Cardiology Disease Profiles Flashcards
1
Q
what is shock
A
Abnormality of circulatory system resulting in inadequate tissue perfusion + oxygenation
2
Q
what is hypovolaemic shock
A
shock due to decrease in blood volume
3
Q
explain the types of hypovolaemic shock
A
haemorrhage- direct blood loss (trauma, surgery), non haemorrhage- decrease in ECFV (vomiting, diarrhoea)
4
Q
pathophysiology of hypovolaemic shock
A
Decrease in BV -> decrease venous return -> decrease EDV -> decrease SV (frank-starling) -> decrease CO + BP -> inadequate tissue perfusion
5
Q
what is myogenic response
A
intrinsic ability of smooth muscle to alter SVR in response to pressure changes
6
Q
what is cardiogenic shock and example of cause
A
Decreased cardiac contractility (eg due to acute MI)
7
Q
what is obstructive shock and example of cause
A
Shock associated with physical obstruction of the great vessels/heart itself
Includes cardiac tamponade, pulmonary embolism and tension pnuemothorax
8
Q
what is distributive shock and the two main types
A
Body can’t get enough blood to heart, brain + kidneys. Happens because blood vessels are extremely dilated which decreases BP.
neurogenic + vasoactive
9
Q
what is neurogenic shock and a cause
A
Eg spinal cord injury
Loss of sympathetic tone to blood vessels + heart -> massive venous and arterial dilation, HR slows -> decrease venous return + SVR -> decrease CO + BP -> inadequate tissue perfusion
10
Q
what is vasoactive shock and possible causes
A
Eg septic shock, anaphylactic shock
Release of massive vasoactive mediators -> massive venous + arterial vasodilation, increased capillary permeability -> decrease venous return + SVR -> decrease CO + BP -> inadequate tissue perfusion
11
Q
treatment for hypovolaemic, cardiogenic, anaphylatic and septic shocks
A
volume replacement, inotropes, adrenaline, vasopressors
12
Q
what is syncope
A
Transient loss of consciousness due to cerebral hypoperfusion, characterized by rapid onset, short duration, and spontaneous complete recovery
13
Q
what is reflex syncope and the 3 types
A
Involves neural reflexes
Vagal stimulation decreases HR which decreases CO and/or
Depression of sympathetic activity to blood vessels -> vasodilation
vasovagal, situational reflex, carotid sinus reflex
14
Q
what triggers vasovagal syncope
A
Faint triggered by emotional distress or orthostatic stress
15
Q
what triggers situational reflex syncope
A
Faint during/immediately after a specific trigger eg cough
16
Q
what triggers carotid sinus reflex syncope
A
Triggered by mechanical manipulation of the neck, eg shaving, tight collar
More common in elderly, especially males
Management- cardiac permanent pacing
17
Q
what is postural hypotension (orthostatic hypotension)
A
Results from failure of baroreceptor responses to gravitational shift in blood when moving from horizontal to vertical position
18
Q
risk factors of postural hypotension
A
old age, certain medications, certain diseases, reduced intravascular volume,prolonged bed rest
19
Q
diagnosis of postural hypotension
A
Positive result indicated by a drop within 3 minutes of standing from lying position- in systolic BP of >20mmHg with/without symptoms, or in diastolic BP of >10mmHg with symptoms
20
Q
what is cardiac syncope
A
Cardiac event causing sudden drop in CO
Eg arrhythmias, MI
21
Q
primary hypertension
A
hypertension with no singular identifiable cause
22
Q
secondary hypertension
A
hypertension caused by an identifiable singular cause
23
Q
causes of secondary hypertension
A
renal disease, endocrine problems, coarction of the aorta, drugs (eg corticosteroids), pregnancy
24
Q
benign hypertension
A
stable elevation of BP over many years, asymptomatic, can lead to LV hypertrophy, renal disease and atheromas
25
malignant hypertension
acute severe elevation of BP, diastolic pressure >130, needs urgent treatment
26
white coat hypertension discrepancy in BP
discrepancy of more than 20/10mmHg between clinic and average daytime ABPM
27
stage 1 hypertension
clinic BP 140/90 or higher, and ABPM 135/85 or higher
28
stage 2 hypertension
clinic BP 160/100 or higher, and ABPM 150/95
29
severe hypertension
clinic systolic BP >180, or clinic diastolic BP >110
30
monitoring hypertension to assess for end organ damage
urine, bloods, fundoscopy, 12 lead ECG, ASSIGN/QRISK3 score
31
step 1 medical manangement of hypertension
if <55 years old use ACEi (ARB if cant tolerate), if >55 or black use CCB
32
