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Phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

which ECG leads do you look at for atria

A

I
II
AVR

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2
Q

what does rigth atrial enlargement look like on an ecg

A

Tall p, pointed p in the limb leads

Don’t sit on a pulmonary problem, its pointy!

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3
Q

what does left atreial enlargement look like on an ECG

A

Notched/m shaped p wave in limb leads

M for mitral in the left side

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4
Q

what is Wolf-Parkinson-White Syndrome and how is it identified on an ECG

A

Short PR interval - (accessory pathway bundle of Kent is working so its conducting too quickly)

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5
Q

how is a first degree heart block shown on an ECG

A

Long PR

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6
Q

what are the three criteria for left ventricular hypertrophy

A

Sokolow and Lyon Criteria:
(S in V1) + (R in V5 or V6) > 35mm

Cornell criteria:
S in V3 + R in AVL > 28 in men or 20 in women

Modified Cornell:
R in AVL>12

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7
Q

how long should the PR interval be

A

120-200ms

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8
Q

how wide should teh QRS be

A

no wider than 110ms (3 small squares)

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9
Q

on whihc leads should teh QRS always be upright

A

I and II

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10
Q

in whihc lead are all waves negative

A

AVR

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11
Q

how do the chest leads change and what are teh best at looking at

A

QRS complex

* R wave increases in size from V1-V4, S wave grows from V1 to 3 and is absent in V6
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12
Q

what should teh ST segment look like in the leads

A

ST segment is isoelectric in all leads except V1 and V2 where it may be slightly raised (very raised is bad)

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13
Q

in which leads should the p and t wave be upright in

A

I II V2-V6

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14
Q

what is teh rule for q waves in i, ii, V2-V6

A

There should be no Q short waves larger than 0,04s in I, II, V2-V6

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15
Q

how many ms is a big and a small box worth on an ecg

A

big - 0.2ms
small - 0.004 ms

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16
Q

how to remeber whihc colour of elecrode goes to which limb

A

snow on grass, smoke on fire (remember white is right)

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17
Q

how do you meausre rhythem on an ECG

A

meausre teh distance between teh Rs

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18
Q

how do you measure the heart rate on an ECG

A

300/number of boxes between each R

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19
Q

which leads looks at the inferior section of the heart

A

II
III
AVF

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20
Q

whihc leads looks at the lateral section of teh heart

A

I
AVL
V5
V6

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21
Q

which leads look at the septal portion of the heart

A

V1
V2

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22
Q

which leads look at the anterior portion of the heart

A

V1
V2
V3
V4

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23
Q

how do you work out the heart rate on an ecg, gor both methods

A

300/1500 method:
this si or regular rhythems
count teh number of big boxes between two QRS complexes and then do 300 divided by this number.

Or cound te small boxes and then do 1500 divided by this number.

10 second rule:
for irrculagr rhythems, you need to cound teh number of qrs complexes on each sheet, as its a 10 second peicie, multiply it by 6 and this gets a pulse.

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24
Q

how much is a big square and a small square worth on an ECG

A

small - 0.04
big - 0.2

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25
Q

how does one work out the heart axis

A

looks at lead 1 and avf QRS complex

they should be both positive whihc means its in teh normal range

If lead 1 is negative it might mean that there is a a right axis deviation

if lead avf is negative then it is left deviated

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26
Q

what is the normla heart axis

A

-30 to +90

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27
Q

what is teh 10 step process to reading an ECG

A

PS really randy alligators play quickly, sex quickly too.

Patient details
Situation details
Rate
Rhthm
Axis
P-wave and P-R interval
Q-wave and QRS complex
ST segment
QT interval
T-wave

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28
Q

what are the infections caues of pericarditis

A
  • Virus - enterovirusl adenovirus, herpesvirus, parovirus
    Bacteria - mycobacterium tuberculosis
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29
Q

what are the most common non infections causes of pericarditisq

A

NEOPLASTIC - secondary metastatic tumours

automimmne conditions - rheumatoid arthiritus, sjogren syndrome

metabolic - ureamia, myoxedema

trauma and iantrogenic - penatrating injury, radiation injury, postmyocardial infarction syndrome,

other - aortic dissection or chronic heart faliure

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30
Q

what are the three most commen causes of pericarditus

A

Virusus

Neoplasms

Iantrogenic form stents and surgery

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31
Q

what is a key feature of pericarditis

A

pain is worse when lying doen and better when sat sitting forewards

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32
Q

what is pulses paridoxis

A
  • Pulsus paridoxis - an exagerated drop in blood pressure during inspiration
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33
Q

what is pericardial effusion

A

Pericardial effusion - A condition in which extra fluid collects between the heart and the pericardium

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34
Q

what are teh people who ace inhibitors shouldnt be given to, and who are teh people beta blocker cant be given to

A

ace - prgnant ladies
beta - severe asthma

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35
Q

what is teh main side effect of ace inhibitors

A

dry cough

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36
Q

what does an incrased PR interval mean

A

a heart block

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37
Q

what does a saw tooth pattern mean on an ECG

A

atrial flutter

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38
Q

what are teh 4 types of Angina

A

Stable - induced by effort such as exercise
Unstable - increased severity, it occurs at rest as well
Decubitus - occurs when lying down
Nocturnal - occurs when asleep and may wake people up

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39
Q

wht is vasospastic angina

A

Vasospastic angina is also known as prinzmetal angina, variant angina or coronary artery spasm. It develops when a coronary artery supplying blood and oxygen to your heart goes into spasm and suddenly narrows.

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40
Q

what are teh risk factors for angina

A

Smoking, obesity, exercise, diet, alcohol intake sedentary lifestyle.

Hypertension, diabeties , hypercholesteremia, depression

Age, family history , gender, ethnicity

Stress, low social interaction

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41
Q

pathophysioology of angina

A

An imbalance between the supply of oxygen to cardiac muscle and the demand

Athelerocscalorsis causes a narrowing of the coronary arteries which cuases ischemia and pain. The plaque gets bigger and bigger and once its 50% of the lumen size it cant compensate anymore, this leads to remodelling and thee vessle becoming narrowing.
Thjis then imposes inot the lumen and runs the risk of hemmoraging
At first a fatty streak forms, which leads to macrophages forming foam cells, and the smooth muscle grows over eth top of the fat.
The consequences of this are occluiion du to thrombus, chronic narrowing of the vessles, aneuyerism changes

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42
Q

what are teh signs of angina

A

Chets pain comes on and is reslolved by rest or GTN spray
Exasubated by cold, anger and excitement

This can be scored by
Central tight chest pain radiating to arms, neck and jaw
Precipitated by exertion
Relieved by rest or GTN spray
3/3 – typical angina
2/3 – atypical angina
1/3 – non-anginal pain

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43
Q

what are teh symptoms of angina

A

Pain in chest, arms, neck and jaw.
Dyspnoa - shortness of beath
Palpitations
Syncope - fainting

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44
Q

differential diagnosis for angina

A

Pericarditis, pulmonary embolism, chest infection, GORD< dissection of the aorta

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45
Q

what are teh zero to finals reatments for angina -

A
  • There are three principles ror manageent - imiediate ef, long term relief and then secindary orevention of CV duiseases.
    • Immediate - use GTN spray, if there is still pain after 5 mins take again, if there us still pain after 5 mins call an ambulance
    • Long term - beta blocker tor calcium channel blocker
    • Secondary prevention - asprin, atorvastain, ACE inhibitors, beta bloker
    • RAMP managemeeeeeshould also be used. R- refer to cardiolgy, advise them about the diagnosis manegement and when to call an ambulance, medical treatmentm procedural/surgical interventions.
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46
Q

what are the drug treatment for angina

A

Treat underlying conditions such as hypertension and diabeties mellitus

Glyceryl trinitate spray - 1st line treatmen which is taken when needed to relive pain

Beta blockers - (bisoprosol, propanalol) reduce the heart rate and the force of contractipn, its negitivly ionotrophic and chronotropic . DON’T use in pateints with asthma or a heart block

Calcium channel blocker - amlodapine,

Anti platelet - asprin inhibits platelet aggregation, by inhibiting COX. Clopidogrel can also be used.

