moves the membrane potential further away from threshold (-55m/v)

64
Q

how does sympathetic stimulation impact HR

A

increases Ca2+ currents and causes faster depolarisation (moves membrane potential closer to the threshold)

65
Q

what structures involved in sympathetic innervation of heart

A

spinal chord
preganglionic fibres
sympathetic chain
postganglionic fibres
NA/NE
beta1 and beta2 receptors

66
Q

what structures involved in parasympathetic innervation of heart

A

brain stem
vagal nuclei
preganglionic fibres
post ganglionic fibres
Ach
M2 muscarinic receptors

67
Q

ecg for atrial fibrillation

A

-lack of p waves consistently
-ireggularly irregular ventricular rhythm
-can be rapid or slow ventricular response depending on bpm

68
Q

ecg for atrial flutter

A

-rapid 300 bpm
-atrial re entry circuit
-saw tooth due to inverted P waves
-a type of supra ventricular tachycardia
-various ratios eg 2:1 (150 bpm)

69
Q

ecg for pvc (premature ventricular contractions)

A

-widened QRS complex
-compensatory pause

70
Q

ecg for pac (premature atrial contractions)

A

-non sinus p wave followed by QRS complex

71
Q

ecg for left bundle branch blocks

A

-wide QRS
-deep S in V1(W) and prolonged R in V6(M)

(WILLLIAM)

72
Q

ecg for right bundle branch blocks

A

-wide QRS
-RSR in V1 (M) and prolonged S in V6(W)

(MARROW)

73
Q

describe the pathogenesis of atrial fibrillation

A

Triggers:
-Ectopic impulses, often from pulmonary veins.
-multiple reentrant circuits
Electrical Remodeling:
-Shortened refractory period.
-Irregular atrial conduction.
Structural Remodeling:
-Fibrosis and atrial dilation disrupt pathways.
-Linked to hypertension, heart failure, and valvular disease.
Consequences:
-Atria quiver, leading to inefficient blood flow.
-Increased risk of thrombus and stroke.

74
Q

describe the pathogenesis of atrial flutter

A

Macro-Reentrant Circuit:
-Circular reentrant electrical circuit in the right atrium that wraps around the annulus of the tricuspid valve
Trigger:
-Often starts with a premature atrial contraction.
Electrical Remodeling:
-Rapid, organized atrial contractions (250-350 bpm).
-Characteristic sawtooth pattern on ECG.
Structural Remodeling:
-Associated with atrial enlargement, fibrosis, or scarring.
Consequences:
-Reduced cardiac output.
-Increased risk of thrombus and stroke.

75
Q

list the classifications of atrial fibrillation

A

paroxysmal
persistent
long standing persistent
permanent

76
Q

what is paroxysmal atrial fibrillation

A

AF that spontaneously terminates within 7 days

77
Q

what is persistent atrial fibrillation

A

AF that continues for more than 7 days or requires cardio version

78
Q

what is long standing persistent atrial fibrillation

A

AF that is continuous for over 12 months

79
Q

what is permanent atrial fibrillation

A

AF cases in which attempts to restore sinus rhythms have been abandoned

80
Q

what are risk factors for AF

A

advanced age
HTN
Genetics/familial risk
obesity/adiposity
alcohol intake
cardiac disease

81
Q

what is ectopic firing

A

-initiation of the cardiac cycle from a beat that does not arise from the SA node

82
Q

AF symptoms list

A

palpitations
dyspnea
exercise intolerance
chest discomfort
dizziness
syncope

83
Q

why does AF present with palpitations

A

irregularity or racing heart beat can be felt by patients

84
Q

why does AF present with dyspnoea

A

compromised cardiac output and abnormal atrial haemodynamics elevate left sided heart pressure

85
Q

why does AF present with exercise intolerance

A

caused by compromised cardiac function

86
Q

why does AF present with chest discomfort

A

caused by compromised cardiac function

87
Q

why does AF present with fatigue

A

caused by compromised cardiac function

88
Q

why does AF present with dizziness

A

high ventricular rates and inconsistent preservation of atrial pressure can cause disruption to blood flow to the brain