step 2 and 3 of medical management of hypertension
combine CCB and ACEi/ARB,
add thiazide like diuretic (indapamide)
33
if blood potassium is <4.5mmol/L in treatment of hypertension then add
spironolactone
34
if blood potassium >4.5mmol/L in treatment of hypertension then
increase thiazide like diuretic, add alpha blocker or add beta blocker
35
BP target for <80 years
<140/90mmHg
36
BP target for diabetics
<130/80mmHg
37
causes of heart failure
IHD, dilated cardiomyopathy, hypertension, arrhythmias, infections, diabetes, congenital heart disease
38
ejection fraction
% of blood pumped out of heart during each beat (SV/EDV x 100)
39
HFrEF
EF <40%, reduced contractility -> systolic ventricular dysfunction -> decreased LVEF -> decreased CO
commonly caused by IHD
40
HFpEF
EF >50%, decreased ventricular compliance -> diastolic ventricular dysfunction -> reduced ventricular filling and increased diastolic pressure -> decreased CO
causes are increased stiffness of ventricle and impaired relaxation of the ventricle
41
left sided heart failure
increased LV afterload - increased aortic pressure (arterial hypertension) or by outflow obstruction (aortic stenosis_
increased LV preload - left ventricular volume overload (backflow into LV caused by aortic insufficiency)
42
right sided heart failure
increased RV afterload - increase in pulmonary artery pressure (pulmonary hypertension)
increased RV preload - RV volume overload (tricuspid valve regurgitation)
43
compensation mechanisms for heart failure
increased adrenergic activity, increase of RAAS- increased angiotensin II secretion + increased aldosterone secretion, secretion of BNP
44
forward failure, consequence of heart failure
reduced CO results poor organ perfusion leading to organ dysfunction
45
LV backward failure, consequence of HF
increased LV pressure -> backflow of blood into the lungs -> increased capillary pressure -> pulmonary oedema
46
RV backward failure, consequence of HF
increased pulmonary artery pressure from LV failure decreases right sided CO -> systemic venous congestion -> peripheral oedema + progressive congestion of internal organs
47
symptoms of HF
exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue
48
signs of HF
tachycardia, elevated jugular venous pressure, cardiomegaly, 3rd+4th heart sounds, bi-basal crackles, pleural effusion, ankle oedema, ascites
49
signs of HF on CXR
pulmonary oedema- kerley B lines, bat wing shadowing, cardiomegaly
50
medical treatment for HFpEF
loop diuretic to relieve symptoms of fluid overload (furosemide)
51
medical management of HFrEF
ABAL- ACEi, Beta blocker, Aldosterone antagonist when symptoms not controlled with A+B, loop diuretics to improve symptoms
52
medical management for acute HF presentation
LMNOP- Lasix (furosemide), Morphine, Nitrates, Oxygen, Position (sit patient up)
53
complications of HF
arrhythmias, depression, cachexia, chronic kidney disease, sudden cardiac death
54
pathophysiology of atherosclerosis
primary endothelial injury -> uptake of LDL from blood into intima of artery -> macrophages migrate into intima where take up LDL and become foam cells (fatty streak) -> macrophages release cytokines + growth factors, results in deposition of collagen -> as plaque enlarges flow is compromised -> unstable angina/MI when plaque ruptures and thrombus occludes artery
55
risk factors for atherosclerosis
smoking, hypertension, obesity, hypercholesterolaemia, diabetes, alcohol, male, old age, family history
56
pathophysiology of stable angina
narrowing of coronary arteries (atherosclerosis) reduces flow to myocardium, during times of high demand there is insufficient supply of blood
57
clinical presentation of stable angina
central/left sided chest discomfort, tight/crushing sensation, may be SoB, results from exertion, symptoms relieved by rest (+GTN)
58
diagnosing angina
clinical diagnosis, ECG (may be normal), CT coronary angiography (diagnostic), exercise tolerance test, myocardial perfusion scan, catheter angiography
59
immediate symptomatic relief for angina
GTN spray
60
long sympathetic relief for angina
B blocker or CCB if not tolerated, other options- long acting nitrates, nicorandil, ivabradine, ranolazine
61
secondary prevention for angina
aspirin, atorvastatin, ACEi
62
surgical interventions for angina
PCI with coronary angioplasty offered to patients with extensive disease on CT
CABG offered to patients with severe stenosis
63
name the acute coronary syndromes