Statins - reduce cholesterol levels, atorvastatin, simvastatin.

ACE inhibitors - for blood pressure controll such as ramapril

Ivabradine - ibibits the pacemaker current in the SAN and therefore reduced heart rate and decreased blood pressure

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47
Q

what are the social traeatments for angina

A

Work out the Qrisk, this takes into account BP, age, smoking status, cholesterol, rhemuatid arthiritus, diabetes mellitus, BMI

Weigth loss, quit smoking, more exercise

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48
Q

what are teh surgical treatments for angina

A

Percutaneous cononary intervention - stentin or balooning of the artery, however this runs the risk of restenosis. Drug eluting stents slowly release medication t oprevent blood clots.

Coronary artery bypass graft - good preognosis but longer recovery

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49
Q

what are the three acute coronary syndromes

A

Unstable angina - cardiac chest pain with a creshendo pattern

STEMI - a major occlusion of a coronary arterym full thickness muscle damage,
Diagnosed by ECG at resintation

NSTEMI - occurs by developing a complete occlusion of a minor coronary artery or partial occlusion of a major coronary artery previously affected by atherosclerosis

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50
Q

what is teh pathophysiology of acute coronary syndromes

A

Rupture or erosion of fibrous cap of a coronary plaque with subsequent formation of a platelet rich clot, inflammation, and vasoconstriction produced by platelet release of serotonin and thromboxane A2

Unstable angina differs from NSTEMI because in NSTEMIs the occluding thrombus is sufficant to cause myocardial damage and an elevation in serum markers of myocardia injury (troponin and creatine kinase)

The main causes if the rupture of atherosclerotic plaque, and consequent arterial thrombosis. The more uncommon causes of it care coronary vasospasm, drug abuse, dissection of coronary artery.

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51
Q

what are teh tests for acute coronary syndromes

A

ECG:
UNSTABLE ANGINA - there is a normal one or slight T depression

STEMI - ST elevation and tall T waves, will produce pathological Q waves sometime after an MI

LEFT BRANCH BUNDLE BLOCK. Remember WilliaM - V1 is W and then M is for V6

NSTEMI - a retrospective diagnosis - will see ST depression and/or T wave inversion

Ischemia - ST depression, T wave flattening or inversion

Q waves - evidence of previous infarction, pathological Q waves are wider than normal, >35% QRS hight and wider than one small square) the larger the infarction is the more likely it will result in a pathological Q.

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52
Q

what are the tests for unstable angina

A

History
FBC – anaemia aggravates it
Cardiac enzymes (troponin normal) – excludes infarction
ECG – ST depression when patient is in pain
CT Coronary angiography
Risk assessment (QRISK2) – if low risk do an elective stress test

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53
Q

what are the 9 treatment catogorys for unstable angina

A

Risk Factor modification
Stop smoking
Lose weight
Healthy diet
Exercise

PCI (if risk assessment score is medium/high) and CABG

Aspirin (300mg initially then 75mg daily) – irreversibly inhibits COX-1 🡪 less production of thromboxane A2 🡪 less platelet aggregation

Anti-coagulants – Heparin interferes with thrombus formation at site of plaque rupture by inhibiting factors II (prothrombin), VII, IX and X and reduces risk of ischaemic events and death
Fondaparinux (synthetic polysaccharide) inhibits factor Xa of the coagulation cascade and has a lower risk of bleeding than heparin

Nitrates – GTN spray or IV infusion

Beta blockers – metoprolol, bisoprolol

Statins – Reduce cholesterol e.g. atorvastatin, simvastatin

ACE inhibitors - Ramipril

Calcium channel blockers (if beta blocker contraindicated) – amlodipin

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54
Q

what are the three cardiac enzymes to test for

A

TROPONIN T and I, highly sensitive to cardiac muscle injury. It will show a rise within 3-12 hours, peak at 24-48 hours. Normal troponin rules out MI.
CREATINE KINASE- catalyses the conversion of creatine ad it will rise and can be used to determine reinfarction
MYOGLOBIN - cardiac enzymes which rises when heart damaged

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55
Q

what are teh complications of acute coronary syndromes

A

DARTH VADER

Death
Arrhythmias
Ruptured septum
Tamponade
HF
Valve disease
Aneurism of ventricle
Dressler’s syndrome - pericarditis and effusing after 2-12 weeks
Embolism
Reoccurrence of ACS

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56
Q

define MI

A

Necrosis of cardiac tissue due to prolonged myocardial ischemia due to complete occlusion of an artery by a thrombus

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57
Q

MI risk factors

A

Age, make, history of coronry heart diseas, DM, hypertension, hyperlipidemia, family history

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58
Q

MI pathophysiology

A

Due to the rupture of an atherlosclarotic plaque which leads to a clot formation in one of the arteries
Rupture - thrombus - occlusion of artery - myocardial cell death

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59
Q

MI key presintations on an ECG

A

STEMI - ST elevation, Tall T waves, pathological Q waves

NSTEMI - ST depression and t wave inversion

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60
Q

MI signs

A

Longer than 20 mins, not relieved by GTN spray, pain may radiate to the left arm, pulse and blood pressure may vary, patient is gray and sweaty, 4th heat sound

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61
Q

MI symptoms

A

chest pain, sweating, dysponea, fatuigue, nausea, vomiting

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62
Q

MI tests

A

History, ECG
STEMI - ST elevation and tall T waves
NSTEMI - ST depression and T inversion

Cardiac enzymer - Troponin T, creatine Kinase, myoglobin
CT angiogra,
FBC, U&E
Blood glucose and lipid level

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63
Q

MI diffrentai diagnossi

A

Angina, pericarditis, endocarditis, pulmonary embolism, pneumothorax, aortic aneurism

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64
Q

actute and secondary manegement for MI

A

Acute management:
MONA - Morphine, oxygenine if low sats, nitrates, Asprin
12 lead ECH and cardiac moniter
Beta blocker for IV, contraindicated in hypotension, HF, bradycardia and asthma
Referral to PCI
Thrombolysis - alteplase

Secondary:
Modification of risk factors
75mg asprin daily
Clopidogrel, ticagrelor
Statins
Beta blocker, ace inhibitor or calcium chanel blocker
Return to work after 2 months if suitable to, and take it easy!

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65
Q

complications of MI

A

MAPDUM

Myocardial rupture
Arrhythmia
Pericarditus
Dresslers syndrope
Unalive
Mitral incompetance

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66
Q

causes of heart disease

A

schaemic heart disease, hypertension, cardiomyopathy, valvular heart disease, congenital heart disease, alcohol and chemotherapy, arrhythmias anaemia, pregnancy, obesity, hyperthyroidism.

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67
Q

risk factros for heart diease

A

Age, obesity, male, previous MI.

