Cardio Week 5 Flashcards
what causes the decrease of blood flow in acute coronary syndromes
rupture of atherosclerotic plaque resulting in thrombus
what markers does myocardial damage release
troponin T and I (also enzyme CK)
what is the diagnosis of NSTEMI
elevated levels of these markers but no ST elevation
what is the diagnosis of unstable angina
demonstrate symptoms of ACS but have neither ST elevation or raised troponin
what may NSTEMIs and UA be associated with in terms of an ECG
ST depression and T wave inversion
what are the symptoms of UA/NSTEMI
resemble those of stable angina, but are frequently more painful, intense and persistent, often lasting at least 30 minutes
what is the typical presentation of UA/NSTEMI
unrelieved by GTN, angina of recent onset brought on by minimal exertion, angina at rest/minimal exertion or post MI angina
what is the physiopathology of UA/NSTEMI
compared to stable, plaques found in ACS tend to have thinner fibrous cap and larger lipid core - especially vulnerable to being ruptured
this exposed plaque (vulnerability to rupture) causes what
platelet aggregation and thrombosis causes local generation of vasoconstrictors such as thromboxane A2 and seratonin
when is revascularisation considered for patients in UA/NSTEMI
patients with high risk of very significant coronary arerty disease, or if drug treatment fails to control symptoms
what drugs are immediately given in UA/NSTEMI
300mg aspirin (antiplatelet) then 75mg/day for life also clopidogrel which inhibits ADP stimulated platelet aggregation
what drugs could be given in the long term after UA/NSTEMI
LMWH (antithrombin - daltparin), glycoprotein IIb/IIa (antiplatelet - tirofiban - given after PCI) B blockers, nitrates (temporary basis to relieve pain)
how is a coronary artery bypass grafting performed
left internal thoracic (mammary) artery used rather than saphenous vein LITA not disconnected from parent (subclavian) but cut distally and attached to coronary artery Usually performed on bypass
what are the main complications of coronary artery bypass grafting
systemic inflammatory response, atrial fibrillation and persistent neurological abnormalities
what is the steps of percutaneous coronary intervention
guiding catheter introduced via femoral, brachial or radial arteryguided wire then advanced down lumen of coronary artery until it is positioned across stenosisballoon catheter advanced over this wire and inflated at side of stenosis to increase luminal diameter
what was introduced as part of PCI to prevent elastic recoil and restenosis
stent - cylindrical metal mesh or slotted tubes that are implanted into artery at site of balloon expansion
what is a complication of PCI
thrombosis (controlled by aspirin and clopidogrel)
when is a patient preferred to have revascularisation
when at risk of developing worsening ischaemic disease or whom drugs are not controlling symptoms
when is PCI preferred
when one or two arteries diseased, as long as disease is not too diffuse
when is CABG used
when all three main coronary arteries diseased, when left coronary mainstem has significant stenosis, when lesions not amendable to PCI and when LV function poor
in which of PCI and CABG must revascularisation be repeated more often
PCIimprovements in stenting will narrow this difference
ruptured plaque reveals collagen which serves as site of platelet adhesion, activation and aggregation. This results in what
release of TXA2, fibrinogen, 5HT, platelet activating factor and ADP which further promotes platelet aggregation activation of clotting cascade leading to fibrin formation and propagation and stabilisation of occlusive thrombus
what is hypokinesis
immediate loss of contractility in affected myocardium
what is symptoms of MI
crushing chest pain, radiated into arms, neck, jawsweating, anxiety, clammy skinoften little effect on BP and HR
what is the immediate treatment of a STEMI
Morphine, Oxygen, Nitrates, Aspirin + Clopidogrel Also thrombolytics
what is the long term treatment of STEMI
B blocker, aspirin, ACE inhibitor, reduction of risk factors, revascularisation if high risk of further events
what is thrombolysis
dissolution of blood clot - done in community by ambulance if they cant get to hospital in 120 minutes
how does thrombolysis work
they induce fibrinolysis, fragmentation of fibrin strands holding clot together - permits reperfusion of ischaemic zone
what are the main agents used in thrombolysis
streptokinase (SK) and tissue plasminogen activator (tPA)
what are the risks in thrombolysis
bleeding, intracranial haemorrhage