unstable angina, STEMI, NSTEMI
64
pathophysiology of ACS
rupture of plaque -> thrombus forms -> thrombus + vasocontriction produced by platelet release of serotonin + thromboxane A2 causes MI
65
what is unstable angina
subtotal occlusion, supply led ischaemia without infarction
66
what is an NSTEMI
subtotal occlusion
67
what is a STEMI
complete occlusion
68
type 1 MI
traditional MI due to an acute coronary event
69
type 2 MI
ischaemia secondary to increased demand/reduced supply of oxygen (eg severe anaemia, tachycardia, hypotension)
70
type 3 MI
sudden cardiac death or cardiac arrest suggestive of an ischaemic event
71
type 4 MI
associated with PCI/coronary stunting/CABG
72
symptoms of an MI
severe crushing central chest pain at rest, radiates to jaw + arms, not relived by GTN, sweating, nausea, 30 mins or longer
73
atypical presentation of MI
milder symptoms, SoB, fatigue, body aches, discomfort in back/chest/arm/neck/jaw, nausea
74
ECG changes in a STEMI
ST segment elevation in leads consistent with an area of ischaemia or a new left bundle branch block
75
ECG changes in an NSTEMI
may be normal, ST segment depression in a region, deep T wave inversion, pathological Q waves (late sign)
76
ECG changes in unstable angina
may be normal, may have abnormal T waves or ST depression
77
initial management of an MI
MONA-T: morphine, oygen if hypoxic, nitrates if hypertensive/in acute LVF, aspirin, ticagreor/clopidogrel
78
definitive management of STEMI
PCI (if within 2 hours), thrombolysis if PCI not available in 2 hours
79
definitive management of an NSTEMI
receive continuing aspirin and anticoagulant, consider IV nitrate, if high risk consider PCI, low risk may be discharged after repeat negative troponin
80
medications used in secondary prevention of MI
DABS- dual antiplatelet (aspirin for life, P2Y12 inhibitor for 6-12 months), ACEi, B blocker, Statin
81
complications of MI
arrhythmias, HF, structural damage, pericarditis- Dresslers syndome (occurs 2-3 weeks after MI)
82
peripheral vascular disease
narrowing of the peripheral arteries due to atherosclerostic plaques, most commonly affects the legs
83
intermittent claudication
occurs when insufficient blood reaches exercising muscle to due atherosclerosis. presents as exertional discomfort relieved by rest, most commonly in calves
84
severe PVD/critical limb ischaemia
artery is compromised to the point where blood is unable to maintain oxygenation of the tissues at rest. clinical features are pain at rest, ulceration, tissue necrosis, absent peripheral pulses
85
ABPI numbers in claudication
normal = 0.9-1.2
claudication = 0.4-0.85
severe claudication = 0-0.4
86
abdominal aortic aneurysm
permanent dilation of the aorta to >3cm
87
causes of AAA
may occur secondary to atherosclerosis, infection, trauma or may be genetic
88
pathophysiology of AAAs
result from degeneration of the media of the arterial wall. during formation of atheromatous plaques, macrophages release enzymes which break down the collagen and elastin of the media -> media expands
89
presentation of a ruptured AAA
sudden onset abdominal pain radiating to back with an expansile abdominal mass
90
surgical treatment of AAAs
if asymptomatic, elective surgery only performed if >5.5cm in diameter
if symptomatic perform a graft
91
thoracoabdominal aortic aneurysm
aneurysms that coexist in both segments of the aorta (thoracic and abdominal)
92
type A TAA
2/3 of cases, involves ascending aorta (may also include descending), associated with marfans
93
type B TAA
1/3 of cases, affects descending aorta only, occurs secondary to atherosclerosis and syphilis
94
clinical presentation of TAA
sudden tearing chest pain radiating to the back
95
carcinoid syndrome
occurs when neuroendocrine tumour metastasizes to the liver where it produces excess hormones, produces right sided cardiac valve disease -> carcinoid heart disease
96
atrial myoma
primary tumour of the heart. associated with systemic fever and malaise, complications are tumour emboli and endocarditis
97
causes of myocarditis
viral infection is most common cause- coxsackievirus most common in europe + USA, chaga's disease due to trypanosomiasis and diptheria
hypersensitivity reactions- to infection (rheumatic fever), drugs (eosinophilic myocarditis), systemic autoimmune diseases (lupus)
98
signs and symptoms of myocarditis
fever, chest pain, dyspnoea, palpitaitons, prominant 3rd heart sound, tachycardia, cardiac failure