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68
Q

explain systolic and diatlic heart faliure

A
  • Systolic - faloure to contract, ejectio fraciton in less than 40%
    This is cause by MI, HTN,IHD, cardiomyopathy (walls are wrong)
    • Diastolic - inibility to relax and fill- because tehre is reduced preload and the ejaction fraction is greater the 50%
      Caused by constrictve pericaritis, cardiac tamponade, hypertension
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69
Q

explain low output and high output heart faliure

A

Low output heart faliure is cuased by pump faliure, excessive preload, chonic ncreased afterload
High output HF - anaemia, pregnancy, hyperthyroidism

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70
Q

what are teh compensatory mechanisms of heart faliure

A
  • SYMPATHETIC STIMULATION - increased HR and contractility, increasing the preload, incrases afterload which causes redcued CO eventually
    • RAAS - fall in CO leads to diminished renal perfusion, activation of RAAS, increased salt and water retention which leads to oedema
    • Angiotensin II causes arteriolar constriction leading ot increased after load
    • VENTRICLAR DILATION - the ventricles become stretched due o the increased preload, but too much and so they cant pump as effectivly
    • MYOCYTE HYPERTROPHY
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71
Q

what are teh pathologys caused by teh compnsatory mechanisms of heart faliure

A
  • Increased preload - faliure of the heart leading to more blood being left behind which stretched the myocyted more
    • Increased afterload
    • Salt and water retention, this increases the afterload
    • Myocardial remodelling - due to myocyte damage and increased interstitial fibrosis
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72
Q

what are teh 3 cardina signs of heart faliure

A
  • Dyspnea
    • Fatigue
      Ankle swelling
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73
Q

what are teh chest xray signs of heart faliure

A

A- alveolar oedema (bats wings in the gaps)
B Kereley B lines
C-Cephalisation of the blood vessles
D - dilated upper lobe vessles
E - pleural eflusions

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74
Q

what are teh 4 test to be doen for heart faliure

A

ECG - may show underlying causes such as arrhythmias, hypertrophy and hypertension
Bloods - BNP - brain natriutc peptide maybe be secreted by the ventricles when in stress
Cardiac enzymes - Toponin T, creatine Kinase, myoglobulin
CXR

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75
Q

heart faliure treatment

A

ifestyle factors
Ace inhibitors
Beta blockers
Diuretics
Ventricular assistance device
Surgery heart transplant

If it is an acue condition give 100% oxygen and nitrate spray as well, and some IV opiates

Fr chronic treat in the same maonor as other hyoertensives, ABCD method

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76
Q

what are 4 acyte heart faliure causes

A
  • Hypertension
    • Acute pulmoar oedema
    • Cardiogenic shoc
      Septic shock
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77
Q

causes of lft heart faliure

A

IHD
HTN
Cardiomyopathy (dilated where the chamber grows and wall thins, or restrictive where the heart become stiff)
Aortic Stenosis (narrowing of the aortic valve)

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78
Q

symptoms of left heart faliure

A

Exertianly dyspnoea
Fatuigue
Weight loss
Notcurnal cough
Dysnpena when lying down

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79
Q

signs of left heart faliure

A

Cardiomegaly
Pulmonar oedema
3rd and 4th heart sounds
Pleural effusion
Tachycardia

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80
Q

right sided hear faliure causes

A
  • Left ventricular fliure - it cuases a fluid bulid up in the lungs
  • HTN
  • Pulmonary stenosis
  • Lung disease (cor pulmonale) there is increased pressure in the lungs which means its harder to pump the blood into
    AV shunt -
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81
Q

right heart faliure syptoms

A
  • Dyspnoea
  • Peripheral oedema
  • Ascites (fluid build-up in the abdomen)
  • Nausea
    Anorexia
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82
Q

right heart faliure signs

A
  • Raised JVP
  • Hepatomegaly
  • Pitting oedema
    Fluid weight gain
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83
Q

Aortic aneurism defornition

A

Permanent localised dilation of an artery to 1.5 - 2x the normal diameter

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84
Q

Aortic aneurism causes

A

Trauma
Atheroma
Connectives tissue disorder - Marfans (fibrillin 1 is affected), Ehlers Danols syndrome - collagen

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85
Q

Aortic aneurism risk factors

A

Smoking, family history, age, male, HTN, trauma, COPD, Hypercholesteremia

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86
Q

Aortic aneurism pathophysiology

A
  • It affects all three layers, and has a saccular r fusiform shape
  • Most common arteries: aorta, iliac, popliteal, femoral, thoracic
    Fake aneurisms are where blood collects under the adventia (outer layer) and happens after trauma
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87
Q

Aortic aneurism symptoms

A

sually asymptomatic and picked u[ on a scan

Sometimes there is pain due to pressure on other structures

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88
Q

Aortic aneurism signs

A

Pulsile abdominal swelling
Expansile aorta epigastic pain and hypovoleamic shock
Hypotension
Collapse

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89
Q

Aortic aneurism tests

A

CT or MRI angiogram
Abdominal ultrasounds

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90
Q

diffreenntial diagnosis for aortic anuerism

A

GI bleed
Perforated ulcer
Appendicitis
Pyelonephritis

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91
Q

aortic anyerism tx

A

Monitoring
Surgery to put in a graft

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92
Q

symptoms of a thoraccis anyerism

A

Asymptmetic
Cough if pressing on phrenic nerve, dysphagia

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93
Q

differenticlal diagnosis of thorassic anyerism

A

MI
bakc pain

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94
Q

aortic dissection epidemiology

A

Males more than females
Common emergency

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95
Q

Aortic dissection causes

A

Chronic hypertension
Connective tissue disorders
Anyerisms
Infection
Atherlosclarosis
Trauma

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96
Q

Aortic dissection pathophysiology

A

Tear in the intima, blood flowing into the intima in high pressure, this creates a flues lumen and splits is leading to occlusion in branches of the aorta

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97
Q

Aortic dissection types

A

Tear in the intima, blood flowing into the intima in high pressure, this creates a flues lumen and splits is leading to occlusion in branches of the aorta

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98
Q

Aortic dissection signs

A

Absent peripheral pulse
Unequal pulse
Neurological signs
Aortic regurgitation
Cardiac tamponade
Compression of other arteries - renal subclavian

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99
Q

Aortic dissection symptoms

A

Sever tearing central chain pain radiating down back and arms

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100
Q

Aortic dissection manegemt

A

Type A - surgical repair
Type B - surgical repair, medication or control blood pressure

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101
Q

atrial flutter
Definition

Aetiology

Risk Factors

A

The atria is in random extreme tachycardia, it is due to circular current running through the atrium. It is a regular but sped up beating, it is less severe than atrial fibrillation.

They often have underling heart problems such as - coronary heart disease, heart valbve disease, congenital heart disease, high blood pressure

Increased age
Valvular dysfunction
Atrial septal defects
Atrial dilation

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102
Q

atrial fibrillation
Definition

Aetiology

Risk Factors

A

Chaotic rhythem with no regularity

Hypertension
Heart faliure
Coronary artery disease
Rheumatic heart diseas
Thyrotoxicosis

Most common supraventircular arrhythmia

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103
Q

AVRNT Definition

Aetiology

Risk Factors

A

AV Node re-entry tachycardia, they have an extra electical conduction pathway that causes tehheart t beat more

Three are two pathways this cuases xtra heartbeets due to a circualr fashion.

They are electrical bondes which means that it loops back round

Twice as common in women than in men

Caffine, alcohol
Exertion

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104
Q

AVRT defornition, and causes

A

AV re-entering (or reciprocating) tachycardia

Its caused by extra connection between the atria and centricels

They are electrical bondes which means that it loops back round

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105
Q

Aortic dissectionatrial flutter
Pathophysiology

Key presentations

A

A heart rate of between 250-320 bpm and it is fluttering, it is shown on an ECG as a sawtooth pattern most commonly shown in II, III, aVF, V1

Palpitations
Fatuigue
Light-headedness
Jugluar venous pulsation
Chest pain

Worsening heart faliure

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106
Q

atrial fibrillation
Pathophysiology

Key presentations

A

Atrial activation 300-600 a mmin

Only a small propotion travel to the ventircles

Aysmptomitic
Palpitations
Fatuigue
Dyspnoea
Heart faliure

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107
Q

AVNRT

Key presentations

A

Regular rapid palpations
Neck pulsation 9JV pulsations)
Polyuria due to release of ANP
Chest pain and SOB

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108
Q

AVRT
Pathophysiology

Key presentations

A

There is extra electircal condiiction pahway which send signals back into the atria and into the ventrcles againe

This is wolff parkinson white syndrome, the extra bundle here is called the bundle of kent, this cuases a short pR interval

There is a slurred start to te hQRS interval

Palpitatoins
Diziness
Dysponea
Chest pain
Syncope

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109
Q

atrial flutter

Tests and treatment

A

ECG - will show as sawtooth patterns
Full blood count
Thyroid function tests
Renal function and serum electrolytes
Troponin T levels

If its an emergency- electrical cardioversion to shock the heart back into working

Give antigoagulation to prevent lots form forming in the artium

Treat the underlying cases - beta blockers

Catheter ablation - putting tubes through blood vessles into the heart to destory atches of the tissue

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110
Q

arial fibrillation

Tests and treatment

A

ECG - irregular waves, no clear p, irregular QRS complex

Rate control- reduce the heart rate by ising beta bi=locker, and anti arrhythias such as amiodarone

Cardioversin therapy

If they don have heart disease yo ucan use sotalol

CHADSVASC score to asses if they are at risk form a sroke and give anti coaguletns as appropriate

Atrial fibriallation can causes thrombs to form - warfrin, heparin, rivaroxiban

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111
Q

AVNRT
Tests and treatment

A

Blood test
Thyrpid function test

Ecg - p waves not visable or immediately after QRS complex.

