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2a systems > Cardiology > Flashcards

Cardiology Flashcards

1
Q

how do you treat arterial thrombosis in coronary system- 3

A

aspirin and other antiplatelets
thrombolytic therapy- tissue plasminogen activator, streptokinase
reperfusion- catheter directed treatments and stents

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2
Q

how do you treat arterial thrombosis in brain

A

aspirin and other anti-platlets
thrombolysis

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3
Q

3 main antiplatelets

A

aspirin
clopidogrel
dipyridamole

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4
Q

where would you find a venous thrombus

A

peripherally in leg and cerebral

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5
Q

what is d dimer

A

a test to EXCLUDE dvt/ pe

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6
Q

treatments for venous thrombosis- 3

A

DOAC (direct oral anticoagulation- tablet)
warfarin
heparin or low molecular weight heparin

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7
Q

disadvantage of low molecular weight heparin

A

injectable only

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8
Q

prevention for venous thrombosis

A

VTE prophylaxis- mechanical (like stockings) or chemical
early mobilization and good hydration

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9
Q

difference between heparin and low molecular weight heparin

A

heparin- continuous IV infusion, requires monitoring with APTT , short half life
LMWH- subcutaneous injection in tummy, once a day , used for treatment and prophylaxis

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10
Q

how does warfarin work

A

prevents synthesis of factor 2,7,9,10
antagonist of vitamin K
prolongs prothrombin time

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11
Q

signs and symptoms of DVT

A

symptoms: leg pain, swelling
signs- tenderness, swelling, warmth, discoloration

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12
Q

signs and symptoms of pulmonary embomism

A

signs- tachycardia, tachypnoea
symptoms- breathlessness, pleuritic chest pain

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13
Q

what heart failure results from pulmonary embolism

A

right heart failure- cor pulmonale

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14
Q

what conditions present with pleuritic chest pain and how to differentiate

A

pe, pneumothorax, pneumonia
cxr- pe= normal, pneumonia and pneumothorax is diagnostic

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15
Q

what is in a athersoscleortic plaque structure

A

lipid
necrotic core
connective tissue
fibrous cap

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16
Q

what are the major cell types in atherogenesis

A

endothelium
macrophages
smooth muscle cells
platelets

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17
Q

risk factors for venous thromboembolism

A

VIRCHOWS TRIAD

  • venous stasis (change in blood flow)- immobility- long haul flights, after surgery. you get aggregation of clotting factors
  • Endothelial injury- smoking, trauma, surgery. damaged endothelim cant secrete anticoagulants
  • Hypercoagubility- preggo, obesity, sepsis, contraceptives
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18
Q

what does venous thromboemolim usually result in

A

PE
DVT

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19
Q

presentation + scoring for dvt

A

sudden onset PLEURETIC CHEST PAIN

dyspnoea with evidence of dvt (swollen calf and immonilsation)

haemoptysis

tachycardic, hypotensive, ankle oedema

wells score for pe is >4= likely pe.
4 or less is unlikely

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20
Q

investigations for PE

A

if pe is likely (wells score>4)- CTPA (CT pulmonary angiogram that looks for clots in the lungs)

1st line is D-dimer test (in blood)- if raised then PE is likely and should do a CTPA, if not raised then its not a PE- it excludes this but isnt diagnostic

x ray would look normal in a PE

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21
Q

treatment for pe

A

if massive PE- thrombolytics

if not massive (more common)- give anticoagulants - DOAC- 1st line DOAC is apixaban/ rivaroxaban

if renal impairment- LMWH

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22
Q

presentation of dvt + scoring

A

unilateral swollen calf with engorged leg veins- typically warm and oedematous

if complete occlusion- severe ischemic leg turns blue

on wells score, >1= likely DVT

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23
Q

investigations for dvt (first line and gold standard

A

wells score less than 1- d dimer to exclude
if raised then do duplex ultrasound which is gold standard!
duplex ultrasound gives you an idea of blood flow and is always gold standard when investigating veins

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24
Q

treatment for dvt

A

same as non-massive PE

  • anticoagulant DOACs- apixaban and Rivaroxiban
  • LMHW if renal impairment
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25
Q

differentials for dvt

A

cellulitis which presents with swollen inflamed calf-
but this will show leukocytosis which is indicative of infection on blood test while dvt doesnt. dvt also conformed with d-dimer and duplex ultrasound

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26
Q

definition of abdominal aortic aneurysm, where is it typically, what is false

A

weakening of arterial walls leading to dilation where diameter is >3cm

typically infrarenal (below renal arteries)

true aneurysm is where all 3 layers of vascular tunic are degraded (usually genetic)

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27
Q

risk factors for aaa

A

(basically risk factors for atherosclerosis)- smoking, obesity, hypertension, trauma, increasing age, family history

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28
Q

pathophysiology of aaa

A

smooth muscle, elastic and structural degradation in all 3 layers of the vascular tunic (intima, media, adventitia)

  • if not all 3 layers then a pseudoaneurysm

dilation >3cn

above 5.5cm is a very high risk of rupture and a rurpture is a surgical emergency