99
ECG changes in myocarditis
may see ST elevation/depression, T wave inversion, atrial arrhythmias, transient AV block
100
hypertrophic cardiomyopathy
autosomal dominant genetic disorder characterised by LVH, impaired diastolic filling and abnormalities of mitral valve
101
clinical presentation of hypertrophic cardiomyopathy
most cases asymptomatic, sudden death in adolescents + young adults
102
ECG changes in hypertrophic cardiomyopathy
LV hypertrophy, ST and T wave changes, abnormal Q waves
103
management of hypertrophic cardiomyopathy
patients with 2 or more risk factors for sudden cardiac death (massive LV hypertrophy, unexplained syncope, family history of SCD) should be assessed for ICD insertion
104
arrhythmogenic right ventricular cardiomyopathy
inherited condition, affects RV with fatty/fibro-fatty replacement of myocytes, leading to segmental or global dilation
105
medical management of arrhythmogenic right ventricular cardiomyopathy
beta blockers for non life-threatening arrhythmias
amiodarone/sotalol for symptomatic arrhythmias
ICD for life-threatening arrhythmias
106
dilated cardiomyopathy
most common form, enlarged ventricular size with normal ventricular wall thickness and systolic dysfunction
107
causes of dilated cardiomyopathy
genetic mutation, toxins (drugs, alcohol, chemotherapy), myocarditis, autoimmune disorders, endocrine disorders, neuromuscular disorders
108
clinical presentation of dilated cardiomyopathy
HF, arrhythmias, conduction defects, thromboembolism, sudden death
109
ECG and ECHO findings with dilated cardiomyopathy
ECG- ST segment and T wave changes
ECHO- dilation of left and right ventricle with poor contraction function
110
restrictive cardiomyopathy
normal/decreased volume of both ventricles with bi-atrial enlargement, normal wall thickness and valves, impaired ventricular filling but near normal systolic function
111
causes of restrictive cardiomyopathy
infiltration of myocardium by an invasive substance (sarcoidosis, amyloid, tumours)
fibrotic myocardium without an external invasive substance (eg result of radiation exposure)
112
pathophysiology of restrictive cardiomyopathy
walls of ventricles become stiff but not necessarily thickened
compliance of ventricular walls during diastolic filling is reduced, clinical features of HF
113
ECG changes in restrictive cardiomyopathy
reduced QRS, ST segment and T wave changes
114
2 factors causing endocarditis
presence of organisms in the bloodstream
abnormal cardiac endothelium that facilitates their adherence and growth
115
risk factors for abnormal cardiac endothelium in endocarditis
rheumatic HD, congenital HD, age related valve degeneration, prosthetic valve
116
risk factors for organisms in the bloodstream in endocarditis
PWID, ICED, IV lines, septicaemia
117
most common causative organisms of IE for all groups, in native valves and in prosthetic valves
staph aureus (all groups), viridans streptoccoci (native valves), staph epidermidis (prosthetic valves)
118
most common causative organisms in IE in PWID
candida and staph aureus
right sided valves usually effected, especially tricuspid
119
atypical causative organisms of IE
coxiella burneti (farming, aortic valve), HACEK bacteria (associated with poor dental hygiene), brucella (goats), fungi (in immunocompromised patients)
120
signs of infective endocarditis
FROM JANE- finger clubbing, roth spots, osler nodes, murmur, janeway lesions, anaemia, nail bed haemorrhages, emboli
121
investigations in IE
take 3 sets of blood cultures, consider serology if blood cultures are negative to look for 'atypical' organisms
122
treatment for native valve severe sepsis (acute)
flucloxacillin
123
treatment for native valve IE subacute
amoxicillin and gentamicin
124
treatment for prosthetic valve IE
vancomycin and gentamicin, add rifampicin on days 3-5
125
treatment for suspected MRSA IE
vancomycin and gentamicin, add rifampicin on days 3-5
126
treatment for IE in PWID
flucloxicillin
127
treatment for staph aureus IE
flucloxacillin
128
treatment for viridans streptococci IE
benzylpenicillin and gentamicin
129
treatment for staphylococcus epidermidis IE
vancomycin and gentamicin, add rifampicin on days 3-5
130
treatment for enterococcus sp. IE
amoxicillin/vancomycin and gentamicin
131
non-bacterial thrombotic endocarditis
multiple small sterile vegetations which do not destroy valves
can cause embolic disease
132