what are the contradictions in thrombolysis
recent haemorrhagic stroke, recent surgery or trauma and severe hypertension
death is an obvious complication of STEMI. What is the arrhythmic complications
ventricular tachycadia
what is the structural complications of STEMI
cardiac rupture, ventricular septal defect, mitral regurgitation, acute pericarditis
what is Dresslers syndrome
structural complication - pericarditis many weeks post MI, damages heart muscle release previously un-encountered material that stimulates an immune response
what are functional complications of STEMI
ventricular dysfunction (L, R or both), chronic HF, cardiogenic shock
what is the secondary prevention measures of MI
healthy lifestyle, smoking cessation, good control of BP cholesterol and diabetes
what are the four phases of cardiac rehabilitation
in patient, early post discharge period, structured exercise programme (hospital based), long term maintenance of physical activity and life style change
what are the targets of MI rehabilitation and secondary prevention
avoid smoking, healthy diet, regular aerobic exercise, optimal drug therapy, cholesterol <4.0mmol/l BP<140/85mmHg
what is the role of interstitial fluid
acts as the go between blood and body cells
terminal arterioles regulate regional blood flow to capillary bed in most tissues - what regulates flow in a few (eg mesentery)
precapillary sphincters
what substances cannot cross capillary wall
plasma proteins
what is the movement of lipid soluble substances
go through endothelial cells of capillary
what is the movement of water soluble substances
go through water filled pores
how are exchangeable proteins moved across wall
by vesicular transport
what is net filtration pressure proportional to
forces favouring filtration - forces opposing filtration
what are the starling forces which favour filtration
PC - capillary hydrostatic pressure (most important) - 35mmHg at arteriolar, 17mmHg at venule πi - interstitial fluid osmotic pressure - 1mmHg (arteriolar)
what are the starling forced opposing filtration
π c - capillary osmotic pressure - 25mmHgPi - interstitial fluid hydrostatic pressure - 1mmHg
how to calculate net filtration pressure
(PC + πi) - (πc + Pi)
what is NFP at arteriolar end
+10mmHg
what is NFP at venular end
-8mmHg
what do starling forces favour
filtration at arteriolar end, reabsorption at venular end
what is oedema
accumulation of fluid in interstitial fluid
what causes the raised capillary cause of oedema
arteriolar dilation raised venous pressure - left ventricular failure (pulmonary oedema), RVF (peripheral oedema - pitting oedema in ankles or sacram)or prolonged standing
what is the plasma osmotic pressure in oedema and what causes this reduction
<30g/l by malnutrition, protein malabsorption, excessive renal excretion of protein and hepatic failure
what causes the lymphatic insufficiency cause of oedema
lymph node damage, filariasis - elephantiasis
what causes the change in capillary permeability cause of oedema
inflammation, histamine increases leakage of protein
what does left sided CCF cause
IHD (MI), cardiomyopathy, vascular disease
what does right sided CCF cause
2nd to LHF, cor pulmonale (any severe lung disease put strain on right side of heart) and congenital heart disease
what is symptoms of left sided heart failure
dyspnoea on exertion/rest, orthopnoea, paroxysmal nocturnal dysponoea and pulmonary oedema (sudden dysponoea pink, frothy sputum)
what are the signs of left sided heart failure
tachycardia, fine crepitations, pleural effusion, S3 (gallop rhythm, s3 + tachycardia)
what does left sided heart failure look like on CXR
cardiomegaly (abnormal enlargement of heart) bats wing shadows esp lower zones, interstitial fluid
what is the symptoms of right sided heart failure
oedema
what is the signs of right sided heart failure
ankle/sacral oedema, JVP elevated (>4cm above sternal angle), heptomealy and ascites (fluid in abdomen)
what does right sided heart failure look like on CXR
normal
what is treatment of CCF caused by previous MIs and cardiomyopathies
standard medical therapy for CCF
what is the treatment of CCF caused by cor pulmonale (enlargement of right side of heart due to disease of lungs or pulmonary vessels)
Rx diuretics and oxygen only
what is treatment of CCF caused by valvular disease
surgery ideally
what is treatment of CCF cased by fast AF
digoxin or DC shock
what is the standard medical treatment of heart failure
diuretics to excrete retained fluidACE inhibitors B blockers Digoxin Other vasodilators (nitrates, hydralazine)(transplant?)