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29
Q

presentation of aaa

A

asymptomatic until high rupture risk

pulsatile mass in abdomen

ruptured= sudden epigastric pain radiating to flank, hypotensive and tachycardic

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30
Q

diagnosis of aaa

A

1st line + diagnostic is abdominal ultrasound

also can do ct angiogram which is more detailed

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31
Q

treatment of aaa

A

non ruptured:

  • manage rf- stop smoking, lower bmi, statins..
  • if expanding 1cm+/year- surgery
    • endovascular repair- stent though femoral artery
    • open surgery- fewer complications but more invasive

ruptured:

  • stabilise abcde, fluids
  • AAA graft surgery- replace weakened walls with graft
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32
Q

diffential for aaa

A

differential is acute pancreatitis, but in that the mass is not pulsatile

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33
Q

definition of peripheral vascular disease

A

narrowing of the arteries supplying the peripheries (mostly calf- basically ihd of lower limb arteries)

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34
Q

risk factors for peripheral vascular disease

A

smoking, hypertension, ageing, obesity, CKD, T2DM

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35
Q

what are the stages of peripheral vascular disease

A

intermitted claudication
critical ischemia
acute- acute limb ischemia

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36
Q

pathophysiology and presentation of peripheral vascular disease- pathophysiology of each stage

A

caused by atherosclerotic plaque

intermittent claudication = least severe. astherosclortic partial lumen occlusion, crampy pain usually in calves after walking a certain distance. stops after few minutes of rest

critical limb ischemia= most severe. very big occlusion and blood supply is barely adequate to meet metabolic demand. pain at rest and risk of gangrene

  • 6Ps!!!- present in critical limb ischemia but the more you have, the more life threatening, present in acute limb ischemia too
    • pulselessness
    • pallor
    • pain- burning and worse at night
    • perishingly cold
    • parasthesia (pins and needles)
    • paralysis

acute limb ischemia = complication where theres total occlusion of vessel due to embolic/ thrombolic formation at site of critical limb ischemia rapid onset of ischaemia in a limb

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37
Q

tests and indications of peripheral vascular disease

A

buerger test positive- elevate legs 45 degrees for one minute - pallor then reactive hyperemia when put down

skin changes on leg- cooler and ulcerations

ankle-brachial pressure index <0.9- lower perfusion to legs than arms and lack of lower leg pulse

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38
Q

treatment of peripheral vascular disease- different phases

A

drugs- atorvastatin, clopidogrel

intermittent claudication- RF management- smoking cessation, lower BMI, statins, aspirin/ clopidogrel

critical limb ischemia- revascularization surgery- endovascular by stent or surgical bypass

acute limb threatening ischemia- revascularization surgery within 4-6 hours

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39
Q

complication of peripheral vascular disease

A

amputations, permanent limb weakness, increased risk of cerebrovascular accidents

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40
Q

cardiomyopathy definition and categories

A

refers to diseases of the myocardium- heart muscular/ conduction defects

categorised into hypertrophic obstructive , restrictive, dilated

inherited cardiac condition

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41
Q

hypertrophic obstructive cardiomyopathy- cause

A

autosomal dominant genetic condition- defect in sarcomeres

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42
Q

hypertrophic obstructive cardiomyopathy- pathophysiology

A

left ventricle becomes hypertrophic, blocks blood flow out the left ventricle, decreased compliance and decreased CO

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43
Q

presentation of hypertrophic obstructive cardiomyopathy

A

often with sudden death, other is angina, exertional sob, syncope, palpitations
SAD

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44
Q

diagnosis of hypertrophic obstructive cardiomyopathy

A

ecg showing left ventricular hypertrophy, echo=definitive, genetic testing

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45
Q

treatment of hypertrophic obstructive cardiomyopathy

A

bb,ccb, amiodarone (anti-arrhythmic)

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46
Q

what cardiomyopathy is main cause of sudden death in young people

A

hypertrophic obstructive cardiomyopathy

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47
Q

dilated cardiomyopathy cause

A

autosomal dominant- often cytoskeleton gene mutation

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48
Q

what type of cardiomyopathy is most common

A

dilated cardiomyopathy

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49
Q

pathophysiology of dilated cardiomyopathy

A

dilated heart chambers- thin cardiac walls poorly contract- reduced CO

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50
Q

presentation of dilated cardiomyopathy

A

sob, heart failure, atrial fibrilation, thromboemboli

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51
Q

diagnosis for dilated cardiomyopathy

A

echo, ecg

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52
Q

treatment of dilated cardiomyopathy

A

treat underlying conditions and control symptoms

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53
Q

what is the rarest type of cardiomyopathy

A

restrictive cardiomyopathy

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54
Q

causes and pathophysiology of restrictive cardiomyopathy

A

causes- granulomatous disease- sarcoidosis, idiopathic

path- rigid fibrotic myocardium fills poorly and contracts poorly- reduced CO

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55
Q

presentation and diagnostic of restrive cardiomyopathy

A

px- dyspnoea, oedema, congestive hf

dx- ecg, echo, cardiac catherterisation is definitive

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56
Q

treatment of restrictive cardiomyopathy

A

tx- none- consider transplant

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57
Q

values for hypertension

A

clinical blood pressure >140/90
home/ ambulance > 135/85

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58
Q

causes of hypertension

A

most common= primary HTN= idiopathic

secondary HTN= bc of known secondary cause- ROPED- renal disease (ckd), obesity, pregnancy, endocrine (conns, cushings, phaeochromocytoma), drugs- (nsaids, steroids)

