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cardio Flashcards

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1
Q

what is stable angina

A

heavy tight gripping chest pain relieved by rest and worse on exertion
a symptom that occurs as a consequence of restricted coronary blood flow

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2
Q

Rfs of angina

A

diabetes mellitus
smoking
hypertension

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3
Q

when does angina occur (e.g of each)

A

when oxygen demand does not meet supply

  1. blood flow impaired (proximal arterial stenosis)
  2. increasted distal resistance (LV hypertrophy)
  3. decrease in o2 capacity of blood (anaemia)
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4
Q

why does a small change in radius cause large change in blood flow

A

pouiselles law - r^4

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5
Q

what is an example of blood flow impairment causing angina

A

proximal arterial stenosis

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6
Q

causes of angina (stable)

A

atheroma
anaemia
cardiac abnormalities (aortic stenosis)

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7
Q

pathophysiology behind angina mismatch on exertion

A

epicardial resistance high therefore microvasc is low to compensate (dilates to increase bf)
when excercise o2 demmand increases but cannot dilate further as already compensated so chest pain =angina

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8
Q

classifications of angina

A 
3/3 = typical angina
2/3 = atypical 
1/3 = non anginal pain
constricting heavy chest pain radiating to chest/jaw/neck/arm
occurs w exertion/stress
relieved by rest or GTN spray
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9
Q

clinical features of stable angina

A

heavy constricting chest pain radiating to chest jaw neck arm occuring on exertion/stress relieved by rest/ gtn spray
SOBOE
fatigue
N&V
sweating
xanthoma (lipid deposition in skin) = A SIGN

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10
Q

what is unstable angina

A 
deteriation of previiously stable angina with symptoms frequently occuring at rest
recent onset (<24hrs)
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11
Q

unstable angina buzz word clin features

A 
crescendo pattern chest pain
increasing freq and severity
breathless
new onset chest pain - pleuritic
INDIGESTION
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12
Q

difference between unstable angina and NSTEMI

A

no occludinig thrombus in unstable angina so no myocardial necrosis
= NORMAL TROPONIN or CK-MB

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13
Q

NSTEMI occlusions?

A

partial major coronary artery occlusion
complete minor coron artery occlusion
previously effected by atherosclerosis

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14
Q

NSTEMI muscle damage description

A

only partial thickness damage of heart muscle

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15
Q

what is an acute coronary syndrome an umbrella term fro

A

unstable angina nstemi and stemi

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16
Q

what is a STEMI

A

comlete occlusion of major coron artery previously affected by atherosclerosis
full thickness dameae of heard muscles so sub enthothelial myocardium - infarct zone spreads to subepicardial myocardium = transmural Q wave

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17
Q

bloods results from stemi

A

elevated troponin T and I (most sensitive)

high creatine kinase MB (CK-MB)

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18
Q

ECG of STEMI at presentation

A

pathological Q wave
ST elevation
tall T waves

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19
Q

DDx of an MI

A 
stabel and unstable angina 
pneumonia
pneuomothorax
GORD
acute gastritis
pancreatitis
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20
Q

Signs of an MI

A 
pallor and clammy
sweating
signif hypotension
4th heart sound (forceful atria contraction overcoming stiff dysfunctional ventricle)
pansystolic murmur
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21
Q

symptoms of MI

A 
sharp crushing chest pain over 20mins - radiate jaw, LEFT ARM, neck
doesnt respond to GTN spray
nausea
SOB
palpatations
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22
Q

Lifestyle MI modifications

A

stop smoking
healthy diet
2’ prevention - statins, warfarin, ACEi

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23
Q

ACUTE Mx of an MI

A 
MONA
Morphine
Oxygen
Nitrates
Aspirin
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24
Q

