cardio Flashcards
what is stable angina
heavy tight gripping chest pain relieved by rest and worse on exertion
a symptom that occurs as a consequence of restricted coronary blood flow
Rfs of angina
diabetes mellitus
smoking
hypertension
when does angina occur (e.g of each)
when oxygen demand does not meet supply
- blood flow impaired (proximal arterial stenosis)
- increasted distal resistance (LV hypertrophy)
- decrease in o2 capacity of blood (anaemia)
why does a small change in radius cause large change in blood flow
pouiselles law - r^4
what is an example of blood flow impairment causing angina
proximal arterial stenosis
causes of angina (stable)
atheroma
anaemia
cardiac abnormalities (aortic stenosis)
pathophysiology behind angina mismatch on exertion
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
classifications of angina
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
clinical features of stable angina
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
what is unstable angina
deteriation of previiously stable angina with symptoms frequently occuring at rest recent onset (<24hrs)
unstable angina buzz word clin features
crescendo pattern chest pain increasing freq and severity breathless new onset chest pain - pleuritic INDIGESTION
difference between unstable angina and NSTEMI
no occludinig thrombus in unstable angina so no myocardial necrosis
= NORMAL TROPONIN or CK-MB
NSTEMI occlusions?
partial major coronary artery occlusion
complete minor coron artery occlusion
previously effected by atherosclerosis
NSTEMI muscle damage description
only partial thickness damage of heart muscle
what is an acute coronary syndrome an umbrella term fro
unstable angina nstemi and stemi
what is a STEMI
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
bloods results from stemi
elevated troponin T and I (most sensitive)
high creatine kinase MB (CK-MB)
ECG of STEMI at presentation
pathological Q wave
ST elevation
tall T waves
DDx of an MI
stabel and unstable angina pneumonia pneuomothorax GORD acute gastritis pancreatitis
Signs of an MI
pallor and clammy sweating signif hypotension 4th heart sound (forceful atria contraction overcoming stiff dysfunctional ventricle) pansystolic murmur
symptoms of MI
sharp crushing chest pain over 20mins - radiate jaw, LEFT ARM, neck doesnt respond to GTN spray nausea SOB palpatations
Lifestyle MI modifications
stop smoking
healthy diet
2’ prevention - statins, warfarin, ACEi
ACUTE Mx of an MI
MONA Morphine Oxygen Nitrates Aspirin
STEMI Mx
if in 2hrs = PCI
BB (atenolol)
ACEi
Clopidogrel
complications of an MI
cardiac arrest unstable angina bradycardias, heart block tachyarrythmias pericarditis (STEMI) DVT/PE/systemi embolism heart failure (ventric dysfunction post necrosis)
causes of LBBB
ischaemic heart disease
aortic valve disease
LV hypertrophy
causes of RBBB
pulm embolism
ischaemic heart disease
atrial/ventric septal defects
RHV
Tx of BBBs
pacemakers
appearance of v1 and v6 leads in RBBB
MaRRoW
v1 = M
v6 = W
appearance of v1 and v6 leads in LBBB
WiLLiaM
v1=W
v6=M
1st degree AV block findings
PR prolongations (>0.22s) constant every atrial signal - ventricle but w delay
2nd degree AV block findings (type 1 / Mobitz 1)
PR interval progressivley longer until dropped beat (no QRS complex) - ventricle escape beats
2nd degree AV block findings Mobitz 2
PR interval constant, QRS complexes randomly dropped
failure to conduct through purkinje system
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
what heart block type does an anterior MI cause
2nd degree/ mobitz 2
what type of heart block does a inferior MI cause
1st degree (and 2nd degree mobitz 1)
symptoms of a 1st degree AV block
none
symptoms of a 2nd degree mobitz 1 AV heart block
usually none but lightheaded, dizziness, syncope
symptoms of a 2nd degree mobitz 2 AV block
SOB, postural HTN, chest pain
symptoms of a 3rd degree AV block
fatigue, lightheadedness, blackout
causes of a 2nd degree mobitz 2 av block
anterior MI
mitral valve surgery
SLE
rheumatic fever
Causes of a 2nd degree mobitz 1 AV bock
AVN blockers so BB or CCBs or Digoxin
or inferior MI
causes of 1st degree AV block
inferior MI, hypokalaemia, AVN drugs (BBs, CCBs, Digoxin)
Tx of 2nd degree mobitz 2 block
pacemaker