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59
Q

risk factors for hypertension

A

increased age

black ethnicity

overweight, lack of excersize, diavetes

stress

increased salt intake

family history

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60
Q

stages of hypertension

A
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61
Q

blood pressure targets

A

under 80- less than 140/90 or 135/85

over 80- less than 150/90 or 145/85

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62
Q

pathophysiology of hypertension

A

all mechanisms will increase raas and sns activity and tpt

blood pressure increases bc bp= co x tpr

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63
Q

presentation of hypertension

A

mostly asymptomtic

pulsatile headache, visual disturbances, seizures

consider secondary causes - phaeochromocytoma, cushings, conns

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64
Q

diagnosis of hypertension

A

bp reading in hospital 140/90 mmHg then ABMP for 24 hours to confirm (bp 135/85+ throughout the day)

asses end organ damage

  • urinanalysis and egfr to check renal function
  • echo/ecg to check LVH
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65
Q

treatment for hypertension

A
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66
Q

complications of hypertension

A

heart failure, severe increased risk of ihd, ckd, increased risk of cerebrovascular accident

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67
Q

what is the most common valvular disease

A

aortic stenosis

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68
Q

where do you hear the aortic valve

A

right of sternum, 2nd intercostal space

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69
Q

what is aortic stenosis

A

narrowing of aortic valve

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70
Q

causes of aortic stenosis

A
  • idiopathic age-related calcification
  • bicuspid aortic valve- congenital (its normally tricuspid)- need family screening after finding this
  • rhematic heart disease
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71
Q

pathophysiology of aortic stenosis

A
  • pressure gradianet develops between left ventricle and aorta- increased afterload
  • left ventricle initially compensates by hypertrophying so it can eject more blood
  • when the left ventricle compensatory mechanism of hypertropjy gets exhaused, the lv functon declines
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72
Q

presentation including heart sound for aortic stenosis

A
  • triad: exertional synope, angina, exertional dyspnoea (SAD)
  • slow rising carotid pulse and decreased pulse amplitude
  • second heart sound (made by closing of aortic+ pulmonary valve) becomes soft or absent ( the aortic valve is not moving and therfore not closing)
  • murmer- ejection systolic murmer- cresendo-decresendo character-radiates to carotid- louder and softer
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73
Q

gold standard investigation for aortic stenosis + what are you looking for

A

echocardiogram- look for left ventricular size and function, and aortic valve area (doppler derived). the aortic valve will barely open

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74
Q

treatment of aortic stenosis

A
  • dental hygiene, consider infective endocarditis prophylaxis
  • if symptomatic- surgery for aortic valve replacement TAVI- transcatheter aortic valve implant- stents the valve open
  • in asymptomatic patients with severe as- consider intervention if adverse features on excersize testing
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75
Q

what is malignant hypertension

A

very high blood pressure causing immediate end organ damage- eg aki, acute stroke, acute coronary syndrome

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76
Q

in terms of dilation and hypertrophy, what do regurgitation and stenosis cause

A

regurgitation- proximal chamber dilation
stenosis- increases upstream pressure and causes proximal chamber dilation and hypertrophy

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77
Q

which valve disorders causes systolic murmers and which cause diastolic

A

systolic: asmr!- atrial stenosis, mitral regurgitation
diastolic: arms!- aortic regurgitation, mitral stenosis

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78
Q

how can you best hear murmers

A

rile!- right- inspiration
left- expiration

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79
Q

where do you hear mitral valve

A

left midclavicular line, 5th intercostal space

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80
Q

what is mitral regurgitation

A

backflow of blood from LV to LA during systole- volume overload

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81
Q

causes of mitral regurgitation

A
  • MYXOMATIOUS MITRAL VALVE (mitral valve prolapse)- main cause
  • IE
  • rhematic heart disease
  • dilated cardiomyopathy
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82
Q

pathophysiology of mitral regurgitation

A

volume overload- left atrial enlargement to compensate and lvh- get pulmonary hypertension- this causes exertional dyspnoea

progressive left ventricular volume overload leads to dilation and progressive heart failure

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83
Q

presentation + murmur type for MR

A
  • ascultation: pansystolic blowing murmer at apex radiating to axilla- simmilarly in volume throughout systole
  • murmer correlates to severity
  • exertional dyspnoea - due to pulmonary hypertension from backlogged blood
  • displaced apex beat because ventricle gets bigger
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84
Q

investigation for MR

A

gs= echocardiogram- la and lv size and function,

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85
Q

treatment for MR

A
  • if severe/ symptoms at rest- - valve replace or repair,
  • anticoag, bb, ccb if AF
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86
Q

what is aortic regurgitation

A

leakage of blood into lv during diastole due to ineffectve aoritc cusps

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87
Q

causes of AR

A
  • biscuspid aortic valve- congenital (mc)
  • rheumatic heart disease
  • IE
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88
Q