STEMI Mx

A

if in 2hrs = PCI
BB (atenolol)
ACEi
Clopidogrel

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25
complications of an MI
``` cardiac arrest unstable angina bradycardias, heart block tachyarrythmias pericarditis (STEMI) DVT/PE/systemi embolism heart failure (ventric dysfunction post necrosis) ```
26
causes of LBBB
ischaemic heart disease aortic valve disease LV hypertrophy
27
causes of RBBB
pulm embolism ischaemic heart disease atrial/ventric septal defects RHV
28
Tx of BBBs
pacemakers
29
appearance of v1 and v6 leads in RBBB
MaRRoW v1 = M v6 = W
30
appearance of v1 and v6 leads in LBBB
WiLLiaM v1=W v6=M
31
1st degree AV block findings
``` PR prolongations (>0.22s) constant every atrial signal - ventricle but w delay ```
32
2nd degree AV block findings (type 1 / Mobitz 1)
PR interval progressivley longer until dropped beat (no QRS complex) - ventricle escape beats
33
2nd degree AV block findings Mobitz 2
PR interval constant, QRS complexes randomly dropped | failure to conduct through purkinje system
34
3rd degree AV block
signal blocked completely = no electrical pulses to ventricles A and V act INDEPENDENTLY = no assos between PR and QRS slow ventric escape beats
35
what heart block type does an anterior MI cause
2nd degree/ mobitz 2
36
what type of heart block does a inferior MI cause
1st degree (and 2nd degree mobitz 1)
37
symptoms of a 1st degree AV block
none
38
symptoms of a 2nd degree mobitz 1 AV heart block
usually none but lightheaded, dizziness, syncope
39
symptoms of a 2nd degree mobitz 2 AV block
SOB, postural HTN, chest pain
40
symptoms of a 3rd degree AV block
fatigue, lightheadedness, blackout
41
causes of a 2nd degree mobitz 2 av block
anterior MI mitral valve surgery SLE rheumatic fever
42
Causes of a 2nd degree mobitz 1 AV bock
AVN blockers so BB or CCBs or Digoxin | or inferior MI
43
causes of 1st degree AV block
inferior MI, hypokalaemia, AVN drugs (BBs, CCBs, Digoxin)
44
Tx of 2nd degree mobitz 2 block
pacemaker
45
tx of 3rd degree av block
IV atropine (slows HR) but if chronic = pacemaker
46
what can u see on BBBs ECG
wide QRS complex w abnormal pattern shape depending on L or R BBB (due to ventric contraction longer due to delay)
47
what do you see on the CXR of heart failure
``` Alevolar oedema B- kerley B lines Cardiomegaly Dilated prominaent upper lobe vessels Effusion (pleural) ```
48
What is heart failure
a clinical syndrome in whihc eh heart cannot provide sufficient output to meet the bodys demands
49
causes of heart failure principals
systolic - V cant contract normally = decreased EF diastolic - inability to relax and fill = incomplete filling hypertension - increased afterload = compensatory hypertrophy = less space for filling = lowers CO increase myocardial work
50
causes of heart failure -
``` ischaemic heart disease MI Cardiomyopathy ventric hypertrophy - HTN aortic stenosis mitral/ aortic regurg anaemia obesity hyperthyroidism ```
51
3 cardinal features of Heart Failure
SOB fatigue ankle oedema
52
L sided heart failure what happpens
blood backs up into lungs
53
R sided heart failure what happens
blood backs up to the body (liver etc)
54
L sided heart failure sympotoms
SOB, lowered exercise tolerance, frothy sputum cough (nocturnal), fatigue, paraoxysmal norturnal dypsnoea (SOB at night)
55
L sided heart failure signs
``` tachycardia cardiomegaly (displaced apex beat) crepitations in lung bases cool peripheries 3rd n 4th heart sounds ```
56
R sided heart failure symptoms
``` peripheral oedema ascites fatigue nausea anorexia ```
57
R sided heart failure signs
``` peripheral oedema increased JVP hepatomegaly pitting oedema ascites weight gain (fuid) ```
58
heart failure pathophysiology
starts to fail so initiates compensatory changes to maintain CO and peripheral perfusion) as heart failure progresses the mechanisms get overwhelmed and turn pathological = DECOMPENSATION