when does non-bacterial thrombotic endocarditis occur
during a hypercoaguable state, eg pregnancy or cancer
133
libmen-sacks endocarditis
small sterile emboli, often under surfaces of valves or on the chords
occurs more often in patients with lupus
thought to be due to deposition of immune complexes
134
what are cyanotic defects
conditions that cause deoxygenated blood to bypass the lungs and enter systemic circulation, or a mi of oxygenated and deoxygenated blood to enter circulation
135
examples of cyanotic defects
all the T's- truncus arteriosus, tertraology of fallout (ventricular septal defect, pulmonary stenosis, overriding aorta + RV hypertrophy), transposition of the great vessels, tons of others
136
what are acyanotic defects
involve left to right shunting or no shunting
137
examples of acyanotic defects
septal defects- ASD, VSD, AVSD, patient ductus arteriosus (high incidence in pre-term babies), aortic and pulmonary stenosis
138
what medication is used to keep the duct open until alternative shunt/definitive surgery in a newborn duct dependent circulation
IV PGE2
139
what is persistent pulmonary hypertension of the newborn
persitence of/reversion to pulmonary arteriolar constriction, causing a severe reduction in pulmonary blood flow and right to left shunting at the artrial and/or ductal level
140
clinical presentation of persistent pulmonary hypertension
severe cyanosis which does not improve with administration of 100% oxygen
tachypnoea
141
pathophysiology of persistent pulmonary hypertension
elevated resistance in pulmonary arteries -> abnormal smooth muscle development + hypertrophy in walls + right to left shunting via foramen ovale -> systemic hypoxaemia
resistance causes increased load on heart -> right heart dilation, tricuspid insufficiency + right heart failure
142
management of persistent pulmonary hypertension
oxygen, mechanical ventilation support, inhaled nitric oxide, circulatory support
143
causes of pericarditis
viral (mainly echoviruses), bacterial (travel infection elsewhere via bloodstream), fungi (immunosupressed), TB (caseous material in pericardial sac), dresslers sydrome, rheumatic fever, connective tissue disorder
144
what is dresslers syndrome
pericarditis that occurs 4-6 weeks post MI, assumed to be immune mediated
145
symptoms and signs of pericarditis
pleuritic chest pain, worse on inspiration, relieved by sitting up
low grade fever, pericardial friction rub
146
ECG changes with pericarditis
saddle shaped ST elevation, PR interval depression
147
complications of pericarditis
pericardial effusion, tamponade, constrictive pericarditis, cardiac failure, death
148
virchows triad
hypercoagulable state (pregnancy, sepsis, malignancy), endothelial injury (trauma, surgery, venous disorders), circulatory stasis (LV disfunction, immobility, venous obstruction)
149
symptoms and signs of DVT
calf- warm, tender, swelling, redness
pitting oedema
150
investigations for DVT
D dimer test rules out DVT for patients unlikely to have it
US doppler leg scan is diagnostic
151
acute management of DVT
anticoagulation- apixaban/rivaroxaban is first line
152
secondary prevention of DVT
long term anticoagulation with warfarin, a DOAC or LMWH
treatment should be continued for at least 3 months, longer if unprovoked/irreversible factors
153
causes of PE
DVT, atrial fibrillation- blood clots form in atria due to stasis and then embolize to pulmonary arteries
154
clinical presentation of PE
dyspnoea (acute onset), pleuritic chest pain, DVT symptoms, collapse, fever, haemoptysis
155
investigations for likely and unlikely PE
likely- CTPA
unlikely- D-dimer, if positive do CTPA
156
when is V/Q scan used in diagnosing PE
alternative to CTPA
used in patients with renal impairment, contrast allergy, at risk from radiation, pregnant
157
CXR in PE
normal early on in PE (before infarction), used to rule out other causes, wedge-shaped infarct indicates PE
158
acute management of a PE
anticoagulation- apixaban/rivaroxiban is first line
thrombolysis recommended as first line treatment for PE where there is circulatory failure (eg hypotension)
159
secondary prevention of PE
long term anticoagulation- warfarin, a DOAC or LMWH
treatment should be continued for at least 3 months
160
haemorrhagic stroke
bleeding inside/around brain tissue due to rupture of a vessel
caused by hypertension or by a weakened vessel wall
161
ischaemic stroke
clot blocks blood flow to area of brain