presentation of AR

A
  • wide pulse pressure- high systolic and low diastolic
  • displaced apical pulse
  • ascultation- early diastolic blowing murmur at left sternal border 2nd space and systiloc ejection murmur
  • decrescendo
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89
Q

investigation for AR

A

gs= echo= evalulate aortic valve and root + dimension

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90
Q

treatment for AR

A
  • consider ie prophylaxis
  • serial echocardiograms to monitor progression
  • medical management of any heart failure
  • surgery if symptomatic with severe ar, and asymptomatic with lv systolic dysfunction
91
Q

what is mitral stenosis

A
  • rare
  • obstruction of lv inflow that prevents proper filling during diastole
92
Q

main cause of mitral stenosis

A

rhematic heart disease

93
Q

patho of mitral stenosis

A
  • rhd causes mitral inflammation, excacerbated over years with calcification. left atria dilates causing pulmonary hypertension- causing right heart failure symptoms
94
Q

presentation of mitral stenosis

A
  • malar cheek flush
  • association with A.fib
  • low pitched mid diastolic murmur- most prominent at apex- heard best when patients lying on elft
  • intensity of murmer doesnt correlate with severity
95
Q

investigation for mitral stenosis

A

echo- gs

96
Q

treatment for mitral stenosis

A
  • if present with a.fib- treat with anticoagulation
  • asymptomatic- serial echocardiogram
  • symptomatic- percutaneous mitral balloon valvotomy, mitral valve surgery or replacement
97
Q

what do calcium channel blockers usually end in + give an example

A

-dipine
amlodipine
also verapamil

98
Q

what do angiotensin 2 receptor blocker drugs end in

A

-artan

99
Q

definition of aortic dissection

A

tear in intima of aorta, blood dissects into media. type of pseudoanyeurism, intramural

100
Q

causes/ rf of aortic dissection

A

age, male, smoking, cholesterol, hypertension, sedentary lifestyle, CABG

101
Q

main location of aortic dissection + types

A

right lateral area of arch- under the most stress. type a is ascending aorta before brachiocephalic. type b= descending aorta after left subclavian

102
Q

pathophysiology of aortic dissection

A

blood dissects media, pools in the false lumen, can propagate forward or backward (anterograde or retrograde) causing low perfusion to end organs, organ failure and shock

103
Q

presentation of aortic dissection

A

sudden onset ripping chest pain

(not mi- thats crushing and heavy)

back pain, abdomen pain

hypotension, hear an aortic regurg, syncope, low left arm peripheral pulse

104
Q

investigation of aortic dissection

A

ct scan= gold standard
cxr shows widened mediastinum
toe = helpful

105
Q

treatment of aortic dissection

A

surgical emergency

  • type a= open surgery to remove section of aorta and replace with graft
  • b- endovascular repair- catheter thry femoral and stent graft

medically- beta blocker- esmolol

if hypotensive- iv fluids, blood transfusion

106
Q

complications of aortic dissection

A

mi, stroke, cardiac tamponade, death

107
Q

what is cardiac tamponade

A

a medical or traumatic emergency that happens when enough fluid accumulates in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock

108
Q

definition of peicarditis

A

typically acute inflammation of pericardium, with or without effusion

  • effusion can be dry (fibrous) or wet (most common, exudative, hemorrhagic)
109
Q

risk factors for pericarditis

A

male- age 20-50

viral infection

transmural mi

110
Q

causes of pericarditis including main cause

A

idiopathic

main- VIRUS- coxsackie, ebv, cmv, herpes

bacteria- mycobacterium tuberculosis !

common- autoimmune- sle, sjrogens, RA

dresslers syndrome -post mi

111
Q

pathophysiology of pericarditis

A

inflamed pericardial layers rub against eachother and cause further inflammation. inflammation causes narrowing of the pericardial space and if not treated it may remain dry or can lead to pericardial effusion

112
Q

presentation of pericarditis overview

A

triad of signs: sharp chest pain, pericardial friction rub (to and fro sound when pt leans forward) and ecg changes

pain is worse lying down and worse with inspiration, better sitting forward

pain radiates to left shoulder and back (trapezius)

myalgia, tripod position to relieve pain,

signs of right sided heart failure (raised jvp and peripheral oedema)

113
Q

in pericarditis- where is the pain and when is it better and worse

A

sharp chest pain that radiates to your left shoulder and back (traps)
its better in a tripod forward position and worse when lying down

114
Q

what is the triad of signs for pericarditis

A

sharp chest pain
pericardial friction rub- leans forwards- a to and fro sound
ecg changes

115
Q

investigations for pericarditis, which is diagnostic

A

ecg= diagnostic- widespread saddle shaped st elevation and pr depression

blood test shows raised wbc (infective), crp, esr (may show autoimmune)

cxr may show cardiomegalic heart

116
Q

treatment for pericarditis

A

idiopathic + viral- NSAIDS eg aspirin + CHOLCHICINE (long term)

if bacterial consider abx

117
Q

complications of pericarditis

A

pericardial effusion leading to CARDIAC TAMPONADE!, constrictive pericarditis

118
Q

definition of atrial fibrilation- rhythm

A

electrical activity in the atria becomes disorganized, leading to random muscle twitching and an irregularly irregular pulse

119
Q

causes of atrial fibrilation and what makes it worse

A

SMITH

-sepsis, mitral stenosis/regurgitation, IHD, thyrotoxocisis, hypertension

alcohol and caffeine make it worse

120
Q

pathophysiology of A fib and why do you get complications

A

electric activity of heart is disorganized- san is overridden by random signals in atria- causes atria to twitch and contract at different times- causes irregularly irregular ventricular contraction

blood stagnates in atria forming a thrombus- may travel to brain causing ischaemic stroke (really high risk)

121
Q

presentation of A fib

A
  • palpitations
  • irregularly irregular pulse
  • thromboemoli (ischaemic stroke)
  • chest pain, syncope, hypotension
122
Q

diagnostic test of A fib and what you see

A

diagnostic= ecg.