59
role of Sympathetic stim in heart failure
pos inotropic effect (force of contraction) pos chronotropic effect incresaes heart rate in heart failure - down regulates receptors and CO no longer increases in response
60
role of increasing preload in heart fail
heart muscle falure so more blood in ventricles after systole = increase in diastolic vol = stretches the myocardium = gets to point where no longing increses contraction force (STARLINGS)
61
increasing afterload heart fail patho
resistance against which the ventricle contracts increases - increases in afterload - increase end diastolic vol and decreases stroke vol = decrease cardiac output. V dilates - fither excaberates the issue
62
effect of RAAS in heart failure patho
decreasing cardiac output decresaes renal perfusion this activates RAAS increase in aldosterone - increases NA reabsorption and h2O reabsoption - ADH release = H2O retention this increases blood volume increasing BP and venous p. therefore increase preload and the stretch and force of heart contraction incresae of contraction req more energy and blood to cardiac myoctyes - heart fail = no increase in blood so die and force decreases along with CO === toxic effects
63
what does adrenic activation do to heart in heart failure
increases HR/contractility hence increasing cardiac work = myocyte damage = decrease in CO causes vasocontriction = increases afterload = increases cardiac work and thus myocyte damage thus decreasing CO
64
what does a lack of renal perfusion cause in iheart fail
RAAS activation - Na and h2O retention = increases preload as increases vol of blood = increasing cardiac work and thus myoctye dmage causes vasocontriction increasing afterload and cardiac work
65
what is the Dx of heart failure
CXR, bloods (B type natriuretic peptide, increased ANP, D-dimer, U&Es, FBC) cardiac enzymes - creatine kinase, toponin I and T Echo - LV dysfunction and structural causes
66
Mx of hert failure
diuretics (furosemide) ACEi (SE-cough) Aldosterone antagonists Beta Blockers Digoxin ( SE= yellow rings around lights) - inhibs Na/K Angiotensin-II recep blockers (corsartan)
67
Lifestyle mods for cardiac failure
obesitiy,stop smoking, diet (decrease salt), decrease alcohol
68
acute heart failure management
100% oxygen, nitrates (dilates vessels), IV furosemide (fluid overload) IV opiates (diamorphine)
69
what is found in bloods of heart falure
B type natriuretic peptide - secreted in response to ventricular wall stress CK-MB ANP - myocyte stretch - cardiomegaly troponin I and T
70
what is pericarditis
inflam of the peritoneum - fluid builds up and puts pressure on heart so cannot pump
71
causes of pericarditis
``` CARDIAC RIND C- colagen vasc disease A - aortic anneurysm R - radiation D- drugs - penicillin I- infections - viral (coxsacki B, enterovirus) bacterial (TB) A - acute renal failure - uraemic = ac of toxins C - cardiac infarction ``` R- rheumatic fever/ arthritis I- Injury N - neoplsam D- dresslers - post MI = autoimm secondary form of pericarditis 2-10wks after
72
CFs of pericarditis
chest pain - relieved by sitting forward (ON A HORSE), exacerbated by lying down pleuritic and radiates to trapezium ridge Friction rub Fever Signs of pericardial effusion - dyspnoea
73
Dx pericaditis BUZZ WORDS
SADDLE SHAPED ST ELEVATION "not in a CAR u are on a horse SADDLE shaped ST elevation, lean forward t waves flatten Bloods - increased troponin CXR - cardiomegaly and pericardial effusion
74
what is cardiac tamponade
build up of fluid in pericarditis - constricts the heart | tamponade = p. obsstruction flow = decresed CO, HYPOTENSION, decreased tissue perfusion increased HR
75
what is becks triad
3 Ds Distant heart sounds Distended jug veins Decreased arterial p
76
what is becks triad assos with
pericarditis
77