clot can be thrombotic, embolic, atheroembolism (embolism formed on plaque) or cardioembolism (embolism formed in heart)
162
transient ischaemic attacks (TIA)
small clot occludes an artery stopping blood flow, clot small so can be dissolved by artery -> symptoms are temporary
163
investigation for a stroke
CT brain +/- angiography
164
management for an ischaemic stroke
thrombolysis up to 4.5 hours from onset of syptoms, thrombectomy up to 6 hours from symptoms onset, usually after having thrombolysis
165
pathophysiology of AF
ectopic foci in pulmonary veins cause irregular atrial rhythm, AV unable transmit beats this quickly -> does so intermittently -> irregular ventricular rhythm
filling time reduced -> reduces CO
allows stasis of blood -> increased stroke risk
166
classification of AF
paroxysmal = <48 hours
persistent = >48 hours
permanent = unable to cardiovert to NSR
167
pulse in AF
irregularly irregular pulse
168
ECG in AF
atrial rate >300bpm, irregularly irregular rhythm, no P waves, narrow QRS
169
acute management of AF
offer rate or rhythm control if onset is <48 hours
offer rate control if onset >48 hours
offer heparin
emergency electrical cardioversion in patients with life-threatening haemodynamic instability
170
medications for rate control of AF
beta blocker- first line
CCB- not preferable in HF
digoxin- only in sedentary people, needs monitoring
AV node ablation
171
offer rate control for AF unless patients have these factors, in which case offer rhythm control
reversible cause for AF
AF is of new onset
AF is causing HF
remain symptomatic despite being effectively controlled
172
methods of rhythm control for AF
cardioversion, beta blocker, dronedarone (after successful cardioversion), amiodarone (patients with HF), LA catheter ablation, Maze procedure
173
pharmacological and electrical cardioversion
pharmacological- flecanide, amioderone
electrical- sedation and use of a cardiac defibrillator
174
paroxysmal AF management
pill in the pocket approach if infrequent episodes without any underlying structural heart disease
take pill (flecanide) to terminate AF when feel symptoms starting
175
what is atrial flutter
form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves
176
pathophysiology of atrial flutte
sustained by micro-reentrant circuit, not all P waves make it to the ventricles so the atria 'flutter'
177
ECG of atrial flutter
atrial 300bpm, ventricular 150bpm, P wave: saw tooth 'F' wave, QRS is normal, rhythm is regular, may be variable
178
treatment for recurrent atrial flutter
catheter ablation, AV nodal blocking agents eg B blockers and class III anti arrhythmics (amiodarone)
179
cause of monomorphic VT
caused by increased automaticity, or due to a reentry circuit within the ventricle
most common cause is scarring of the heart muscle from previous MI
180
cause of polymorphic VT
caused by abnormal ventricular repolarisation
eg long QT syndrome, drug toxicity, electrolyte imbalances
181
symptoms and signs of VT
pre-syncope, hypotension, cardiac arrest
pulse rate is 120-220 bpm
182
ECG changes in monomorphic VT
constant QRS morphology, broad complex rhythm, rapid rate
183
ECG changes in polymorphic VT
QRS complex varies in amplitude
184
ECG changes in torsade de pointes
specific polymorphic VT associated with a long QT interval, QRS complexes appear to twist around the isoelectric line
185
medical management of stable VT
anti-arrhythmic drugs (amiodarone, lignocaine), DCCV if fails
186
ECG changes in VF
bizarre irregular waveforms, no recognisable QRS complexes, random frequency and amplitude, uncoordinated electrical activity
187
what is brugada syndrome
inheritable condition, idiopathiv VF with no evidence of causative structural cardiac disease
188
VF triggers in brugada syndrome
sleep, fever, excessive alcohol, large meals, some drugs (b blockers, psychotropics, analgesics, anaesthetics)
189
ECG findings in brugada syndrome
ST elevation, RBBB in V1-3
190
triggers for QT prolongation and torsades de pointes
potassium rich foods, diarrhoea, vomiting, underwater breath holding, exercise, sleep, sudden loud noise
191
clinical presentation of long QT syndrome
develop syncope and palpitations as a result of polymorphic VT (torsades de pointes)
192
ECG findings in long QT syndrome
torsades de pointes, QT interval > 0.5 seconds
193
supraventricular tachycardia
abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart
194
cause of supraventricular tachycardia