tx of 3rd degree av block
IV atropine (slows HR) but if chronic = pacemaker
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)
what do you see on the CXR of heart failure
Alevolar oedema B- kerley B lines Cardiomegaly Dilated prominaent upper lobe vessels Effusion (pleural)
What is heart failure
a clinical syndrome in whihc eh heart cannot provide sufficient output to meet the bodys demands
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
causes of heart failure -
ischaemic heart disease MI Cardiomyopathy ventric hypertrophy - HTN aortic stenosis mitral/ aortic regurg anaemia obesity hyperthyroidism
3 cardinal features of Heart Failure
SOB
fatigue
ankle oedema
L sided heart failure what happpens
blood backs up into lungs
R sided heart failure what happens
blood backs up to the body (liver etc)
L sided heart failure sympotoms
SOB, lowered exercise tolerance, frothy sputum cough (nocturnal), fatigue, paraoxysmal norturnal dypsnoea (SOB at night)
L sided heart failure signs
tachycardia cardiomegaly (displaced apex beat) crepitations in lung bases cool peripheries 3rd n 4th heart sounds
R sided heart failure symptoms
peripheral oedema ascites fatigue nausea anorexia
R sided heart failure signs
peripheral oedema increased JVP hepatomegaly pitting oedema ascites weight gain (fuid)
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
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
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)
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
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
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
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
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
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)
Lifestyle mods for cardiac failure
obesitiy,stop smoking, diet (decrease salt), decrease alcohol
acute heart failure management
100% oxygen, nitrates (dilates vessels), IV furosemide (fluid overload) IV opiates (diamorphine)
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
what is pericarditis
inflam of the peritoneum - fluid builds up and puts pressure on heart so cannot pump
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
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
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
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
what is becks triad
3 Ds
Distant heart sounds
Distended jug veins
Decreased arterial p
what is becks triad assos with
pericarditis
what is a sign of cardiac tamponade
pulsus paradozus (ventric independence) heart cant fully stretch between cotnractions so doesnt filll so CO decreases
what is contrictive pericarditis
caused by TB = thick and fibrous and calcified so inelastic so decerased diastolic filling
what causes constrictive pericarditis
TB
Tx for pericarditis
NSAID OR aspirin
colchicine if symtp still (SE = nausea)
signs of acute periph vasc disease
6 P's! Pain Pallor Pulseless Paresthesia Paralysis Perishingly cold
how diagnose PVD
brachial ankle pulse index (0.5-0.9 =intermit claudication, <0.5 = crit limb ischaemia)
signs of PVT
absent leg pulses
feet cold
first line BP drugs for above 55 and not afro
ACEi or ARBs
70yo bp first line
CCB (CI if have oedema or heart failure risk)
40 year old afro bp first line
CCB
2nd line BP
A + C (CCC)
3rd line BP
A + C + D (thiazide like diuretic)
4th line BP
A + C + D + further D + alpha or beta blocker
SE of ACE-i
dry cough as less aldosterone so bradykinin accumulates = rash also
SE of BB
fatigue and dizzy
BB beta1 selective
cardio (1 = 1 heart)
BB beta2 selective
lungs (2 = 2 lungs)
CCB SE
ankle oedema - vasodilaters and L-type C channel blcokers
why does hypertension cause
PVD
cerebrovascular disease
isch. heart disease
how to diagnose HTN
24hr ambulatory bp monitoring
assess QRISK2 (for heart risk)
sphygmomanometer,
what is classed as hypertension (figures)
over 140/90mmHg
135/85mmHg if 24hr ambulatory bp monitoring
what are the 2 types of HTN
primary/essential - idiopathic
secondary - has a cause
causes of secondary HTN
renal disease oral contraceptive pill pregnancy acromegaly cushings conn's CKD
what is malignant HTN
rapid rise in BP - vascular damage MED EMERGENCY