Holter monitoer- a portable ecg you wear for eth whole day
Echocardiogram

Listen for bruit - a breathy vaaaa sound,

Most don’t require management

Vagal manoeuvres - dunking head in water, carotid sinus massage

Beat blockers
Calcium channel blockers

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112
Q

AVRT Tests and treatment

A

Blood test
Thyrpid function test

Ecg - p waves not visable or immediately after QRS complex.

Holter monitoer- a portable ecg you wear for eth whole day
Echocardiogram

Listen for bruit - a breathy vaaaa sound,

Vagal manouvers

IV Adenosine - causes a complete heart block for a fraction of a second which leads to termination of the crcuit K

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113
Q

Ventricular ectopic defornition and causes

A

Type of arrhythmias where there is an extra beat every so often

Infection, muscle disease, channel ion disease, electrolyte imbalence

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114
Q

Ventricular ectopic signs and symptoms

A

Diziness
Fainting
#palpitation
Tiredness
Cold peripheries
Dyspnoa

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115
Q

Ventricular ectopic tests

A

ECG to took for it
Echocardiogram
Exercise stress test
Blood test for infection markers

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116
Q

ventricular ectopic treatment

A

Beta blockers
Calcium channel blockers

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117
Q

what is toursaire de pintes: defornitoin, symptoms, causes, treatmetn

A

Toursardes de pointes - a complicatio hwat causes the ventricles to beat out of time with the atria. It will case a very raplily up and down ECG, butu blood ion tests should also be conducted. It can causes sudden cardiac death

Symptoms include:
Heart palpitation
Diziness
nausuea
Cold sweats
Chest pain
Shortness of breath
Rapid pulse
Low blood pressure
Syncope
Cardiac arrest

It is often brought on by stress and exercise, and also some types of drugs.

It is treated by beta blockers, pacemakers, implantabe cardioverter defibrillator

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118
Q

Prelonged QT syndrome defornition and risk factors

A

Prolonged qt interval on an ECG which ma be congenital or aquired

It can lead to sudden cardiac death due to ventricular tacharrhythmias

PT interval prolonging drugs (amioderone)
Gene mutations

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119
Q

Prelonged QT syndrome pathophysiology

A

In congenital - they have gene mutaions affecting ion channles which prevent the signals passing on

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120
Q

Prelonged QT syndrome key presintation sna dsymptoms

A

History of gene mutations
Drugs or circumstances known to prelong QT
Syncope dueing heighted adrenergic tone
Syncope during arousal or surprise

Dizziness
Angina
Fatigue
Oliguria

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121
Q

Prelonged QT syndrome tests

A

ECG!!!

Echocardiogram
Genetic testing
Exercise tolerance test

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122
Q

Prelonged QT syndrome treatment

A

Beta blockers
Implantable cardioverter defibrillator
Lifestyle modification

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123
Q

type 1 heart block
Definition

Aetiology

A

Delayed AV conduction that causes a prolonged PR interval

  • LEV disease
  • IHD - scar tissue forms myocyte blocks the conduction pathway
  • Myocarditis
  • Hypokalaemia
  • Drugs such as beta blockers
  • Increased vagal tone
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124
Q

type 1 heart block key presintations, and manegemnt

A

asymptomatic

no manegement heheheeh what a prank card lol

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125
Q

1st degree heart block ECG findings

A

ECG - prolonged PR interval of over 0.22 seconds

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126
Q

type 2 heart block moblitz 1 defornition and aitiology

A

2- Mobitz I - prolonged PR which increases until a QRS is missed and then the cycle restarts

you make my heart miss a beat (or a ventricular contraction)

Moblitz I (wenckebach)- caused by AV node block and results in progressive PR interval prolongation until a p wave fails to conduct and a QRS is skipped. Its normally cyclical and the QRS is missed every n times.

Caused by MI, drugs, increased vagal tone, hyperkalaemia

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127
Q

type 2 heart block moblitz 1 key presintations and ECG findings

A

light headedness, diziness, syncope

increasing PR interval length untill a beat is skipped

128
Q

type 2 heart block moblitz 1 treatment

A

Atropine if it causes bradycardia or hypotension

129
Q

type 2 heart block moblitz 2 defornition and cause

A

2 - Mobliz II - just a missed QRS every so often

Some atrial impulses fail to reach the ventricles

Mobitz 2 (hay) - there is no incrased PR interval, just an intermittent QRS missing. Sometimes a fixed ratio of missing QRS.

Structural heart disease, MI or fibrosis, cardiomyopathy

Its gerally seen in serious changes to the hearts structure.

130
Q

type 2 heart block moblitz 2 key presintations and ECG findings

A

Chest pain, dyspnoea, syncope. Postural hypertension.

○ QRS is widened and QRS complexes are dropped without PR prolongation

○ FBC to look for electrolyte imbalance

131
Q

type 2 heart block moblitz 2 treatmetns

A

NEVER GIVE ATROPINE

Stopping medication that slow nodal conduction (beta blocker/digoxin/calcium channel blocker)

Adress electolycte imbalances

Pacemaker

132
Q

type 2 heart block moblitz 2 complications

A

Risk of sudden death, risk of asystole, needs a pacemaker placed

Don’t give atropine!! It can increased the chance f complete heart block or asystole

133
Q

type 3 heart block defornition and causes

A

3 -
Occurs when there is complete dissociation between atrial and ventricular activity. E.g. atrial BPM is 60, ventricular is 30 BPM

CHD
Infection
Hypertension
Myocaridal infarction

134
Q

type 3 heart block key presintations and EXG findings

A

Syncope
Dysnpnoea
Chest pain
Confusion

ECG - p waves that don’t lead to QRS ever and more p waves than qrs

Ventricular contaction is sustained below the sight of block in the pathway

If the HIS system is changed i

135
Q

type 3 heart block tx

A

Dopamine, adrenaline, IV atrpopine
Pacemaker insertion

136
Q

BBB defornition

A

BBB - complete block f a bundle branch oto eiter the left or the right, which leads to late contraction of theventricle

137
Q

causes of LBBB

A

Left:
Coronary artery disease
High blood pressure
Heart valve disease
Enlarged or weakened heart muscle (cardiomyopathy)
Heart infection (myocarditis)
Heart attack
Congenital heart defects
Certain heart rhythm medicines

138
Q

Causes of RBBB

A

Right:
Myocarditis.
Trauma to your chest.
Heart attack (myocardial infarction).
Right heart catheterization or other procedures.
Changes in branch structure, such as stretching.
Pulmonary hypertension
Pulmonary emobolism
Copd

139
Q

ecg results for left and right BBB

A

ECG - WiLLiaM MaRRow

For a left bundle branch block, there is a W in V1 and an M in V6 in the right bundle branch block there is M in lead 1 and W in V6

Wide QRS which is lasting longer

140
Q

treatment for bbb

A

pacemaker!