89
Q

why does AF present with syncope

A

high ventricular rates and inconsistent preservation of atrial pressure can cause disruption to blood flow to the brain

90
Q

list the 4 main treatments for AF

A

rate control
rhythm control
anticoagulation
risk management

91
Q

ways for ‘rate control’ in AF

A

beta blockers
calcium channel antagonists

92
Q

why is rate control used to treat AF

A

reduce ventricular rate to alleviate symptoms; promote haemodynamic stability, reduce tachyarrythmic effects

93
Q

ways for ‘rhythm control’ in AF

A

Catheter ablation, anti arrhythmic meds eg amiodarone

94
Q

why’s is rhythm control used used to treat AF

A

attempt to achieve and maintain sinus rhythm, reduce AF symptoms, reverse remodelling

95
Q

why is anticoagulation used to treat AF

A

reduce risk of stroke (if elevated risk score)

96
Q

way to achieve anticoagultion in AF

A

factor XA inhibition, direct thrombin inhibitors

97
Q

ways to manage risks in AF

A

weight loss
glucose control
exercise

98
Q

why is risk management used for treating AF

A

reduce risk factors promoting maintenance and progression of AF

99
Q

Describe the pathophysiology linking atrial fibrillation and stroke risk

A

-cardiac endothelial damage and cardiac inflammation can lead to abnormal atrial flow
-causing blood stasis within the LA
-blood clot forms due to hypercoagulabilty
-embolisation
-blood vessel coagulation

100
Q

test for quantifying stroke risk with AF

A

CHA(2)DS(2)VAS
-all worth one point
-except A and S
-add up to 9

101
Q

what does CHADSVAS stand for

A

Congestive heart failure
Hypertension
Advanced age (75+)
Diabetes mellitus
Stroke/TIA/thromboembolism
vascular disease
semi advanced age (65-74)
sex

102
Q

score of 0 on CHADSVAS means

A

no anticoagulation

103
Q

score of 1 (female) on CHADSVAS means

A

no anticoagulation

104
Q

score of 1 (male) on CHADSVAS means

A

anticoagulation needed

105
Q

score of 2+ on CHADSVAS means

A

anticoagulation needed

106
Q

list the common forms of bradyarrythmias

A

sinus bradycardia
sinus arrhythmia
sinus node ageing
sick sinus syndrome

107
Q

what is a sinus bradycardia

A

-sinus node discharge rate is below 50 bpm
-common in elite athletes and people with high levels of aerobic exercise

108
Q

what can cause sinus bradycardia

A

-high vagal tone
-decreased sympathetic tone
-sinus node dysfunction/modelling
-effects of medication

109
Q

what is a sinus arrhythmia

A

-describes phasic variation
Normal arrhythmia:
-respiratory sinus arrhythmia
-low HR with high vagal tone

-during inspiration HR is typically faster, while it is slower during expiration
-has normal P wave morphology
-PR intervals >120 ms

110
Q

what is sinus node ageing

A

-intrinsic heart rate is the SA node discharge rate in the absence of autonomic activity
-intrinsic HR declines progressively with increasing age
-the likelihood and prevalence of sinus bradyarrhythmias is much higher in elderly patients

111
Q

examples of sick sinus syndrome

A

-persistent sinus bradycardia
-sinus arrest or exit block
-combinations of SA and AV node abnormalities
-alteration of rapid tachyarrhythmias with periods of slow atrial and ventricular rates

112
Q

characteristics of SND (sinus node syndrome)

A

-fibrosis in the proximity to the SA node and atrial scar
-nodal atrial discontinuity
-inflammatory/degenerative changes
-ion channel remodelling

113
Q

what are the categories of AV block

A

1st degree
2nd degree (type 1 and 2)
3rd degree

114
Q

what is a 1st degree AV block

A

-impulses are conducted but conduction time is prolonged (PR interval >200ms)

