Week 4 Cardiovascular Flashcards
1
Q
what are the triggers for inflammatory heart disease
A
-pathogens, damaged cells and irritants
2
Q
outline the mechanism of inflammatory heart disease
A
- Triggering Event:
- Infection (e.g., bacteria, viruses)
- Autoimmunity
- Toxins/Drugs
- Immune System Activation
- Immune cells (macrophages, T-cells) respond to infection or damage.
- Cytokines amplify inflammation.
- Chronic Activation Against Self-Antigens:
-Molecular mimicry: Immune system mistakes heart tissue for foreign antigens.- Leads to autoimmunity (e.g., Rheumatic heart disease).
- Inflammation and Damage:
-Inflammation and fluid accumulation around the heart. - Outcome:
- Persistent inflammation → fibrosis, impaired heart function, heart failure.
3
Q
define pericarditis
A
inflammation of the fibrous sac surrounding the pericardium
4
Q
define myocarditis
A
inflammation of the heart muscle (cardiac myocytes)
5
Q
define endocarditis
A
inflammation of the inner layer of the heart (endocardium); involves heart valves
6
Q
what are lesions present in endocarditis called
A
vegetations (include mass of platelets, fibrin, organisms, inflammatory cells)
7
Q
endocarditis effects which parts of the heart
A
can impact: IV septum, chordae tendinae, cardiac devices, valves
8
Q
is endocarditis infective or non infective
A
can be both
9
Q
causes of myocarditis
A
-virus
-other infections
-immune conditions
-drugs/toxins
-vaccination
-physical trauma
10
Q
investigation features of myocarditis
A
-ECG changes
-raised cardiac enzyme levels
-inflammatory markers
11
Q
findings for pericarditis
A
-sharp chest pain, postural
-ST elevation
-Pericardial rub
-pericardial effusion
12
Q
list the types of pericardial effusion
A
serous
serosanguineous
chylous
13
Q
what causes serous pericardial effusion
A
CCF. low albumin
14
Q
what causes serosanguineous pericardial effusion
A
blunt chest trauma
malignancy
ruptured MI
aortic dissection
15
Q
what causes chylous pericardial effusion
A
mediastinal lymphatic obstruction
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
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
18
Q
how does RHD cause chest pain
A
obstructed blood flow and increased pressure in the heart chambers can cause chest pain
19
Q
how does RHD cause fatigue
A
inefficient pumping due to valve lesions requires the heart to work harder, leading to fatigue
20
Q
how does RHD causes palpitations
A
irregular blood flow and turbulence can cause palpitations, especially in regurgitant valves
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
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.
23
Q
when are immune complexes removed from the circulation
A
when Ag=Ab (if Ab smaller than it won’t be removed)
24
Q
what symptoms are present upon exposure to strep A
A
sore throat, skin sores
25
how long do symptoms after exposure to strep A last
10 days to 6 weeks
26
what are the symptoms of ARF
acute fever
27
how long do the symptoms of ARF last
5-15 years
28
what are the symptoms of RHD
complications to cardiac functions
29
how long do the symptoms of RHD last
until death
30
major diagnostic criteria for RHD
| jones
chorea
carditis
arthritis
subcutaneous nodules
erythema marginatum
CCASE
31
minor diagnostic criteria for RHD
| jones
fever
raised inflammatory markers
arthralgia
ECG (PR segment prolongation)
previous RF
frapp
32
what are erythema marginatum
Pink or red rings with clear centers, usually not itchy. (bulls eye)
33
what is chorea
Involuntary, jerky movements, often associated with neurological disorders
34
consequences of native RHD with MVR
heart failure
Afib
stroke
infective endocarditis
pregnancy issues
35
consequences of RHD with MVR only
acute surgical complications
36
consequences of native RHD only
acute valvulitis
37
what is native RHD
RHD that affects the patient's own original heart valves
38
list the causes of endocarditis
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%)
39
what are the complications of endocarditis
uncontrolled infection
emboli
HF
mycotic aneurisms
40
what are mycotic aneurysm
infectious organisms, typically bacteria from the heart valve infection, spread through the bloodstream and infect the arterial wall.
41
Outline a basic approach to managing infective endocarditis
-antibiotics (broad-->specific)
-heart failure management eg diuresis
-surgery is used in 50% of cases
42
Explain the pathogenesis of infective endocarditis
-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
43
clinical signs of infective endocarditis
Janeway lesions
osler nodes
Roth spots
septic:spleen, kidney, lung, vertebra ,arthritis
-abscess, stroke, seizures
-synovitis
-glomerulonephritis
44
what is abscess
A localized collection of pus, often causing pain and swelling.