141
Q

hypertension criteria

A

140/90mmhg on at least two separate occasions

142
Q

hypertension causes

A

95% of cases - is a primary origin
Secondary - renal, endocrine (cushings, acromegally), coarctation of the aorta, preeclampsia occuring in the third trimester, drugs

143
Q

hypertension risk factors

A

Family history
Old age
Low birthweight
Male
Afro-caribean heritage
Unhealthy diet
Lack of physical activity
Obesity

144
Q

hypertension pathophysiology

A

Vascular changes - atherosclerosis which causes thickening og the media of muscular arteries
Heart changes
Nervous system - intracerebral haemorrhaging
Kidneys - renal disease can causes water retention
Malignant - raised diastolic blood pressure, progressive renal disease,

145
Q

hypertension key presintations

A

Asymptomatic apart from in malignant
May cause the occasional headache

146
Q

hypertension tests

A

Take the blood pressure - if it is >140/90 confirm on a second reading and use a 24 hour ambulatory BP monitor, and a multiple hoe BP monitoring

Test to asses end organ damage - urine analysis to check the kidney function
ECG and echo
Fundoscopy to check hypertension retinopathy
Bloods - creatine, eGFR, glucose
Clinical history of previous MI

147
Q

hypertension manegemtne

A

Calculate the QRISK of heart attack!!

If there is end organ damage or high QRISK then it needs to be treated

Lifestyle changes - smoking cessation, low fat diet, reduced alcohol and salt, increased exercise, Weigth loss

Drugs - ABCD
Ace inhibitor - ramopril
Beta blocker - bisoprolol, propanol
Calcium channel blockers - amlodipine
Diuretics - furosemide

148
Q

what is malignant and severe hypertension

A

Malignany hyertention - ca rapid rise in BP cuain vascular damagem and might give sympotms of headache and visual disturbances

Severe hypertentions of > 200/130

It ca cuase hypertensie emergancies wych as acute kidney injury and HF

Treat with sodium nitroprusside!!

149
Q

Deep vein thrombosis defornition

A

Occlusion in normal vessles most commenl deep I the vien so te leg. Thet often occur after periods of imobalisation

150
Q

Deep vein thrombosis risk factors

A

Age
Obesity
Vacrose veins
Long haul flights
Immobility and bed rest
Plasminogen deficiency
Pregnancy

151
Q

Deep vein thrombosis causes

A

Surgery
Immobility
Leg fractures
Oral contraceptive pill
Long haul flights
Pregnancy

152
Q

Deep vein thrombosis key oresintations

A

Calf pain and swelling
Warmth
Redness
Ankle oedema
Pitting oedema
Gangrene
cyanotic discoloration

153
Q

Deep vein thrombosis tests

A
  • Look for the D dimer - this si a protien reeased form eth breakdown of clots which if its there it ight be DVT and if its nt, it excludes VDT
  • FBC including plateltes
  • Doppler - compression ultrasound which uses sound waves to see the blood flow through the vessles, looks at the poplitel vein
154
Q

Deep vein thrombosis treatmetns

A

The main aim is to prevent PE

* LMW heparin (enoxaparin)  to inactivate factor Xa and stop the clotting 
* Warfarin  - antagonist of 1 9 7 2 clotting factors 
* Direct acting oral anticoagulants; apixaban, rivaroxaban , they work by inhibiting Xa factors but don’t need monitoring like warfin does

Prevention:
* Compression stockings
* Early mobilisation
Leg elevation

155
Q

Deep vein thrombosis complications

A

PE
Post thrombolytic syndrome - damage to the veins and valves causes ulcers and pain, vacrose veins and swelling
Reoccurrence of thrombosis

156
Q

pulmonary emoblism - dfornition causes and risk factors

A

Dislodged thrombi occludes pulmonary vasculature, it might causes right sided heart failure and cardiac arrest

Deep vein thrombosis

Increasing age
Obesity
Surgery

157
Q

pulmonary emoblism test and assesment scoring system

A

CTPA
Echocardiogram
D-dimer test t to look for clot proteins
Full blood count
ARTIERIAK BLOOD GAS
Chest x ray
ECG - sinus tachycardia

Looks for Prescence of DVT

Use the wells score for diagnosis-
Clinical signs and symptoms of DVT +3
PE is #1 diagnosis OR equally likely +3
Heart rate > 100 +1.5
Immobilization at least 3 days OR surgery in the previous 4 weeks +1.5
Previous, objectively diagnosed PE or DVT +1.5
Haemoptysis +1
Malignancy w/ treatment within 6 months or palliative +1

SOCRE OF >4 MEAN PE LIKELY

158
Q

pulmonary emoblism - key presintations

A

Dyspnoea
Chest pain
Signs of DVT
Risk factors
Cough
Fever

159
Q

pulmonary emoblism - diffreentila diagnosis

A

Unstable angina
NSTMI
STEMI
Pnumonia
bronchitis
Pericarditis
Cardiac tamponade

160
Q

pulmonary emoblism tx

A

HEAMODYNAMICALLY UNSTABLE:
* Give oxygen
* give thrombolytics to break it down
* It can cause low blood pressure so giving salone (500ml/0.9%) or hartmans solutinon
* Anticoagulation - given to haemodynamically stable patients - apixaban, rivaroxaban, or LMWH.

HEAMODYNAMICALLY STABLE:
Anticoagulation and monitor closely for signs of becoming haemodynamically unstable

161
Q

pulmoary empbolism complications

A

Heart failure
MI

162
Q

peripheheral vascular disease 4 stages

A

Legs most commonly affected
4 stages:
1. Asymptomatic
2. Intermittent claudication (pain in the arms or legs that occurs when the blood supply s narrowed)
3. Rest pain or nocturnal pain
Necrosis/gangrene

163
Q

peripheheral vascular disease causes and risk factors

A

ATHERLOSCLAROSIS!

Smoking
Diabetes
Dyslipidaemia- increased fat levels in the blood
Hypertension

164
Q

peripheheral vascular disease pathophysiology

A

If its in the hip or buttocks - aorta or iliac
Thihgh - common femoral
Upper 2/3rd of calf - superior femiar aryert
Lower 1/3 of calf - popliteal artyer
Fooot - tibeal ot peroneal artyer

The pain is cases by the released of adenosine in response to muscle ischemia

There is a narrowing of the vessles which occludes the blood flow leading to ishecemia and pain

165
Q

peripheheral vascular disease signs and symptoms

A

Absent pulses
Punched out ulcers

Cramping pian in calves ,thighs and buttocks
Pain is relieved by rest
Postural colour change - buegers test (foot turns white when elevated and red when lowered)

There are 6 Ps of limb ischemia
* Pain
* Pallor
* Pulseless
* Perishing cold
* Paraesthesia
* Paralysis

166
Q

peripheheral vascular disease tests

A
  • Ankle brachial pressure index - this is the difference in pressure between the ankle and the arm. The blood pressure is measured using a cuff and sopper ultrasound device. The ankle should normally have a higher blood pressure than the arm, but in peripheral vascular disease the ration changes. It is ankle/arm which should be less than 0.9 to be abnormal.
  • COLOUR DUPLEX USS - quick and non invaseive, can show the vessles and blood flow within them
  • AUSICLATIONS - bruits due to the turbulent blood flow
  • Creatine kinase MM - a marker that shows muscle breakdown
167
Q

peripheheral vascular disease differentials

A

diabetes mellitus, arthritis, anaemia, renal disease

168
Q

peripheheral vascular disease tx

A

Risk factor modification - smoking, hypertension, cholesterol, improves diabetes, diet
Medications - antiplatelet therapy (clopidogrel)
Exercise programs - improve blood flow
Percutaneous transluminal angioplasty (stent)

