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Cardio Week 5 Flashcards

1
Q

what causes the decrease of blood flow in acute coronary syndromes

A

rupture of atherosclerotic plaque resulting in thrombus

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2
Q

what markers does myocardial damage release

A

troponin T and I (also enzyme CK)

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3
Q

what is the diagnosis of NSTEMI

A

elevated levels of these markers but no ST elevation

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4
Q

what is the diagnosis of unstable angina

A

demonstrate symptoms of ACS but have neither ST elevation or raised troponin

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5
Q

what may NSTEMIs and UA be associated with in terms of an ECG

A

ST depression and T wave inversion

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6
Q

what are the symptoms of UA/NSTEMI

A

resemble those of stable angina, but are frequently more painful, intense and persistent, often lasting at least 30 minutes

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7
Q

what is the typical presentation of UA/NSTEMI

A

unrelieved by GTN, angina of recent onset brought on by minimal exertion, angina at rest/minimal exertion or post MI angina

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8
Q

what is the physiopathology of UA/NSTEMI

A

compared to stable, plaques found in ACS tend to have thinner fibrous cap and larger lipid core - especially vulnerable to being ruptured

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9
Q

this exposed plaque (vulnerability to rupture) causes what

A

platelet aggregation and thrombosis causes local generation of vasoconstrictors such as thromboxane A2 and seratonin

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10
Q

when is revascularisation considered for patients in UA/NSTEMI

A

patients with high risk of very significant coronary arerty disease, or if drug treatment fails to control symptoms

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11
Q

what drugs are immediately given in UA/NSTEMI

A

300mg aspirin (antiplatelet) then 75mg/day for life also clopidogrel which inhibits ADP stimulated platelet aggregation

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12
Q

what drugs could be given in the long term after UA/NSTEMI

A

LMWH (antithrombin - daltparin), glycoprotein IIb/IIa (antiplatelet - tirofiban - given after PCI) B blockers, nitrates (temporary basis to relieve pain)

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13
Q

how is a coronary artery bypass grafting performed

A

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

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14
Q

what are the main complications of coronary artery bypass grafting

A

systemic inflammatory response, atrial fibrillation and persistent neurological abnormalities

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15
Q

what is the steps of percutaneous coronary intervention

A

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

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16
Q

what was introduced as part of PCI to prevent elastic recoil and restenosis

A

stent - cylindrical metal mesh or slotted tubes that are implanted into artery at site of balloon expansion

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17
Q

what is a complication of PCI

A

thrombosis (controlled by aspirin and clopidogrel)

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18
Q

when is a patient preferred to have revascularisation

A

when at risk of developing worsening ischaemic disease or whom drugs are not controlling symptoms

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19
Q

when is PCI preferred

A

when one or two arteries diseased, as long as disease is not too diffuse

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20
Q

when is CABG used

A

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

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21
Q

in which of PCI and CABG must revascularisation be repeated more often

A

PCIimprovements in stenting will narrow this difference

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22
Q

ruptured plaque reveals collagen which serves as site of platelet adhesion, activation and aggregation. This results in what

A

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

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23
Q

what is hypokinesis

A

immediate loss of contractility in affected myocardium

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24
Q

what is symptoms of MI

A

crushing chest pain, radiated into arms, neck, jawsweating, anxiety, clammy skinoften little effect on BP and HR

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25
Q

what is the immediate treatment of a STEMI

A

Morphine, Oxygen, Nitrates, Aspirin + Clopidogrel Also thrombolytics

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26
Q

what is the long term treatment of STEMI

A

B blocker, aspirin, ACE inhibitor, reduction of risk factors, revascularisation if high risk of further events

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27
Q

what is thrombolysis

A

dissolution of blood clot - done in community by ambulance if they cant get to hospital in 120 minutes

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28
Q

how does thrombolysis work

A

they induce fibrinolysis, fragmentation of fibrin strands holding clot together - permits reperfusion of ischaemic zone

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29
Q

what are the main agents used in thrombolysis

A

streptokinase (SK) and tissue plasminogen activator (tPA)

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30
Q

what are the risks in thrombolysis

A

bleeding, intracranial haemorrhage

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31
Q

what are the contradictions in thrombolysis

A

recent haemorrhagic stroke, recent surgery or trauma and severe hypertension

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32
Q

death is an obvious complication of STEMI. What is the arrhythmic complications

A

ventricular tachycadia

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33
Q

what is the structural complications of STEMI

A

cardiac rupture, ventricular septal defect, mitral regurgitation, acute pericarditis

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34
Q

what is Dresslers syndrome

A

structural complication - pericarditis many weeks post MI, damages heart muscle release previously un-encountered material that stimulates an immune response