what is a sign of cardiac tamponade
``` pulsus paradozus (ventric independence) heart cant fully stretch between cotnractions so doesnt filll so CO decreases ```
78
what is contrictive pericarditis
caused by TB = thick and fibrous and calcified so inelastic so decerased diastolic filling
79
what causes constrictive pericarditis
TB
80
Tx for pericarditis
NSAID OR aspirin | colchicine if symtp still (SE = nausea)
81
signs of acute periph vasc disease
``` 6 P's! Pain Pallor Pulseless Paresthesia Paralysis Perishingly cold ```
82
how diagnose PVD
brachial ankle pulse index (0.5-0.9 =intermit claudication, <0.5 = crit limb ischaemia)
83
signs of PVT
absent leg pulses | feet cold
84
first line BP drugs for above 55 and not afro
ACEi or ARBs
85
70yo bp first line
CCB (CI if have oedema or heart failure risk)
86
40 year old afro bp first line
CCB
87
2nd line BP
A + C (CCC)
88
3rd line BP
A + C + D (thiazide like diuretic)
89
4th line BP
A + C + D + further D + alpha or beta blocker
90
SE of ACE-i
dry cough as less aldosterone so bradykinin accumulates = rash also
91
SE of BB
fatigue and dizzy
92
BB beta1 selective
cardio (1 = 1 heart)
93
BB beta2 selective
lungs (2 = 2 lungs)
94
CCB SE
ankle oedema - vasodilaters and L-type C channel blcokers
95
why does hypertension cause
PVD cerebrovascular disease isch. heart disease
96
how to diagnose HTN
24hr ambulatory bp monitoring assess QRISK2 (for heart risk) sphygmomanometer,
97
what is classed as hypertension (figures)
over 140/90mmHg | 135/85mmHg if 24hr ambulatory bp monitoring
98
what are the 2 types of HTN
primary/essential - idiopathic | secondary - has a cause
99
causes of secondary HTN
``` renal disease oral contraceptive pill pregnancy acromegaly cushings conn's CKD ```
100
what is malignant HTN
rapid rise in BP - vascular damage MED EMERGENCY | >200/120mmHg
101
CFs of malignant hypertenstion
headaches, visual distrubances, bilateral retinal haemorrhages
102
Complications of malignant HTN if not treat quick
aortic disection, MI, pulm oedema
103
things you look for to assess HTN endstage organ damage
FUNDOSCOPY - eyes - papilloedema, retinal haemorrhage CARDIAC - ECG - LV hypertrophy KIDNEYS - urinalysis
104
RFs of HTN
afro carrib high BMI lifestyle (smoking sedatory life style alchol diet)
105
Atrial fib complicatios
increases stroke risk by 5x
106
what do you give patients with AF to prevent stroke risk
warfarin
107
what is atrial fib
continuous rapid activation of the atria causing uncoordinated depolarisation with not all impulses going to the ventricles = decresae in cardiac output
108
what do you see on an ECG with AF
quivering baseline, irreg QRS complexes, 100-175bpm
109
what causes AF
``` anything that increases atrial pressure/muscle mass/inflam/fibrosis rheumatoid heart disease heart failure XS alcohol HTN valv heart disease ```
110
CFs of AF
``` palpitations fatigue dizziness chest pain IRREGULARLY IRREGULAR PULSE ```
111
Dx of AF
ECG - no P waves (fine oscillations), QRS = irregular | IRREG IRREG PULSE
112
DDx of AF
atrial flutter, supraventricular tachycardias
113
how would you treat chronic AF
``` rate control (BBs CCBs) and anticoag (DOACs, warfarin) cardioversion - convert to sinus rhythm AND GIVE LMWH to reduce thromboemboli risk ```
114
how would you manage acute atrial fib
rate control + anticoag + correct metabolite imbalance
115
how to you control rate with AF
AV node blockers - CCB (verapamil) | BBs (bisoprolol) digoxin, amiodarone
116
RF of AF
age, DM, obesity, XS alcohol, CVD, hyperthyroidism
117
what is infective endocarditis
infection of heart valve or areas lined by endocardium
118
how do you diagnose infective endocarditis
DUKES CRITERIA major - pos blood culture, endocarium involvment, new valve regurg minor - vasc signs, pos echo, fever over 38 degrees, preidsposition (IVDU) IE if 2x major or 1x major + 3x minor OR all minor