169
Q

pericarditis causes

A
  • Idiopathic
  • Infection - mainly viral but could by TB or fungal
  • MI
  • Autoimmune - SLE, sjoogrens
  • Dressler dynrom - inflamation of the pericardium after the MI damagining it, a delayed response
  • Iantrogenic - caused by surgery or medications
  • Uraemia - build p of toxins due to kidney faliure
  • Malignancy - breast lung leukeamia
170
Q

pericarditis key presintations, signs, sympotoms

A

Pericardial rub
Pain worse when lying flat and reilved when sat forewards

Raised JVP

Chest pain, sever, sharp and not with a crushing feeling
Dysnopea
Hiccups and cough due to phrenic involvement
Fever

171
Q

pericarditis tests

A

ECG - sadle shapped ST in all leads
PR depression
PeRicardiTiS

Bloods - cardiac enzymes
C reative pritiens
FBC

Echocardiogram
CXR - show water bottle shape and cardiomegaly f there is effusio

172
Q

pericardidits pathophysiology

A

It become inflamed with peripher vascularisation and infiltraiotn y polymorphonuler leukocytes

173
Q

pericarditis tx

A

NSAIDS
Colchine - inhibits migration of neutrophils
f=drainigle of fluid
Rest
Treat underlying cuases- steriods for autoimmune cases

174
Q

pericarditis complications

A

Pericardial effusion
Cardiac tamponade - there is so much pericardial effusion that the heart can no longer beat anymore
Chroninic constricitve pericarditis - there is a rigid pericardil sack which prevents diastolic filling f the ventricels

175
Q

what is constricitve pericarditis

A

Constrictive pericarditis:

Normally idiopathic or restrictive cardiomyopathy
Signs and symptoms simmilar to right sided heart faliure, Juglar veouns distention, dependant oedema, hepatomegaly, ascites

Kussmals sign - JVP rises with inspiration
Pulsus paridoxus
AF
Pericardial knock

Chest xray - show norma heart and ericardial calcification
CT or MRI - diagnostic to show pericardial thickening
echcardiogram

176
Q

pericardial effusion and cardiac tamoponade defornition

A

Effustion - fluid in the space
Tamponade - effcects on the hearts ability to pump

177
Q

pericardial effusion signs

A

Effusion obsucres apex beat
Hypotension tachcardia
Elevated JVP
Pulsus paridosis - a blood pressure fall of more than 10mmHg during inspiration
Causes more venous return to eh right side of the heat

178
Q

pericardial effusion tests

A

Echocardiogram
Chest xray
ECG - shows low voltage complexes with sinus tachycardia
#

  • Pericardial effusion
    ○ CXR – large heart
    ○ ECG – low voltage QRS complexes and sinus tachycardia
    ○ Echocardiogram
  • Cardiac Tamponade
    ○ CXR – large heart
    ○ Beck’s triad
    § Falling BP
    § Rising JVP
    § Muffled heart sounds
    ○ ECG
    Echocardiogram
179
Q

pericardial effusion and cardiac tamponade manegemtnet

A

Effusions normally resolve themselves
Tamponade requires emergency pericardiocentesis
If effusion reoccurs excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics

180
Q

infective endocarditis defornition

A

Infection of the heart valves and endocardial lining within the heart

181
Q

infective endocarditis epidemiology/risk factors

A

Elederyly
IV drug abusers
Congenital heart disease
Poor dental hygiene
Prosthetic valves or pacemakers
More commen in men

182
Q

infective endocarditis bacterial causes (name teh bacteria)

A

S.aureus is the most common
Pseudomonas aeruginosa
Streptococcus viridians (from dental problems)

183
Q

infective endocarditis key presintations

A

FROM JANE

Fever
Roths spots
Oslers nodes
Murmur
Janeway lesions
Aneamia
Nailbed splinter hemmorages
Emboli - MI storke PVD

There are two main diagnostic criteria - bugs grown form cultures and evidance of endocarditis on an echo or new valve leak

There are 5 minor ones:
Risk factors
Fever
Vascular or immue phenomena
Equivocal blood cultures

184
Q

infective endocarditis sympotms

A

Fever + prosthetic material in heart, risk factor, newly developed arrhythmias

Headaches
Fever
Malaise
Confusion
Night sweats

185
Q

infective endocarditis signs

A

Splinter haemorrhages
Roth spots (haemorrhages in the retina)
Osler nodes in fingers (tender nodules in the fingers)
Janeway lesions - haemorrhages and nodules in fingers
Clubbing

186
Q

infective endocarditis tests

A

Transoesophogel echo - diagnostic
Transthoraci echo
ECG
CXR
Blood cultures

187
Q

infective endocarditis treatment

A

Antimicrobials - IV for 6 weeks
If not staph use benzylpenicillin and gentamycin
If staph use vancomycin and rifampicin
Always treat with 2 antibiotics at the same time so it’s a broad specturm.

Treat complications - arrhythmias, HF heeart block and embolisation
Stroke rehab abscess drainage
Surgery

188
Q

shock defornition

A

Acute circulatory failure where there is inappropriate tissue perfusion resulting in hypoxia. It also causes low BP below 90.

There are compensatory mechanisms:
Hypotension causes baroreceptors in thee aortic arch and carotid sinus to stimulate adrenaline release, this causes vasoconstriction and increase CO.

Reduced perfusion of the renal cortex causes renin release. This incr

189
Q

shock key presintations

A
  • Pallor
  • Rapid weak pulse
  • Presuced pulse pressure
  • Reduced urine output
  • Confusion, weakness, collapse, coma
    Reduced capillary r
190
Q

shock first line tests

A

○ FBC
○ Serum creatinine
○ Electrolytes
○ Blood glucose
○ Coagulation
○ Blood gases
Liver biochemistry

191
Q

shock tx

A

Airways
Breathing - 100% O2
Circulation - IV acess, fluid for blood loss, stop bleeding, give adrenaline to cause vasoconstiction

192
Q

define hypovolemic shock

A

Loss of large amounts of blood

193
Q

causes of hypovolemic shock

A

There is a reduced preload. This can also be caused by burns which causes plasma leakage, D&V dehydration, intestinal obstruction, pancreatitis

blood loss

194
Q

hypovolemic shock kery presintations

A

inadequate tissue perfiusion
Increased sympathetic tone
Tachycardia
Sweating
Bradycardia

195
Q

anaphyactic shock causes

A

IgE - release of histamine

196
Q

anaphylactic shock key presintations

A
  • Onset of symptoms after antigen exposure
  • Swollen tongue, lips
  • Laryngeal oedema
  • Swollen epiglottis
  • `Warm peripheries and hypotension due to profound vasodilation
  • Urticaria
  • Angio-oedema
  • Wheezing and SOB due to bronchospasm
  • Upper airway obstruction due to laryngeal oedema
    Low BP – due to vasodilation, increased vascular permeability and fluid loss from vascular space
197
Q

anaphylactic shock treat,ent

A
  • Remove antigen
  • Oxygen
  • Adrenaline
  • Fluids (500ml 0.9 saline)
    Observation
198
Q

septic shock pathophysiology

A

Vasodilation due to inflammatory cytokines

Systemic inflammatory respnse, temtruture is raised, tachycardia, increased resp rate

Severe sepsis – sepsis with dysfunction of one or more organs
Septic shock – persisting tissue hypoperfusion after a fluid challenge

Endotoxins cuases lower perfusion which causes dameg to endothelium and there is inflamation
There is increased clotting

199
Q

septic shock key presintations

A
  • Pyrexia and rigors (increased body temptriute which auses the person to feel cold untill they reach it and shake (rigours)
  • Nausea and vomiting
  • Vasodilation with warm peripheries
    Bounding
200
Q

septic shock tests

A

BLOOD CULTREIS LOOKING FOR BACTERIA

○ FBC
○ Serum creatinine
○ Electrolytes
○ Blood glucose
○ Coagulation
○ Blood gases
Liver biochemistry