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35
Q

what are functional complications of STEMI

A

ventricular dysfunction (L, R or both), chronic HF, cardiogenic shock

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36
Q

what is the secondary prevention measures of MI

A

healthy lifestyle, smoking cessation, good control of BP cholesterol and diabetes

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37
Q

what are the four phases of cardiac rehabilitation

A

in patient, early post discharge period, structured exercise programme (hospital based), long term maintenance of physical activity and life style change

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38
Q

what are the targets of MI rehabilitation and secondary prevention

A

avoid smoking, healthy diet, regular aerobic exercise, optimal drug therapy, cholesterol <4.0mmol/l BP<140/85mmHg

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39
Q

what is the role of interstitial fluid

A

acts as the go between blood and body cells

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40
Q

terminal arterioles regulate regional blood flow to capillary bed in most tissues - what regulates flow in a few (eg mesentery)

A

precapillary sphincters

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41
Q

what substances cannot cross capillary wall

A

plasma proteins

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42
Q

what is the movement of lipid soluble substances

A

go through endothelial cells of capillary

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43
Q

what is the movement of water soluble substances

A

go through water filled pores

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44
Q

how are exchangeable proteins moved across wall

A

by vesicular transport

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45
Q

what is net filtration pressure proportional to

A

forces favouring filtration - forces opposing filtration

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46
Q

what are the starling forces which favour filtration

A

PC - capillary hydrostatic pressure (most important) - 35mmHg at arteriolar, 17mmHg at venule πi - interstitial fluid osmotic pressure - 1mmHg (arteriolar)

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47
Q

what are the starling forced opposing filtration

A

π c - capillary osmotic pressure - 25mmHgPi - interstitial fluid hydrostatic pressure - 1mmHg

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48
Q

how to calculate net filtration pressure

A

(PC + πi) - (πc + Pi)

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49
Q

what is NFP at arteriolar end

A

+10mmHg

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50
Q

what is NFP at venular end

A

-8mmHg

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51
Q

what do starling forces favour

A

filtration at arteriolar end, reabsorption at venular end

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52
Q

what is oedema

A

accumulation of fluid in interstitial fluid

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53
Q

what causes the raised capillary cause of oedema

A

arteriolar dilation raised venous pressure - left ventricular failure (pulmonary oedema), RVF (peripheral oedema - pitting oedema in ankles or sacram)or prolonged standing

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54
Q

what is the plasma osmotic pressure in oedema and what causes this reduction

A

<30g/l by malnutrition, protein malabsorption, excessive renal excretion of protein and hepatic failure

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55
Q

what causes the lymphatic insufficiency cause of oedema

A

lymph node damage, filariasis - elephantiasis

56
Q

what causes the change in capillary permeability cause of oedema

A

inflammation, histamine increases leakage of protein

57
Q

what does left sided CCF cause

A

IHD (MI), cardiomyopathy, vascular disease

58
Q

what does right sided CCF cause

A

2nd to LHF, cor pulmonale (any severe lung disease put strain on right side of heart) and congenital heart disease

59
Q

what is symptoms of left sided heart failure

A

dyspnoea on exertion/rest, orthopnoea, paroxysmal nocturnal dysponoea and pulmonary oedema (sudden dysponoea pink, frothy sputum)

60
Q

what are the signs of left sided heart failure

A

tachycardia, fine crepitations, pleural effusion, S3 (gallop rhythm, s3 + tachycardia)

61
Q

what does left sided heart failure look like on CXR

A

cardiomegaly (abnormal enlargement of heart) bats wing shadows esp lower zones, interstitial fluid

62
Q

what is the symptoms of right sided heart failure

A

oedema

63
Q

what is the signs of right sided heart failure

A

ankle/sacral oedema, JVP elevated (>4cm above sternal angle), heptomealy and ascites (fluid in abdomen)

64
Q

what does right sided heart failure look like on CXR

A

normal

65
Q

what is treatment of CCF caused by previous MIs and cardiomyopathies

A

standard medical therapy for CCF

66
Q

what is the treatment of CCF caused by cor pulmonale (enlargement of right side of heart due to disease of lungs or pulmonary vessels)

A

Rx diuretics and oxygen only

67
Q

what is treatment of CCF caused by valvular disease

A

surgery ideally

68
Q

what is treatment of CCF cased by fast AF

A

digoxin or DC shock

69
Q

what is the standard medical treatment of heart failure

A

diuretics to excrete retained fluidACE inhibitors B blockers Digoxin Other vasodilators (nitrates, hydralazine)(transplant?)