119
RF for Infective endocarditis
``` IVDU IV cannula pacemaker poor dental hygiene cardiac surgery ```
120
causes of infective endocarditis - organisms
Staph aureus - IVDU, surgery, diabetes Strep virdians - dental Staph epidermis
121
Tx of staph aureus caused infection endocarditis
flucoxacilli
122
Tx of strep virdians caused IE
Benzylpenicillin + Gentamycin
123
Tx of IE
ABx - specific to blood cultures organism (4-6wks) surgery to remove infected devices tx complications (heart failure, arrhytmias)
124
why do organisms grow in IE
damaged endocardium promotes platelet and fibrin depostion and organisms adhere and grow = vegitaiton
125
CF pneumonic for IE
FROM JANE
126
Cf of IE
Fever Roth spots (retina) Osler nodes (fingers n toes) Murmor (NEW) Janeway lesions - non tneder red fingers palms, soles Anaemia Nail haemorrhages - splinters, haemorrhage Emboli (---STROKE, MI, kindey dysfunction) also clubbing and splenomegaly
127
how to Dx IE - tests done
Echo - transoesphageal, transthoracic bugs grown on cultures - 3x diff sites over 24hrs bloods - normocytic, normochromic anaemia, increased ESR, CRP, neutrophilia
128
Causes of IE
abnormal valves (regurg or prosthetic) surgery bacteriaemia malignancy/prev IE
129
characteristic feature of aortic dissection
TEARING chest pain radiates to back | vomiting, LoC, sweating and shock
130
what is aortic diessection
a tear inside of the aorta and blow flows in between the layers forcing them apart creating a false lumen
131
causes of aortic dissection
atherosclerotic, marfans, trauma, cocaine
132
why do you get unequal pressure in arms in aortic disection
as disection extends, branches seclude sequentially causing hemiplagia (L sided paralysis)
133
why can you get neurological symptoms in severe aortic disection
spinal cord blood supply cut off
134
characteristic CT scan sign for aortic disection
tennis ball sign
135
Dx of aortic disection
absent peripheral pulses CT - tennis ball sign CXR - widened mediastinum
136
Mx of aortic disection
BBs (metorolol), oxygen, BP ocntrol, surgical repair, morphine (analgesia)
137
what is an aneurysm
permanent dilation of an artery cause by weaknes in vessel wall - cant withdtand pressure so diameter increases. assos w fibrosis and myocyte atrophy
138
2 types of annueurysm
if dilation over 50% orginial diameter true - involves all layers false (=pseudoanneurysm) blood collects in outer layer only (adventitia)
139
causes of aortic aneurysm
``` atherosclerosis connective tissue (marfans) HTN obesity trauma ```
140
CFs of aortic ann
asymtp if unruptured - abdo back loin gorun pain. pulastile abdo swelling ruptured - intermit or continuous abdo pain radiates to back-iliac fossa- groin tachycardia anaemia sudden death hypotension collapse and shock
141
Dx of AAA
abdo US - >3cm across | CT or MRI angiography scans
142
DDx of AAA
GI bleed, isch bowel dis, appendicitus
143
Tx of AAA
treat underlying cause Rf modification - anti hypertensives, stop smoking Surgery - graft onto aorta
144
characteristic finding of atrial flutter
saw tooth flutter waves (F waves) between QRS
145
4 features of tetralogy of fallot
pulm stenosis r ventric hypertrophy overriding aorta ventric septal defect
146
CXR finding of tetralogy of fallot
boot shaped (due to RV hypertrophy)
147
why do children w tet of fallot squat alot
kinks femoral arteries, incresaing periph vascuarl resistance causing increasing p of systemic circulation - increase p of LV till becomes greater than RV causing shunt to REVERSE -- from L to R again and blood gets oygenated - decrease cyanosis
148
CFs of tet of fallot
``` syncope squatting fail to thrive clubbing CYANOSIS ```
149
why tet of fallot cyanosed
shunt from r to left so less blood to lungs to get oxygenated

2a RRS (26 decks)

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