201
Q

septic shock treatmetn

A
  • Airways
  • Breathing
  • Circulation
  • Antibiotics
    ○ Community-acquired pneumonia – ceftriaxone
    ○ MRSA – vancomycin
    ○ Pseudomonas – cefepime + metronidazole
  • Treat underlying cause
  • Coagulopathy
  • Acute kidney injury
202
Q

cardiogenic shock pathophysiology

A

Heart isn’t pumping well

Myocardial flaure signs
* Chest pain
* Respiratory distress
* JV distention
* Hypotensino
* Crackles in lungs
* ST elevation
Gallop rhythem

203
Q

cariogenic shock causes

A

MI
Myocarditis
Atrial and ventricular arrhythmias
Bradycardia
Rupture of valve cusp
PE
Tension pneumothorax
Cardiac tamponade

204
Q

cardiogenic shock tests

A

○ D-dimers
○ Echocardiogram

FBC
○ Serum creatinine
○ Electrolytes
○ Blood glucose
○ Coagulation
○ Blood gases
Liver biochemistry

205
Q

what is ARDS

A

ARDS: caused by : sick, head injury , near drowning, chemical pneumotisk sepsis

  • Alveolar capillary membrane injury results in leakage of fluid into alveolar spaces
  • There is resulting neutrophil invasion which attracts more neutrophils = Exudative phase
  • Eventually, fibroblasts come in and initiate healing = proliferative phase
  • Scar tissue then forms due to fibroblasts = fibrotic phase
  • Results in severely stiff lungs and therefore severe difficulty in ventilation and O2 blood perfusion
    Causes cynosis, tachycardia periphera vasodilation
206
Q

neurogenic shock pathophysiology

A

Damage to Ns mean bp can’t be controlled as well, caused norallly by a spinal injury above T6

207
Q

define cardiomyopathy

A

Disease in the myocardium which effect the mechanical or electrical function of the heart

208
Q

hypertropic cardiomyopathy defornition cna causes

A

Hypertrophic- heart is stiff and doesn’t relax properly.

caused by autosomal dominant mutation

209
Q

hypertrophic cardiomyopathy key presintations

A

Angina
Dyspnoea
Palpitations
Dizzy spells
Syncope
Crescendo decrescendo murmur
S4 sound

210
Q

hypertrophic cardiomyopathy tests

A

Microscopically - myocyte disary, fibrossi is an electrica insulator and the curretn goes though the fibrosis and casues arrhythmia

ECG - abnormal, deep T wave inversion

Echocardiogram

211
Q

hypertrophc cardiomyopathy tx

A

Amidarone - antu arrhythmia
Calcium channel blockers
Beta blocker
Digocin contraindicated
Surgery

212
Q

dialated cardiomyopathy defornition

A

Muscle is normal or thin and the chamber is large. This eams that they arent as sting and cant work as effectively

213
Q

dialated cardiomyopathy causes

A

diopathic
Infectio
Ischemia
Alcohol
Genetic

214
Q

dialated cardiomyopathy key presintations

A

Heart faliure sympotms
Dysponea
Arrhythmias
Increase JVP

215
Q

dialated cardiomyopathy tests

A

CXR - learge heart
ECG
Echo

216
Q

dialated cardiomyopathy treatment

A

HF and AF treated in the normal way
Left ventricular assist device
Heart transpplant if thinning s too great

217
Q

Arrthymogenic cardiomyopathy defornition

A

Presents with arrhythmias

There is a replacement of the heart muscle with fat, therefore it cant beat as well

May be little structural or directly involve RV and LV

218
Q

Arrthymogenic cardiomyopathy key presintations

A

Arrhythmia
Syncope
RHF

219
Q

Arrthymogenic cardiomyopathy tests

A

Histology - more fatty layers

ECG - in V123, ther eare epsilion wave and t wave inversion

Genetic testing

Echo

220
Q

Arrthymogenic cardiomyopathy manegement

A

Beta blockers
Arrhythmias - amiodarone

221
Q

restrictive cardiomyopathy defornition

A

Ventricles are stiffer and ledd compleinet
This leads to less CO and HF

Poor dilation of the heart restricts its ability to take on blood and pass it onto the rest of the body

222
Q

restrictive cardiomyopathy causes

A

Amyloidosis - misfolded protiens which are insoluble
Acrcoidosis - formation of granulmas I the heart walk
Idiopathc
Endocardia fibrolastosis
Iron overload

223
Q

restrictive cardiomyopathy key presintations

A

Similar to constrictive pericarditis
Dysponea, elevated JVP
Heaptomegaly
Acitis
3rd and 4th heart sounds

224
Q

restrictive cardiomyopathy tests

A

CXR
ECG
Echo
Cardiac catherisaition

225
Q

restrictive cardiomyopathy treatments

A

Treat underlying causes

Heart transplantation

226
Q

Rheumatic fever defornition

A

An autoimmune diseae that occurs after a group A strp infection which can affect many systems such as chroic rheumatic disease, without long term pernicillin it can reoccur and cases damage to the cardiac valvular tissues. The antibodies to the bacteria also react and damage the myocardium. It normally occurs 2-4 weeks after infection.

227
Q

Rheumatic fever risk factors

A

Less developed countries
Lower income
Family history of rheumatic fever
Genetic susceptibility

228
Q

Rheumatic fever pathophysiology

A

Carditis caused by the attack of the immune system. Pericarditis, myo and endo as well.

229
Q

Rheumatic fever signs and symptos

A

Fever, joint pain

Recent sore throat, skin infection, chest pain, dyspnoea, heart palpitations, heart murmur, pericardial rub, swollen joints which apperar migratory as different joint get inflamed at different times

Skin lesions - painless nodules, Erythema marginatum rash

Nervous suste involvelemt - chorea which is irreglar uncorntrolled rapid movemt of the limbs

230
Q

Rheumatic fever tests

A

Throat swab for bacteria culture
ASO antiboy titres - antibodies againt streptococcus, which indicate recent infection
Echocardiogram
ECG
CXR

231
Q

Rheumatic fever trteatment

A

Penocymethypnicillin for 10 days to get rid of infection

NSAIDS for joint pain

Asprin and steroids for carditis

Phrophylactic antibiotics are sued to prevent further steptococcal infections and reoccurance

232
Q

Rheumatic fever complications

A

Valvular stenossi (mitral normally)
Chronic heart faliur
Reoccurance of RF

233
Q

aortic stenosis causes

A

Due to the narrowing there is obstructed LV emptying which causes a pressure gradient to develop between LV and the aorta which means an incrased afterload whih cleads to left ventricle hypertrophy

Tis then leads to increased myocradial oxygen demand, angina and LV faliure

234
Q

aortic stenosis risk factors

A

Congentital bicuspid valve
Old age leading to calcificationa nd degeneration of normal valves
Rheumatic heart disease

235
Q

aortic stenosis signs and symptoms

A

○ Exertional syncope
○ Angina
○ Dyspnoea – due to HF

Slow reisinf and weak carotid pulse
Soft or absent 2nd heart sound and preominenet 4th heart sound due to LV hypertrophy
Ejection systilic murmur - sounds like a whooshing noise

Heart faliure

236
Q

aortic stenosis tests

A

Chest xray - shows noral heart size, LVH, prominence of ascending aorta and calcular calcification
ECG - may show signs of LV stress patterns and ST depression and T wave invesrsion in aVL V5 and V^

echocardiogram is teh main diagnostic tool!!