45
major criteria for infective endocarditis
| DUKES
-microbiological evidence of endocarditis
-positive echo showing vegetation and associated valve damage
46
minor criteria for infective endocarditis
| DUKES
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
47
what are Roth spots
retinal hemorrhages with pale centers
48
location of the SA node
border between the superior vena cava and right atrium
49
location of the atrioventricular node
border between the right atrium and right ventricle
50
location of the bundle of HIS
within the right atrium, distal to the AV node near the tricuspid valve
51
location of bundle branches
subendocardial, along the IV septum towards the apex
52
location of purkinje fibres
lateral extensions of the left and right bundle branches
53
explain the cardiac conduction system process
-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
54
features of the conduction system of heart
-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
55
Outline how the electrical, signal spreads though the myocardium
-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
56
function of SA node
Primary pacemaker of the heart, initiating the electrical impulse that causes atrial contraction.
57
function of AV node
Delays the electrical impulse, allowing time for the ventricles to fill with blood before they contract.
58
function of bundle of HIS
ransmits impulses from the AV node to the ventricles.
59
function of bundle branches
Conduct impulses to the respective ventricles
60
function of purkinje fibres
Distribute the electrical impulse to the ventricular myocardium, causing ventricular contraction.
61
Describe the process of excitation-contraction coupling in cardiac muscle.
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
How is the action potential generation modified by the autonomic NS
-without control, SA node would fire 100-110 Ap's per minute
-symp--->increases HR
-parasymp--> decreases HR
63
how does parasympathetic stimulation impact HR
-increases K+ currents and causes hyper polarisation, which slows depolarisation and moves the membrane potential further away from threshold (-55m/v)
64
how does sympathetic stimulation impact HR
increases Ca2+ currents and causes faster depolarisation (moves membrane potential closer to the threshold)
65
what structures involved in sympathetic innervation of heart
spinal chord
preganglionic fibres
sympathetic chain
postganglionic fibres
NA/NE
beta1 and beta2 receptors
66
what structures involved in parasympathetic innervation of heart
brain stem
vagal nuclei
preganglionic fibres
post ganglionic fibres
Ach
M2 muscarinic receptors
67
ecg for atrial fibrillation
-lack of p waves consistently
-ireggularly irregular ventricular rhythm
-can be rapid or slow ventricular response depending on bpm
68
ecg for atrial flutter
-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
ecg for pvc (premature ventricular contractions)
-widened QRS complex
-compensatory pause
70
ecg for pac (premature atrial contractions)
-non sinus p wave followed by QRS complex
71
ecg for left bundle branch blocks
-wide QRS
-deep S in V1(W) and prolonged R in V6(M)
(WILLLIAM)
72
ecg for right bundle branch blocks
-wide QRS
-RSR in V1 (M) and prolonged S in V6(W)
(MARROW)
73
describe the pathogenesis of atrial fibrillation
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
describe the pathogenesis of atrial flutter
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
list the classifications of atrial fibrillation
paroxysmal
persistent
long standing persistent
permanent
76
what is paroxysmal atrial fibrillation
AF that spontaneously terminates within 7 days
77
what is persistent atrial fibrillation
AF that continues for more than 7 days or requires cardio version
78
what is long standing persistent atrial fibrillation
AF that is continuous for over 12 months
79
what is permanent atrial fibrillation
AF cases in which attempts to restore sinus rhythms have been abandoned
80
what are risk factors for AF
advanced age
HTN
Genetics/familial risk
obesity/adiposity
alcohol intake
cardiac disease
81
what is ectopic firing
-initiation of the cardiac cycle from a beat that does not arise from the SA node
82
AF symptoms list
palpitations
dyspnea
exercise intolerance
chest discomfort
dizziness
syncope
83
why does AF present with palpitations
irregularity or racing heart beat can be felt by patients
84
why does AF present with dyspnoea
compromised cardiac output and abnormal atrial haemodynamics elevate left sided heart pressure
85
why does AF present with exercise intolerance
caused by compromised cardiac function
86
why does AF present with chest discomfort
caused by compromised cardiac function
87
why does AF present with fatigue
caused by compromised cardiac function
88
why does AF present with dizziness
high ventricular rates and inconsistent preservation of atrial pressure can cause disruption to blood flow to the brain
89
why does AF present with syncope
high ventricular rates and inconsistent preservation of atrial pressure can cause disruption to blood flow to the brain
90
list the 4 main treatments for AF
rate control
rhythm control
anticoagulation
risk management
91
ways for 'rate control' in AF
beta blockers
calcium channel antagonists
92
why is rate control used to treat AF
reduce ventricular rate to alleviate symptoms; promote haemodynamic stability, reduce tachyarrythmic effects
93
ways for 'rhythm control' in AF
Catheter ablation, anti arrhythmic meds eg amiodarone
94