70
Q

what is spironolactone and when is it used

A

aldosterone receptor antagonist, used in severe CCF (on top of ACE)side effects - hyperkalaemia, renal dysfunction, gynaecomastia (enlargement of male breast)

71
Q

what are the new drugs which can be used in heart failure

A

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)

72
Q

what is the therapy for acute LVF

A

Sit upOxygen (care in COPD)IV furosemide (loop diuretic)IV diamorphine (not in COPD)

73
Q

what is normal sinus rhythm characterised by what

A

upright P waves in leads I and II and inverted in AVR and VIcan have sinus arrhythmia, sinus bradycardia and sinus tachycardia

74
Q

what is bradycardia caused by and how is it treated

A

failure of impulse formation or conduction (due to hypothermia, hypothyroidism, raised ICP, drug therapy or acute ischaemia) treated by atropine

75
Q

what causes heart block

A

block in AV node of bundle of His results in AV block whereas lower in conduction system produces BBB

76
Q

what is 1st degree AV block

A

simple prolongation of PR (above 0.2 sec) every atrial depolarisation is followed by conduction to ventricles but with delay

77
Q

what are the two different types of second degree AV block

A

morbitz I and morbitz IIcan be 2:1 or 3:1 ie every second or third P wave conducts to ventricles

78
Q

what is the features of Morbitz I

A

progressive PR interval until a P wave fails to conduct

79
Q

what is the features of Mobitz II

A

dropped QRS complexes occur (not preceded by P wave)

80
Q

what is third degree AV block

A

all atrial activity fails to conduct to ventriclesbroad QRS

81
Q

what is BBB

A

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)

82
Q

what is AV junctional tachycardia (superventricular)

A

usually referred to as paroxysmal SVTs and are often seen in young patients with no or little structural heart disease

83
Q

what is AV nodal re-entry tachycardia (supraventricuar)

A

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

84
Q

what is AV reciprocating tachycardia

A

atrial activation occurs after ventricular activation P wave still seen between QRS and T wave

85
Q

distinguishing between AV nodal re-entry tachycadia and AV reciprocating tachycardia is difficult but not usually critical as management similar. What is management?

A

haemodynamically unstable - emergency cardioversionhaemodynamically stable - vagal maneouvers (right carotid massag and valsalva manoeuvre) - if unsuccessful, try IV adenosine

86
Q

what is the basic info regarding atrial fibrillation

A

common cause of CV morbidity/mortality prevelance increases with agechaotic and disorganised electrical activity irregular heartbeat

87
Q

what is the different types of AF

A

paroxysmal (less than 48 hours)persistant (more than 48 hours)permanent

88
Q

what is the symptoms of AF

A

can be asymptomatic palpations, presyncope, syncope, chest pain, dyspnoea, sweatiness, fatigue

89
Q

causes of AF

A

predisposing factorsheart valve abnormality, calcification in elderly, congenital heart disease, post rheumatic fever, IV, IV drug users, alcohol, heart failure, hypertension, prosthetic valve

90
Q

how does a damaged heart cause AF

A

damage - turbulent flow over roughened endothelium - platelet/fibrin exposed - bacteria settle and become vegetation

91
Q

what does ECG look like in AF

A

irregularly irregular, atrial rate >300bpm, absence of P waves

92
Q

what is the treatment in AF

A

pharmacological cardioversion - amiodarone or flecainide electrical cardioversion if haemodynamically unstablelong term management involves rate and rhythm control

93
Q

what do you do if cardioversion not available within 24-48 hours of symptom onset

A

put patient on anticoagulation (warfarin) for 6-8 weeks

94
Q

what is complication of AF

A

stroke

95
Q

what is basic info of atrial flutter

A

often associated with AFsimilar initial therapeutic approach

96
Q

what does atrial flutter look like on ECG

A

sawtooth-like waves 250-350bpm

97
Q

how is atrial flutter treated

A

electric cardioversion recurrent - radiorequency catheter albation and class IA, IC, II, III, IV and digoxinAV nodal blocking agents may be used if persist

98
Q

what causes atrial tachycardia

A

digitalis poisoning

99
Q

what is treatment of atrial tachycardia

A

adenosine to terminate, class IC, III, radio catheter ablation for prophylaxis

100
Q

what is atrial ectopic beats

A

often no symptoms, may be heaviness of heart beat ECG abnormal and early P waves followed by normal QRSno treatment

101
Q

what is Wolf-Parkinson-White syndrome (superventricular)

A

broad QRS with slurred upstroke on R wave (delta wave)delta wave suggests underlying WPW which can cause SVT