  • irregularly irregular pulse with narrow qrs <120ms
  • no p waves and fibrillatory squigles

maybe echo later

123
Q

treatment for a fib- both acute and chronic

A

acutely if unstable-/ syncope/ shock/ chest pain/ heart failure-synchronized cardioversion (shock)

stable/ long term- bb (heart rate and pulse), oral anticoag (stroke)

124
Q

for a.fib- explain the scoring system to see if anticoag is needed

A

CHADS2-VASc-SCORE- stroke risk so anticoagulation needed

GREATER THAN 2= GIVE ORAL ANTICOAG (apixaban/ rivaroxaban)

congestive heart failure

hypertension

age > 76

DM

stroke

vascular disease

age 65-74

sex (female)

125
Q

in a.fib, explain the score that asses risk of major bleeds in patients taking anticoagulation

A
  • old age
  • renal impairment
  • bleeding previously
  • iron- low hb
  • taking antiplatelet
126
Q
A
127
Q

definition of atrial flutter

A

irregular organised atrial firing- 250-300bpm.

128
Q

risk factors of atrial flutter

A

atrial fib. also similar aetiology to atrial fib

129
Q

pathophysiology of atrial flutter

A

fast atrial ectopic firing (250-300bpm). causes atrial spasm but not as uncoordinated as A.Fib

130
Q

presentation of atrial flutter

A

dyspnea, palpitations

131
Q

diagnostic investigations of atrial flutter

A

ECG= diagnostic. saw tooth pattern on f wave. often with a 2:1 block (2 p waves for every QRS)

132
Q

treatment, acute and stable of atrial flutter

A

acutely unstable- synchronized cardioversion

stable- beta blocker with oral anticoagulation

133
Q

what do you call a large volume of fluid thats enough to impair ventricle filling

A

cardiac tamponade

134
Q

what is pericardial effusion

A

accumulation of fluid in pericardial space accompanying pericarditis

135
Q

causes/ rf of pericardial effusion

A

typically pericarditis

rf all pericarditis related- viral, autoimmune

136
Q

presentation of pericardial effusions and its main complication

A

related to pericarditis

cardiac tamponade (effusion is large enough to raise intra-cranial pressure, squeezing the heart - reduced filling in diastole and decreased CO)-

  • BECKS TRIAD (bless)- blood pressure lowered (hypotension), elevated JVP, soft/ muffled s1+s2 heart sounds
  • pulsus paradoxicus- fall in systolic BC >10mmHg on inspiration- good indicator of tamponade
137
Q

diagnostic investigation of pericardial effusion and other

A

effusion- echocardiogram= diagnostic- asses size fo effusion

cxr will show big globular heart

138
Q

treatment of pericardial effusion and tamponade

A

effusion- treat underlying cause (usually nsaids and colchicine), drain effusion

cardiac tamponade- urgent paricardiocentesis

139
Q

definition of heart block and bundle block and bundle branch block

A

when the av delays for too long

bundle block is when delay is in bundle of his (before split into r+l)- the r and l delay is bundle branch block

140
Q

what is the av delay represented by on ecg and how long should this be

A

pr interval- 200ms/5 small boxes (120-200)

141
Q

what is one small box on ecg equal to

A

0.04s

142
Q

first degree heart block- what is it and treatment

A

the avn delay is just too long

prolonged pr interval (>200ms)

usually asymptomatic- so no treatment

143
Q

what are the subcategories of type 2 heart block

A

mobitz 1/ wenckebach- progressive delay
mobitz 2- no progression, all or nothing

144
Q

explain mobitz 1 in second degree heart block and treatment

A

MOBITZ 1/ wenckebach - delay gets progressively longer until you drop a beat

pr gets progressively longer until a beat is dropped and theres no qrs, and then normal pr returns

no tx unless theres symptoms eg syncope. tx= pacemaker

145
Q

explain mobitz type 2 second degree heart block and treatment

A

MOBITZ 2- conduction through av node is all or nothing- atrial impulse goes through with no delay or it doesnt go through at all

pr interval is consistently prolonged (not progressively) and theres random dropped qrs , then the prolonged pr returns

treatment= pacemaker

146
Q

what does a 3:1 heart block mean

A

p waves for every qrs is a 3:1 block

147
Q

explain 3rd degree/ complete heart block and treatment

A

no impulses are conducted

ventricles recognixe they don’t get impulses so generate their own ventricular escape rhythm

the atria and ventricles now each have their own pacemaker and contract independantly of eachother- av dissasociation- reduced CO- syncope or sudden cardiac death

p and qrs waves appear at their own rates

NEEDS treatment- pacemaker.