115
Q

what is the intervention for a 1st degree AV block

A

nil

116
Q

what is a 2nd degree/type 1 AV block

A

progressive lengthening of a conduction time until an impulse is not conducted

117
Q

intervention for a 2nd degree/type 1 AV block

A

nil

118
Q

what is a 2nd degree/type 2 AV block

A

intermittent block of conduction without prior lengthening of conduction time

119
Q

intervention for 2nd degree/type 2 AV block

A

nil

120
Q

what is a 3rd degree AV block

A

complete dissociation between atrial and ventricular impulses

121
Q

intervention for 3rd degree AV block

A

urgent pacemaker

122
Q

ECG characteristic for a first degree AV block

A

prolonged (consistent) PR interval

123
Q

ECG characteristics for a second degree/type 1 Av block

A

PR intervals get progressively longer, eventually no conduction

124
Q

ECG characteristics for a second degree/type 2 AV block

A

PR interval consistent on first few cycles; no AV conduction afterwards

125
Q

ECG characteristics for a third degree AV block

A

complete AV dissociation, PR intervals are not coupled with QRS complexes

126
Q

what does each part of ECG represent

A

P Wave: Atrial depolarization.

PR Interval: Time from atrial to ventricular activation.

QRS Complex: Ventricular depolarization.

ST Segment: Transition from depolarization to repolarization.

T Wave: Ventricular repolarization.

QT Interval: Total time for ventricular activity (depolarization + repolarization).

U Wave (if present): Final phase of ventricular repolarization.

127
Q

what are the ways for pacing in bradycardic patients

A

single chamber
dual chamber
biventricular

128
Q

what is a single chamber pacemaker

A

used for atrial pacing only

129
Q

what is a duel chamber pacemaker

A

atrial and R ventricular pacing

130
Q

what is a biventricular pacemaker

A

atrial, R/L ventricular pacing

131
Q

what is sudden cardiac arrest

A

sudden and unexpected death occurring within an hour of the onset of symptoms or in patients found dead within 24hrs of being asymptomatic to a cardiac arrhythmia or haemo-dynamic catastrophe

132
Q

what are the cardiac causes for SCA

A

coronary heart disease
cardiomyopathies
inherited arrhythmias
valvular heart disease

133
Q

what are the reversible causes of SCA

A

hypoxia
hypovolaemia
hypokalaemia
hypo/hyperthermia

toxins
tension pneumothorax
thrombosis
tamponade

134
Q

modifiable risk factors for SCD/SCA

A

HTN
dyslipidaemia
cigarette smoking
obesity
depression/anxiety
poor diet
limited physical activity
heavy alcohol use

135
Q

non modifiable risk factors for SCD/SCA

A

advanced age
being male
being African or non asian
diabetes
FHx of SCD
mutations
CV conditions
congenital abnormalities

136
Q

list the forms of ventricular arrhythmias

A

-sustained ventricular tachycardia
-non sustained ventricular tachycardia
-polymorphic ventricular tachycardia
-Torsades de Pointes (Ballerina)

137
Q

what is sustained ventricular tachycardia

A

-cardia arrhythmia of >3 consecutive complexes
* > 100 bpm
*VT lasts >30s and/or requires termination

138
Q

what is non sustained ventricular tachycardia

A

-cardiac arrhythmia of >3 consecutive complexes
* >100bpm
*terminates spontaneously <30s

139
Q

what is polymorphic ventricular tachycardia

A

multiform QRS morphology from beat to beat; indicates ischemia

140
Q

what is Torsades de Pointes

A

long QT segment
polymorphic
twisting of points

141
Q

assessment factors for diagnosing ventricular arrhythmias

A

heart rate and regularity
JVP
sternotomy scars
Elevated BP
murmurs
oedema

142
Q

Community intervention for managing ventricular arrhythmias

A

-educate community members
-screening
-promoting healthy lifestyle
-BLS programs
-community AED provision
-recognition of familial risk –> screening

143
Q

Individual intervention for managing ventricular arrhythmias

A

-AED use
-CAD management (obesity, lipids,HTN)
-internal cadioverter defibrillator
-ant-arrhythmic meds
-specific risk scoring systems
-risk assessment of SCD

Medical Studies 1 (15 decks)

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