caused by electrical signal re-entering the atria from the ventricles
195
AV nodal re-entrant tachycardia
re-entry circuit forms within the AV node, most common cause of SVT in patients with structurally normal heart
196
AV re-entrant tachycardia
involves an accessory pathway usually located in the valvular rings, most commonly caused by Wolff-Parkinson-White syndrome
196
197
ectopic atrial tachycardia
occurs when the electrical signal originates in the atria somewhere other than the sinoatrial node
198
acute management of stable patients with SVT
valsalva manoeuvre, carotid sinus massage, IV adenosine (verapamil is an alternative), DCCV if all fail
199
ECG in supraventricular tachycardia
fast narrow complex tachycardia, QRS < 0.12 seconds
200
long term management of patients with paroxysmal SVT
medication- beta blockers, CCBs, amiodarone
radiofrequency ablation
201
wolff-parkinson-white syndrome
genetic disorder that allows abnormal conduction to occur in the heart via an accessory pathway
202
pathophysiology of w-p-w syndrome
have an accessory pathway called bundle of kent that allows the signal to return to the atria from the ventricles.
this creates a re-entrant loop that predisposes to tachyarrhythmias (AF, AFlutter, AVRT)
203
ECG findings in w-p-w syndrome
slurred upstroke on QRS complex (delta wave), short PR interval, wide QRS complex
204
definitive treatment of w-p-w syndrome
radiofrequency ablation of the accessory pathway
205
1st degree heart block
PR interval > 0.2 seconds, does not usually require treatment, long term follow recommended
206
2nd degree heart block
intermittent absence of QRS complexes- mobitz type 1 and type 2
207
mobitz type 1 heart block
2nd degree heart block, progressive lengthening of PR interval, eventually resulting in a dropped beat (P wave with no QRS)
208
mobitz type 2 heart block
2nd degree heart block, each P wave is associated with a QRS complex until there is one P wave that is not followed by a QRS, often progresses to 3rd degree AV block
209
3rd degree heart block
complete atrial block- atrial contraction is normal but no beats are conducted to the ventricles. no relation between P and QRS but both are present
210
atrial regurgitation
reflux of blood from the aorta through the aortic valve into the LV during diastole
211
causes of aortic regurgitation
valve disease (rheumatic fever, IE, bicuspid aortic valve), aortic root disease (aortic dissection, hypertension, Marfans, Ehler-Danlos
212
signs of aortic regurgitation
high pitched early diastolic murmur best heard at left sternal edge 4th ICS with patient leaning forward and breath held in
collapsing pulse
apex beat displaced laterally and downwards
213
when is valve replacement indicated for aortic regurgitation
symptomatic patients and asymptomatic patients when LV function begins to deteriorate
214
aortic stenosis
aortic valve is too small, narrow or stiff, resulting in obstruction of blood flow from LV to aorta during systole
215
causes of aortic stenosis
younger patients- congenital bicuspid valve, older patients- calcifications on aortic valve, rheumatic heart disease
216
signs of aortic stenosis
ejection systolic murmur best heard at 2nd right ICS right sternal edge, radiates to carotids
217
mitral regurgitation
occurs when blood leaks back through the mitral valve during systole
218
causes of mitral regurgitation
primary valve disorder (IE, MI causing valve prolapse, rheumatic fever), secondary to LV dysfunction (from cardiomyopathy or post MI)
219
signs of mitral regurgitation
pan-systolic murmur best heard at the apex, radiates to the axilla, displaced apex
220
medication for mitral regurgitation
diuretics, ACEi if HF develops
221
mitral stenosis
occurs when there is obstruction to flow throught the mitral valve during diastole
222
causes of mitral stenosis
rheumatic fever, calcification related to age, congenital
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why can mitral stenosis cause AF
MS causes pressure in LA to remain elevated, so atria enlarges -> can cause AF
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signs of mitral stenosis
mid diastolic murmur best heard at apex, malar flush, tapping apex beat
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medication for mitral stenosis
diuretics, treat AF
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what does an innocent murmur sound like
soft, early systolic, short and non-radiating murmur