148
Q

cause of bundle branch block

A

usually caused by fibrosis- ischemia, heart attack , hypertension, CAD, cardiomyopathy

149
Q

explain bundle branch block- how it works

A

conduction block on right bundle branch

sa node- atria contract- av node- bundle of his- at split it goes down left bundle first because right is blocked, so left ventricle contracts first, then to the right. (from left, spreads through purkinjie fibers to right)

150
Q

on the leads what does bundle branch block look like

A

use chest leads- v1-v6

left- william - w in v1, m in v6

right- marrow- m in v1, w in v6

151
Q

in structural heart defects, when is there cyanosis and when isnt there

A

blood shunts left to right- non cyanotic
right to left- cyanotic

152
Q

what are the 4 features of tetralogy of fallot

A
  • ventricular septal defect
  • overriding aorta on top of the ventricular septal defect
  • rv hypertrophy
  • rv outflow obstruction
153
Q

explain whats going on in tetralogy of fallot and what the baby looks like

A
  • cyanotic, ventricular septal defect with rv outflow stenosis
  • right vnetricule is higher pressure than the left, puncures hole in the ventricle, blue blood (deoxygenated) passes from RV to LV- patient is blue.
154
Q

what position improves cyanosis in babies

A

knee to chest squat position

155
Q

what would a chest x ray show in tetralogy of fallot and whats the treatment

A

boot shaped heart
full surgical repair within 2 years of life

156
Q

explain coarctation of aorta- what is it whats happening

A
  • aorta narrows at ductus arteriosus (pul artery to aorta)
  • blood diverts through aortic arch branches- increased perfusion to upper body vs lower body
157
Q

presentation, dx and tx of coarctation of aorta

A
  • presentation- scapular bruits, upper body hypertension
  • dx- cxr show dilated intercostal vessels, ct angiogram
  • tx-surgical repair or stenting
158
Q

what does ductus arteriosus do

A

connects pulmonary artery to aorta

159
Q

what happens in a patent ductus arteriosus, presentation, dx and tx

A

fails to close after burth
- blood shunts from aorta to pulmonary trunk - risk of pulmonary overload + eisenmengers ( high pressure pul blood flow- damaage to pul vasculature- RV
- dyspnoea, failure to thrive- machine like murmur
- dx- echo
- tx- close it surgicially or percutaneously (medically first- ibuprofen, indomethacin)

160
Q

what is an av septal defect , whats its presentation

A

hole down middle of heart
dyspnoea, exersize intolerant- eventually eisenmengers

161
Q

what strucutal heart defect is downs syndrome most commonly associated with

A

atrioventricular septal defect

162
Q

explain ventricular septal defect- whats happening, dx and tx

A

left to right- non cyanotic shunt. risk of eisenmangers + RVH

small vsd- asymptomatic

large vsd- excersize intolerance, failure to thrive,

dx- echo

tx- surgical closure or spontaneous

163
Q

whats happening in an atrial septal defect, dx, tx

A

patient foramen ovale

shunt of blood left to right so non cyanotic

may overload right hand side circulation and cause rvh, worst case is eisenmengers

dx- echo

tx- spontaneous or surgical closure

164
Q

define Infective endocarditis

A

infection of heart valve/ other endocardial strucutres in the heart

165
Q

causes of carditis

A
  • bacteria
    • main cause= staph .aureus
    • strep. viridans ( gram positive, a haemolytic, optochin resistant strep, associated with poor dental hygeine)
    • s. boris- associated with colon cancer
    • HACEK organisms- Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella
166
Q

epidemiology of Infective endocarditis

A

elderly

young iv drug users

young with congenital heart disease

prostetic heart valves

167
Q

what valve is affected in Infective endocarditis

A

ie typically affects MITRAL VALVE on left, but in IV drug users, affects more TRICUSPID

168
Q

pathophysiology of Infective endocarditis

A

abnormal/ damaged endocardium have increased platelet , deposition- bacteria adheres to this and causes vegetations (mass of fibrin, platelets, bacteria and antibodies)

169
Q

presentation of Infective endocarditis

A

FEVER+ NEW MURMUR!

fatigue, chest pain

janeway lesions- painless lesions in palms and soles due to microemboli

splinter haemorrhages in nail bed

osler nodes- painful, red lumps on tips of fingers and toes

roth spots- small ruptured capillaries in the eyewe- seen on funduscope

170
Q

diagnosis of Infective endocarditis- gold standard, what a diagnosis is based on and blood test/ film results

A

GS= transoeseophageal echocardiography- can see vegetations on the valves through this

based on modified duke criteria- 1major+3minor or 5 minor

  • major= persistently positive blood cultures (typical bacteria), echo toe shows vegitations
  • minor- predisposing factors, fever, vascular phenomena, equivocal blood cultures

also have high esr, crp, neutrophillia

171
Q

general treatment for Infective endocarditis

A

iv penicillin and gentamicin

172
Q

treatment for Infective endocarditis if staph aureus is cause

A

vancomycin + rifampicin

173
Q

treatment for Infective endocarditis if strep viridians is the cause

A

benzylpenicillin + gentamicin

174
Q

complication of Infective endocarditis

A

heart failure + septic emobili + sepsis

175
Q

what does one large square on the ecg mean

A

200ms

176
Q

how to calculate heart rate on ecg

A

300/ no of big squares
eg- 2 big boxes (400ms)
300/2= 150 bpm

177
Q

what does the st segment represent

A

isovulemic ventricular relaxation

178
Q

what does the qrs complex show

A

ventricular depolarisation and atrial repolarisation
cant see atrial repolarisation bc its masked by ventricular depol