>200/120mmHg
CFs of malignant hypertenstion
headaches, visual distrubances, bilateral retinal haemorrhages
Complications of malignant HTN if not treat quick
aortic disection, MI, pulm oedema
things you look for to assess HTN endstage organ damage
FUNDOSCOPY - eyes - papilloedema, retinal haemorrhage
CARDIAC - ECG - LV hypertrophy
KIDNEYS - urinalysis
RFs of HTN
afro carrib
high BMI
lifestyle (smoking sedatory life style alchol diet)
Atrial fib complicatios
increases stroke risk by 5x
what do you give patients with AF to prevent stroke risk
warfarin
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
what do you see on an ECG with AF
quivering baseline, irreg QRS complexes, 100-175bpm
what causes AF
anything that increases atrial pressure/muscle mass/inflam/fibrosis rheumatoid heart disease heart failure XS alcohol HTN valv heart disease
CFs of AF
palpitations fatigue dizziness chest pain IRREGULARLY IRREGULAR PULSE
Dx of AF
ECG - no P waves (fine oscillations), QRS = irregular
IRREG IRREG PULSE
DDx of AF
atrial flutter, supraventricular tachycardias
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
how would you manage acute atrial fib
rate control + anticoag + correct metabolite imbalance
how to you control rate with AF
AV node blockers - CCB (verapamil)
BBs (bisoprolol) digoxin, amiodarone
RF of AF
age, DM, obesity, XS alcohol, CVD, hyperthyroidism
what is infective endocarditis
infection of heart valve or areas lined by endocardium
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
RF for Infective endocarditis
IVDU IV cannula pacemaker poor dental hygiene cardiac surgery
causes of infective endocarditis - organisms
Staph aureus - IVDU, surgery, diabetes
Strep virdians - dental
Staph epidermis
Tx of staph aureus caused infection endocarditis
flucoxacilli
Tx of strep virdians caused IE
Benzylpenicillin + Gentamycin
Tx of IE
ABx - specific to blood cultures organism (4-6wks)
surgery to remove infected devices
tx complications (heart failure, arrhytmias)
why do organisms grow in IE
damaged endocardium promotes platelet and fibrin depostion and organisms adhere and grow = vegitaiton
CF pneumonic for IE
FROM JANE
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
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
Causes of IE
abnormal valves (regurg or prosthetic)
surgery
bacteriaemia
malignancy/prev IE
characteristic feature of aortic dissection
TEARING chest pain radiates to back
vomiting, LoC, sweating and shock
what is aortic diessection
a tear inside of the aorta and blow flows in between the layers forcing them apart creating a false lumen
causes of aortic dissection
atherosclerotic, marfans, trauma, cocaine
why do you get unequal pressure in arms in aortic disection
as disection extends, branches seclude sequentially causing hemiplagia (L sided paralysis)
why can you get neurological symptoms in severe aortic disection
spinal cord blood supply cut off
characteristic CT scan sign for aortic disection
tennis ball sign
Dx of aortic disection
absent peripheral pulses
CT - tennis ball sign
CXR - widened mediastinum
Mx of aortic disection
BBs (metorolol), oxygen, BP ocntrol, surgical repair, morphine (analgesia)
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
2 types of annueurysm
if dilation over 50% orginial diameter
true - involves all layers
false (=pseudoanneurysm) blood collects in outer layer only (adventitia)
causes of aortic aneurysm
atherosclerosis connective tissue (marfans) HTN obesity trauma
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
Dx of AAA
abdo US - >3cm across
CT or MRI angiography scans
DDx of AAA
GI bleed, isch bowel dis, appendicitus
Tx of AAA
treat underlying cause
Rf modification - anti hypertensives, stop smoking
Surgery - graft onto aorta
characteristic finding of atrial flutter
saw tooth flutter waves (F waves) between QRS
4 features of tetralogy of fallot
pulm stenosis
r ventric hypertrophy
overriding aorta
ventric septal defect
CXR finding of tetralogy of fallot
boot shaped (due to RV hypertrophy)
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
CFs of tet of fallot
syncope squatting fail to thrive clubbing CYANOSIS
why tet of fallot cyanosed
shunt from r to left so less blood to lungs to get oxygenated