what is spironolactone and when is it used
aldosterone receptor antagonist, used in severe CCF (on top of ACE)side effects - hyperkalaemia, renal dysfunction, gynaecomastia (enlargement of male breast)
what are the new drugs which can be used in heart failure
sucubtril-valsartan, neprilysin (blocks NP), implantable cardiac defibrillator (ICD)cardiac resynchronisation therapy (only for prolonged QRS, 3 pacemakers inserted to force LV and RV to contract together)
what is the therapy for acute LVF
Sit upOxygen (care in COPD)IV furosemide (loop diuretic)IV diamorphine (not in COPD)
what is normal sinus rhythm characterised by what
upright P waves in leads I and II and inverted in AVR and VIcan have sinus arrhythmia, sinus bradycardia and sinus tachycardia
what is bradycardia caused by and how is it treated
failure of impulse formation or conduction (due to hypothermia, hypothyroidism, raised ICP, drug therapy or acute ischaemia) treated by atropine
what causes heart block
block in AV node of bundle of His results in AV block whereas lower in conduction system produces BBB
what is 1st degree AV block
simple prolongation of PR (above 0.2 sec) every atrial depolarisation is followed by conduction to ventricles but with delay
what are the two different types of second degree AV block
morbitz I and morbitz IIcan be 2:1 or 3:1 ie every second or third P wave conducts to ventricles
what is the features of Morbitz I
progressive PR interval until a P wave fails to conduct
what is the features of Mobitz II
dropped QRS complexes occur (not preceded by P wave)
what is third degree AV block
all atrial activity fails to conduct to ventriclesbroad QRS
what is BBB
conduction delay - QRS = 0.11scomplete block of bundle branch - wider QRS >12sshape depends on wether left (W/V in V1 and M in V6) or right (vice versa)
what is AV junctional tachycardia (superventricular)
usually referred to as paroxysmal SVTs and are often seen in young patients with no or little structural heart disease
what is AV nodal re-entry tachycardia (supraventricuar)
there are 2 functionally and anatomically different pathways in AV nodeQRS complex narrow, P waves cant be seen or come immediately before or after QRS
what is AV reciprocating tachycardia
atrial activation occurs after ventricular activation P wave still seen between QRS and T wave
distinguishing between AV nodal re-entry tachycadia and AV reciprocating tachycardia is difficult but not usually critical as management similar. What is management?
haemodynamically unstable - emergency cardioversionhaemodynamically stable - vagal maneouvers (right carotid massag and valsalva manoeuvre) - if unsuccessful, try IV adenosine
what is the basic info regarding atrial fibrillation
common cause of CV morbidity/mortality prevelance increases with agechaotic and disorganised electrical activity irregular heartbeat
what is the different types of AF
paroxysmal (less than 48 hours)persistant (more than 48 hours)permanent
what is the symptoms of AF
can be asymptomatic palpations, presyncope, syncope, chest pain, dyspnoea, sweatiness, fatigue
causes of AF
predisposing factorsheart valve abnormality, calcification in elderly, congenital heart disease, post rheumatic fever, IV, IV drug users, alcohol, heart failure, hypertension, prosthetic valve
how does a damaged heart cause AF
damage - turbulent flow over roughened endothelium - platelet/fibrin exposed - bacteria settle and become vegetation
what does ECG look like in AF
irregularly irregular, atrial rate >300bpm, absence of P waves
what is the treatment in AF
pharmacological cardioversion - amiodarone or flecainide electrical cardioversion if haemodynamically unstablelong term management involves rate and rhythm control
what do you do if cardioversion not available within 24-48 hours of symptom onset
put patient on anticoagulation (warfarin) for 6-8 weeks
what is complication of AF
stroke
what is basic info of atrial flutter
often associated with AFsimilar initial therapeutic approach
what does atrial flutter look like on ECG
sawtooth-like waves 250-350bpm
how is atrial flutter treated
electric cardioversion recurrent - radiorequency catheter albation and class IA, IC, II, III, IV and digoxinAV nodal blocking agents may be used if persist
what causes atrial tachycardia
digitalis poisoning
what is treatment of atrial tachycardia
adenosine to terminate, class IC, III, radio catheter ablation for prophylaxis
what is atrial ectopic beats