179
Q

how long is the p wave normally

A

<120ms wide

180
Q

how long is the pr interval and where is it

A

0.12-0.2 seconds (120-200ms) (3-5 small squares)
from start of p to q of qrs

181
Q

what does the t wave show

A

ventricular repolarisation

182
Q

what does a broad qrs show

A

ventricular conduction delay/ bundle branch block

183
Q

where is the qrs interval and what does it represent

A

start of qrs to end of t wave
ventricular depolarisation and repolarisation

184
Q

how do you know if something is a superventricular rhythms

A

qrs complex is narrow and tachycardia

185
Q

eg of supraventricular rhythms

A

atrial fib
atrial flutter
atrial tachycardia

186
Q

what do ventricular rhythms look like

A

broad qrs- just looks in general a broad rhythm

187
Q

what is cardiac failure

A
  • state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues
  • symptomatic condition- breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output
188
Q

causes of cardiac failure

A
  • IHD!!! main cause
  • hypertension- (as arterial pressu reincreases it gets harder for lv to pump blood out- so lv hypertrophies needing more oxygen, extra muscles also squeeze coronary arteries so less blood to tissue)
  • dilated cardiomyopathy
  • restrictive cardiomyopathy
  • valvular heart disease- mainly aortic stenosis
  • pregnancy, hyperthryodiism, arrhythmias (anything increasing myocardial work)
  • cor pulmonale
189
Q

rf for cardiac failure

A
  • age (65+), smoking, obesity, previous MI, male
190
Q

systolic vs diastolic cardiac failure

A
  • systolic
    • decreased contractility of lv- causing decreased cardiac output- so DECREASED EJECTION FRACTION<40% and INCREASED EDV (bc more blood left over as less is pumped out, combined with diastolic filling)
      • caused by ihd (low contractility as part of it was damaged), mi, hypertension, dilated cardiomyopathy (dilated and weakened)
    diastolic:
    • not enough blood is returning to heart
    • normal ejection fraction and normal edv (as atria is capable of sqeezing more blood into ventricle)
    • end diastolic pressure is HIGH as the venticle is not compliant
      • causes: hypertension, cardiac tamponade, constrictive pericarditis
191
Q

high output vs low output cardiac failure

A

can also be low or high output- low output is decreased co and fails to increase with exertion- could be due to mitral regurgutation, pump failure, high output is like anaemia, pregnancy, hyperthyroidism

192
Q

patho of heart failure

A
  • normally increased preload= increased afterload= increased CO (frank starling law)
  • failing hearts= dysfunctional frank starling= reduced CO
  • compensatory mechanism activates- RAAS & SNS (temporary increase bp with increase in aldosterone, adh, sns), causing vasoconstriction increasing afterload
  • compensation soon fails- cardiac remodeling, the raas will exacerbate fluid remodeling and heart failure will affect both circuits - congestive heart failure
193
Q

cardinal signs of heart failure

A

SOBASFAT
sob

ankle swelling- fluid retention

fatigue

194
Q

left heart failure causes and presentation

A

heart failure with reduced ejection fraction. typically due to systolic (pumping) dysfunction

  • IHD
  • Hypertension
  • Dilated cardiomyopathy (ventricle is dilated + weakened- restrictive is also a rarer cause)
  • aortic stenosis
  • presentation
    symotoms:
    • exertional dyspnoea
    • paroxysmal nocturnal dyspnoea (sob attack at night)
    • orthopnea (usually pt will lie on more pillows to help)
    • fatigue
    • weight loss
    signs:
    • cardiomegaly + displaced apex beat
    • pulmonary oedema
    • pleural effusion
    • 3rd (and 4th) heart sounds
    • crepitations in lung bases (crackles)
    • tachycardia
195
Q

rifht heart failure causes and presentation

A
  • left ventricular failure (increased pressure in pul artery makes it harder for right side to pump blood into it)
  • hypertension
  • pulmonanry stenosis
  • cor pulmonale (lung disease)
  • presentationsymptoms:
    • sob
    • peripheral oedema
    • ascites
    signs:
    • raised JVP
    • hepatomegaly
    • pitting oedema
196
Q

classification of heart failure

A

NHYA- new york heart assocoiation- for hf severity

  • class 1- asymptomatic- no limit on physical activity
  • 2 and 3- mild hf - slight limit on moderate activity and symptomaticallt moderate/ marked limit on moderate and gentle activity
  • class 4- symptomatically severe- symptoms even at rest!
197
Q