why's is rhythm control used used to treat AF
attempt to achieve and maintain sinus rhythm, reduce AF symptoms, reverse remodelling
95
why is anticoagulation used to treat AF
reduce risk of stroke (if elevated risk score)
96
way to achieve anticoagultion in AF
factor XA inhibition, direct thrombin inhibitors
97
ways to manage risks in AF
weight loss
glucose control
exercise
98
why is risk management used for treating AF
reduce risk factors promoting maintenance and progression of AF
99
Describe the pathophysiology linking atrial fibrillation and stroke risk
-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
test for quantifying stroke risk with AF
CHA(2)DS(2)VAS
-all worth one point
-except A and S
-add up to 9
101
what does CHADSVAS stand for
Congestive heart failure
Hypertension
Advanced age (75+)
Diabetes mellitus
Stroke/TIA/thromboembolism
vascular disease
semi advanced age (65-74)
sex
102
score of 0 on CHADSVAS means
no anticoagulation
103
score of 1 (female) on CHADSVAS means
no anticoagulation
104
score of 1 (male) on CHADSVAS means
anticoagulation needed
105
score of 2+ on CHADSVAS means
anticoagulation needed
106
list the common forms of bradyarrythmias
sinus bradycardia
sinus arrhythmia
sinus node ageing
sick sinus syndrome
107
what is a sinus bradycardia
-sinus node discharge rate is below 50 bpm
-common in elite athletes and people with high levels of aerobic exercise
108
what can cause sinus bradycardia
-high vagal tone
-decreased sympathetic tone
-sinus node dysfunction/modelling
-effects of medication
109
what is a sinus arrhythmia
-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
what is sinus node ageing
-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
examples of sick sinus syndrome
-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
characteristics of SND (sinus node syndrome)
-fibrosis in the proximity to the SA node and atrial scar
-nodal atrial discontinuity
-inflammatory/degenerative changes
-ion channel remodelling
113
what are the categories of AV block
1st degree
2nd degree (type 1 and 2)
3rd degree
114
what is a 1st degree AV block
-impulses are conducted but conduction time is prolonged (PR interval >200ms)
115
what is the intervention for a 1st degree AV block
nil
116
what is a 2nd degree/type 1 AV block
progressive lengthening of a conduction time until an impulse is not conducted
117
intervention for a 2nd degree/type 1 AV block
nil
118
what is a 2nd degree/type 2 AV block
intermittent block of conduction without prior lengthening of conduction time
119
intervention for 2nd degree/type 2 AV block
nil
120
what is a 3rd degree AV block
complete dissociation between atrial and ventricular impulses
121
intervention for 3rd degree AV block
urgent pacemaker
122
ECG characteristic for a first degree AV block
prolonged (consistent) PR interval
123
ECG characteristics for a second degree/type 1 Av block
PR intervals get progressively longer, eventually no conduction
124
ECG characteristics for a second degree/type 2 AV block
PR interval consistent on first few cycles; no AV conduction afterwards
125
ECG characteristics for a third degree AV block
complete AV dissociation, PR intervals are not coupled with QRS complexes
126
what does each part of ECG represent
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
what are the ways for pacing in bradycardic patients
single chamber
dual chamber
biventricular
128
what is a single chamber pacemaker
used for atrial pacing only
129
what is a duel chamber pacemaker
atrial and R ventricular pacing
130
what is a biventricular pacemaker
atrial, R/L ventricular pacing
131
what is sudden cardiac arrest
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
what are the cardiac causes for SCA
coronary heart disease
cardiomyopathies
inherited arrhythmias
valvular heart disease
133
what are the reversible causes of SCA
hypoxia
hypovolaemia
hypokalaemia
hypo/hyperthermia
toxins
tension pneumothorax
thrombosis
tamponade
134
modifiable risk factors for SCD/SCA
HTN
dyslipidaemia
cigarette smoking
obesity
depression/anxiety
poor diet
limited physical activity
heavy alcohol use
135
non modifiable risk factors for SCD/SCA
advanced age
being male
being African or non asian
diabetes
FHx of SCD
mutations
CV conditions
congenital abnormalities
136
list the forms of ventricular arrhythmias
-sustained ventricular tachycardia
-non sustained ventricular tachycardia
-polymorphic ventricular tachycardia
-Torsades de Pointes (Ballerina)
137
what is sustained ventricular tachycardia
-cardia arrhythmia of >3 consecutive complexes
* > 100 bpm
*VT lasts >30s and/or requires termination
138
what is non sustained ventricular tachycardia
-cardiac arrhythmia of >3 consecutive complexes
* >100bpm
*terminates spontaneously <30s
139
what is polymorphic ventricular tachycardia
multiform QRS morphology from beat to beat; indicates ischemia
140
what is Torsades de Pointes
long QT segment
polymorphic
twisting of points
141
assessment factors for diagnosing ventricular arrhythmias
heart rate and regularity
JVP
sternotomy scars
Elevated BP
murmurs
oedema
142
Community intervention for managing ventricular arrhythmias
-educate community members
-screening
-promoting healthy lifestyle
-BLS programs
-community AED provision
-recognition of familial risk --> screening
143
Individual intervention for managing ventricular arrhythmias
-AED use
-CAD management (obesity, lipids,HTN)
-internal cadioverter defibrillator
-ant-arrhythmic meds
-specific risk scoring systems
-risk assessment of SCD