often no symptoms, may be heaviness of heart beat ECG abnormal and early P waves followed by normal QRSno treatment
what is Wolf-Parkinson-White syndrome (superventricular)
broad QRS with slurred upstroke on R wave (delta wave)delta wave suggests underlying WPW which can cause SVT
what causes WPW
congenital accessory conduction pathway connecting atria and ventriclesthis accessory pathway does not have the rate lowering properties of AV node and as result, high atrial rates can be conducted to ventricules
what is treatment of WPW
destruction of abnormal electrical pathway by radio frequency ablation by cardiac electrophysiologists (or radio catheter ablation)or if AF - IA, IC and III
what VTs are life threatening
sustained VT and ventricular fibrillation with haemodynamic instability (syncope, hypotension)
what are causes of VT
hypokalaemia, hypomagnesaemia, hypocalcemia, ischaemic heart (most common)
what is sustained VT
> 30sVT more likely than SVT if very broad QRS
what is complications of sustained VT
pre-syncope, syncope, hypotension and cardiac arrest
what does ECG look like in sustained VT
broad, abnormal QRS complexes120-220bpm
if patient haemodynamically compromised (pulseless, hypotensive) what is treatment
emergency DC cardioversion must be considered first
if patient haemodynamically stable, what is treatment
chemical cardioversion
what is drug of choice in sustained VT
IV lignocaine (lidocaine), or amiodaroneDCCV may be necessary if therapy unsuccessful
what is ventricular fibrillation
rapid, irregular ventricular with no mechanical effectmost common cause of death following MI
symptoms of ventricular fibrillation
pulseless and becomes rapidly unconsciouss
what is ECG like in ventricular fibrillation
shapeless, rapid oscillations and there is no hint of organised complexes
what is treatment of ventricular fibrillation
only effective treatment is electrical defibrillation
what is long QT syndrome
describes an ECG where ventricular repolarisation is greatly prolonged can be congenital and on ECG it develops into torsades de pointes
how to recognise patient in cardiac arrest
unresponsive patient, not breathing normally, no pulse preceding hypoxia and hypotension common
what is the equation to calculate the oxygen delivery index
DO2 = SaO2 x [Hb] x 1.36 x CO (HR x SV^2)
how to improve SaO2
increase FiO2, clear airway and adequate breathing
how to improve [Hb]
transfuse trigger, treat anaemia - Gp&S / X-match, IV access (Fe etc)
how to treat bradycardia
atropine or b stimulant
how to fix preload problems
IV fluids, raise legs
how to fix contractility problems
treat cause (PCI for MI)
how to fix afterload problems
excess afterload (HBP) - vasodilator reduced afterload (septic shock) - vasoconstrictors
which airway problems cause cardiorespiratory arrest
CNS depression (tongue), lumen blocked (blood, vomit), swelling (trauma, infection, inflammation), muscle (laryngospasm, bronchospasm)
which breathing problems cause cardiorespiratory arrest
CNS depression, muscle weakness, nerve damage, restrictive chest defect, fractured ribs, pneumothorax, haemothorax, infection, COPD, asthma, PE, ARDS
which circulatory problems cause cardiorespiratory arrest
asphyxia, hypoxaemia, blood loss, hypothermia, septic shock
how to assess SaO2
clinical (not reliable), pulse oximetry or arterial blood gas
how to assess [Hb]
clinical (not reliable) part of FBC or bedside (hemocue)
how to assess heart rate
pulse, pulse oximetry, ECG monitor with sound on, arterial BP monitor
which rhythms are shockable
ventricular fibrillation and ventricular tachycardia (monomorphic VT - broad, rapid rate, constant QRS or polymorphic torsade de pointes)
what is the steps after shocking with defibrillation
continue CPR for 2 mins then give adrenaline after every other shock give amiodarone after 3rd shock as once off
what are non shockable rhythms
asystole (absent QRS, p waves may persist, rarely straight line, adrenaline IV then every 2 CPR cycles)pulseless electrical activity (same adrenaline thing)
what is the four Hs of treatable reversible causes of cardiorespiratory arrest
hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia
what is the four Ts of treatable reversible causes of cardiorespiratory disease
thrombosis, tension pneumothorax, temponade (cardiac - fluid in pericardium) and toxins
post cardiac arrest syndrome includes what
post-cardiac arrest brain injury, post-cardiac arrest myocardial dysfunction, systemic ischaemia/reperfusion response and persistent precipitating pathology