investigations 4 for heart failure

A
  • bloods- brain natriuretic peptide (bnp)- released from stressed ventricles in response to increase mechanical stress
  • CXR- (abcde)
    • alveolar oedema (bat wings)
    • kerley b lines
    • cardiomegaly
    • dilated upper lobe vessel of lung
    • effusion (pleural)
  • echo
  • ecg- may show underlying cause
198
Q

what does a chest x ray show for heart failure

A
  • alveolar oedema (bat wings)
  • kerley b lines
  • cardiomegaly
  • dilated upper lobe vessel of lung
  • effusion (pleural)
199
Q

treatment of heart failure

A
  • lifestyle change- weight loss, excersize , stop smoking and drinking
  • pharmacological: (ABAL) one after the other if it doesnt help
    • Ace inhibitor (or arb)
    • Beta blocker
    • Aldosterone antagonist- spironolactone
    • Loop diuretic- furosemide or thiazide
    in severe- cardiac resynchronisation therapy, or heart transplant
200
Q

cause/ rf of stable angina

A

most common cause is ischaemic heart disease

age, smoking, family history (first relative and under 65ish), diabetes- hyperlipidemia, hypertension, obesity, stress, sedentery…

201
Q

exacerbating factor of stable angina

A

anemia, hypoexemia, hypertension, valvular heart disease

cold weather, emotional stress

big meals

202
Q

patho for stable angina

A

mismatch between hearts oxygen supply and demand- increase in demand and limited supply.

atherosclerosis:

  • fatty streak appears in intimal wall- t cells and macrophages
  • in intimediate lesiosn you get foam cells , t cells and vascular smooth muscle cells. platelet aggregates and adheres to site inside vessel lumen
  • advanced lesion- foam cells, t cells, smooth muscle, fibroblasts, lipid decelop fibrous cap on top of lesion

symptoms will start when lumen is 70-80% occluded.

if plaque ruptures- progressive luminal damage

203
Q

presentation of stable angina

A

central crushing chest pain radiating to neck/jaw

brought on with exertion and worsens from time

relieved with 5 mins rest/ gtn spray

breathlessness

204
Q

1st line and gold standard investigations for stable angina

A

1st line is ecg- normal, wuth excersize shows ischaemia. may see st depression and t wave inversion

GS- CT angiography- shows stenosed athersoscleoric arteries- 70-80% occluded

205
Q

treatment for stable angina

A
  • lifestyle modifying- low weight, stop smoking, healthy diet
  • symptomatic- GTN spray

all pt should 1st line be on CCB- (AMLODIPINE) OR BETA BLOCKER

then ccb AND bb

then ccb and bb and another antianginal eg long acting nitrates

  • contraindications of ccb= heart failure, bb is asthma

consider:- ace-i, aspirin, statin

if pharmacology is unceccessful- referal for revascularisation

  • PCI- balloon stent coronary artery- less invasive but risk of restenosis
  • CABG- bypass graft- more invasive but better prognosis
206
Q

what is prinzmetal angina- who do you see it in and what does it present with

A

prinzmetals angina due to coronary vasospasm- not due to cv vessel atherogenesis. seen in cocains users and ecg shows st elevation

207
Q

what is acs

A

umbrella term for unstable angina, NSTEMI, STEMI

208
Q

patho/ cause of acs

A

usually ischaemic heart disease (mc) -

usuallt result of thrombus from an atherosclerotic plaque blocking a coronary artery

209
Q

presentation of acute coronary syndrome

A

same as stable angina but resting pain with no relief- GTN doesnt help

severe palpitations and sense of impending doom

central, constricting chest pain

  • levine sign is a sign of ischemic chest pain
210
Q

dx and ix for acs

A

ecg

biomarkers- troponin and creatine kinase

ct angiogram to show extent of occlusion

211
Q

long term treatment for acs

A

long term treatment: beta blocker, aspirin, (75mg life), atrovastatin, acei

212
Q

occlusion in unstable angina

A

partial occlusion of minor artery

213
Q

infarction in unstable angina

A

no- ischemia only

214
Q

ecg and troponin in unstable angina

A
  • ecg normal (may be some st depression and t wave inversion)
  • troponin lvls normal
215
Q

presentation of unstable angina

A

chest pain at rest

  • chest pain with cresendo pattern
216
Q

treatment for unstable angina

A

MONAC

  • morphine, o2 if sats are left than 94, nitrates (gtn) aspirin 300mg +clopidogrel (dual antiplatelet)
217
Q

occlusion and infarction of NSTEMI

A

occlusion- major partial/ total minor coronary artery
infarction- sub endothelium infarction- area far away from coronary artery

218
Q

diagnosis on? and other test/ investigation for nstemi

A

retrospective diagnosis based on troponin results (elevated)

ecg- st depression, t wave inversion, NO Q WAVES!

219
Q

treatment for nstemi

A

use GRACE score- if low risk coronary angiography later and if high risk then coronary angiography right there- consider pci
pci only- not thrombolytics

220
Q

occlusion and infarction of stemi

A

total of major coronary artery
transmural infarction through all layers

221
Q

diagnosis based on and other tests for stemi

A

diagnosis made on ECG at presentation
st elevation
pathological Q WAVES after some time

troponin elevated

222
Q

treatment for stemi

A

MONAC
PCI- stenting
if not- thrombolytics

223
Q
A

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