102
Q

what causes WPW

A

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

103
Q

what is treatment of WPW

A

destruction of abnormal electrical pathway by radio frequency ablation by cardiac electrophysiologists (or radio catheter ablation)or if AF - IA, IC and III

104
Q

what VTs are life threatening

A

sustained VT and ventricular fibrillation with haemodynamic instability (syncope, hypotension)

105
Q

what are causes of VT

A

hypokalaemia, hypomagnesaemia, hypocalcemia, ischaemic heart (most common)

106
Q

what is sustained VT

A

> 30sVT more likely than SVT if very broad QRS

107
Q

what is complications of sustained VT

A

pre-syncope, syncope, hypotension and cardiac arrest

108
Q

what does ECG look like in sustained VT

A

broad, abnormal QRS complexes120-220bpm

109
Q

if patient haemodynamically compromised (pulseless, hypotensive) what is treatment

A

emergency DC cardioversion must be considered first

110
Q

if patient haemodynamically stable, what is treatment

A

chemical cardioversion

111
Q

what is drug of choice in sustained VT

A

IV lignocaine (lidocaine), or amiodaroneDCCV may be necessary if therapy unsuccessful

112
Q

what is ventricular fibrillation

A

rapid, irregular ventricular with no mechanical effectmost common cause of death following MI

113
Q

symptoms of ventricular fibrillation

A

pulseless and becomes rapidly unconsciouss

114
Q

what is ECG like in ventricular fibrillation

A

shapeless, rapid oscillations and there is no hint of organised complexes

115
Q

what is treatment of ventricular fibrillation

A

only effective treatment is electrical defibrillation

116
Q

what is long QT syndrome

A

describes an ECG where ventricular repolarisation is greatly prolonged can be congenital and on ECG it develops into torsades de pointes

117
Q

how to recognise patient in cardiac arrest

A

unresponsive patient, not breathing normally, no pulse preceding hypoxia and hypotension common

118
Q

what is the equation to calculate the oxygen delivery index

A

DO2 = SaO2 x [Hb] x 1.36 x CO (HR x SV^2)

119
Q

how to improve SaO2

A

increase FiO2, clear airway and adequate breathing

120
Q

how to improve [Hb]

A

transfuse trigger, treat anaemia - Gp&S / X-match, IV access (Fe etc)

121
Q

how to treat bradycardia

A

atropine or b stimulant

122
Q

how to fix preload problems

A

IV fluids, raise legs

123
Q

how to fix contractility problems

A

treat cause (PCI for MI)

124
Q

how to fix afterload problems

A

excess afterload (HBP) - vasodilator reduced afterload (septic shock) - vasoconstrictors

125
Q

which airway problems cause cardiorespiratory arrest

A

CNS depression (tongue), lumen blocked (blood, vomit), swelling (trauma, infection, inflammation), muscle (laryngospasm, bronchospasm)

126
Q

which breathing problems cause cardiorespiratory arrest

A

CNS depression, muscle weakness, nerve damage, restrictive chest defect, fractured ribs, pneumothorax, haemothorax, infection, COPD, asthma, PE, ARDS

127
Q

which circulatory problems cause cardiorespiratory arrest

A

asphyxia, hypoxaemia, blood loss, hypothermia, septic shock

128
Q

how to assess SaO2

A

clinical (not reliable), pulse oximetry or arterial blood gas

129
Q

how to assess [Hb]

A

clinical (not reliable) part of FBC or bedside (hemocue)

130
Q

how to assess heart rate

A

pulse, pulse oximetry, ECG monitor with sound on, arterial BP monitor

131
Q

which rhythms are shockable

A

ventricular fibrillation and ventricular tachycardia (monomorphic VT - broad, rapid rate, constant QRS or polymorphic torsade de pointes)

132
Q

what is the steps after shocking with defibrillation

A

continue CPR for 2 mins then give adrenaline after every other shock give amiodarone after 3rd shock as once off

133
Q

what are non shockable rhythms

A

asystole (absent QRS, p waves may persist, rarely straight line, adrenaline IV then every 2 CPR cycles)pulseless electrical activity (same adrenaline thing)

134
Q

what is the four Hs of treatable reversible causes of cardiorespiratory arrest

A

hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia

135
Q

what is the four Ts of treatable reversible causes of cardiorespiratory disease

A

thrombosis, tension pneumothorax, temponade (cardiac - fluid in pericardium) and toxins

136
Q

post cardiac arrest syndrome includes what

A

post-cardiac arrest brain injury, post-cardiac arrest myocardial dysfunction, systemic ischaemia/reperfusion response and persistent precipitating pathology

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