237
Q

aortic stenosis

A
238
Q

aortic stenosis treatment

A

Surgical - aortic valve replacemnet - in symptomatic patiens as onset of symptoms associated with 75% mortality at 3 years
General - dental hygine is important as they are at risk of endocarditis

239
Q

aotic regurgitation explination

A

Regurgitation - failure of the valve to work properly
Leakage of blood into LV due to ineffective coaptation of the aortic cuffs

240
Q

define stenosis

A

Stenosis - narrowing of the valve to the point where is 1/4th of the normal size. There are three type, supravalvular, sub, and valvular

241
Q

Aortic Regurgitation causes

A

Idiopathic
Effective endocarditis
Chronic rheumatic fever
Congenital bicuspic aortic valve
Rheumatic fever
Infective endocarditis - acute

242
Q

Aortic Regurgitation pathophysiology

A

Combined pressure and volume overload - LV dilation and LVH

243
Q

Aortic Regurgitation signs

A

Collapsing pulse
Wide pulse pressure
Quincke’s sign - capillary bed
De Mussets sign - head nodding with each heart beat
Mullers sign - visible pulsation of uvula
Heart sounds - displaced hyperdynamic apex beat
Early diastolic murmur at left sternal edge in 4th intercostal space - accentuated when eth patient sits forewards and holds breath
Systolic murmur

244
Q

Aortic Regurgitation symptoms

A

Exertional dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Palpitations
Angina
Syncope
De Mussets sign - head nodding with each heart beat
Mullers sign - visible pulsation of uvula

245
Q

Aortic Regurgitation tests

A

Echocardiogram
ECG - LVH (left ventricular hypertrophy)
CXR - shows a large heart and occasional dilation of ascending aorta

246
Q

Aortic Regurgitation treatment

A

IE prophylaxis (antibiotics for infective endocarditis)
Vasodilators
Surgical - pelplace valve before LV disfunction

247
Q

mitral stenosis defornition

A

Obstruction of LV that prevents proper filling during diastole

248
Q

mitral stenosis causes

A

Rhumatic heart disease causes by rehmatic fever
Infective endocarditis
Mitral annular calcification
Congenital causes

249
Q

mitral stenosis risk factors

A

Unreated strep infections

250
Q

mitral stenosis pathophysiology

A

Thickening and imobility of valve leads to obstruction of blood flow form the LA to the LV which leadsto increase LA pressure, pulmonary hypertention and right heart dysfunction

Atrial fibrillation is commen due to elevation of LA pressure and dilation

Thrombus may fmor in the dilated atrium and could causes a stroke

Elevated LA pressure can lead to pulmonary embolism

251
Q

mitral stenosis signs

A

Mitral facies - extrere cheek flushing due to vasoconstriction
Low volume pulse
Tapping, on disppalced apex beat
Heart souds - loud S1 at apex, if there is a loud S2 with elevated JVP and peripheral oedema it may indicate pulmonary hypertension induing RV overload
Diastolic murmur is a low pitch rumble at the apex and is left heard when the patient is lying on the left hand siede and expiring

252
Q

mitral stenosis symptoms

A

Exertional dyspnoea
Coughing up blood
Haemoptysis - coughing up blood
Right heart failure - fatigue, weakness, lower leg swelling
Palpitations due to AF
Chest pain

253
Q

mitral stenosis tests

A

Echocardiogram
Chest xray - LA enlargeent, pulmonary hypertension, calcifies mitral valce
ECG - AV and LA enlargement

254
Q

mitral stenosis tx

A

Contoell of any AF with beta blockers
Anticpagulents to prevent clot formation in AF
Diuretics for heart faliure
Percutaneous mitral balloon valvotomy to open up the valve more

255
Q

mitral regurgitation defornition

A

Backflow of blood from the LV to the LA during systole

256
Q

mitral regurgitation causes

A

Myxomatouse degeneration
Rehumatic heart disease
Infective endocarditis
Ishcheamic mitral valve
Dialated cardiomyopathy

257
Q

mitral regurgitation risk factors

A

Female
Lower BMI
Age
Renal dysfunction
Previous MI

258
Q

mitral regurgitation pathophysiology

A

Pure volume overload due to leakage form LC into LA

Compemsatory mechanisms - LA enargemet
LV hypertrophy
Increased contractility
Preogressive LA dilation and RV dysfunction due to pulmonary hypertension
Progressive LV volume overload leads to dilation and preogressive HF

259
Q

mitral regurgitation signs

A

Collapsing pulse with wide pulse pressure
Hyperdynamic and displaced apex beat
Heart sounds
Soft S1
Pansystolic murmur
Diastolic blowing urmur
Austin flint murmur
Systolic ejection murmur

260
Q

mitral regurgitation symptoms

A

Exertional dysponea
Fatuige and legarthy
Palpitations
Right sided HF that can lead to congestive failure

261
Q

mitral regurgitation tests

A

CXR - enlarged LA and LV
Echocardiogram - LA LV size and function
ECG

262
Q

mitral regurgitation treatments

A

Consider IE prophylaxis (a hight dose of antibiotics)
Vasodilators
AF control - beta blockers, calcium channel blocks
Anticoagulant for AF and flutter
Serial echocardiogram to manage flutter
Surgical treatment to replace valve if the patient has symptoms at rest or exercise, or if the left ventricle end systolic diameter is >45mm.

263
Q

Tetralogy of Fallot defornition

A

is made up of 4 different heart defects

* Ventricular septal defect 
* Overriding aorta - aorta positioned over VSD instead of LV 
* Pulmonary stenosis  RV hypertrophy
264
Q

Tetralogy of Fallot epidemiology

A

Most common cyanotic cardiac disorder,

10% of all contentive heart defects

265
Q

Tetralogy of Fallot key presintations

A
  • Frequesnt crying in children
  • Toddlers may squat to alleviae some of the L ot R shunt
  • Central cynosis
  • Low birthweigt
  • Dysponea
  • Delayed pubity
  • Systolic ejecion murmus
  • Adults are asymptomatic often
  • Dysponea on exertion
  • Systolic ejection murmurs
    Clubbing
266
Q

Tetralogy of Fallot test

A

CXR shows boot shaped heart
ECG shows RBBB

267
Q

Tetralogy of Fallot treatment

A

Children knee to chest position and give O2
Full surgial treatment is required due to progressive cardiac debiliy and central thrombosis risk

Often pulmonary valve regurgiation in adulthood and require a redo surgery

268
Q

coarctation of aorta defornition

A

There is a narroing in the aorta at the site of the ductus arteriosis

269
Q

coarctation of aorta epidimiology

A

Associated with turners syndrome, berry anyerisms, bicuspid acotic valves

More common in male

270
Q

coarctation of aorta pathophysiology

A

evere - complete obstruction leading to collapse

Mild - raisd blood pressire, systolic murmur form collateral vessles

Can lead to long term problems sucj as hypertension
Coronary artyery disease
Early stokes, subarrachnoid hemmorage
It requires repeat interverntions and enyerisms can form at the rigth o

271
Q

coarctation of aorta key presintations

A
  • Often asymptomaic
  • Right arm hypertension
  • Radio femoral pulse delay (feel the redia pulse before femoral
  • Discrepancies in BP in upper body and lower
  • Bruits (buzzes) over the scapula form collateral vessels
  • murmur
    Headache
272
Q

coarctation of aorta test

A

CXR- show indentation
ECG - LV hypertrophy
CT - can demonstrate coarcation and quantifty flow

273
Q

coarctation of aorta treatment

A

Surgical repair
Percutansous repain
Baloon dilation and stenting

274
Q

Ventricular septal defect defornition

A

there is a hole in teh sepum of teh heart taht allow blood flow
Blood moves form left to right
Increased blood blow to the lungs

275
Q

Ventricular septal defect key presintations

A

Pulmonary hypertension and eisenmengers complex
Smalll breathless baby
Increased resp rate
Tachycardia
Murmur
Increased risk of endocarditis
Cyanosis
Finger clubbing

276
Q

Ventricular septal defect treatment

A

Many will close up naturally
If small no intervention is required

Moderatly sized lesion may need ACE inhibitor, furosemide and digoxin

Consider prophylactic antibiotics for risk of endocarditis

277
Q

Ventricular septal defect risk factora

A

Down syndomre
Materal alcohol consumption
Family history

278
Q

atrial septal defect risk facros

A

age
male

279
Q

atrial septal defect what are teh two types

A

Primium - present earlier
May involve AV node
Affects lowe in eh septum
SECONDUM - the most common, pressure higher in the L than R, causing a left o right shunt
Increased flow to the right hand side and lings
Can lead to right sided heart failure and dyspnoea
Will cause right sided overload and dilation
It can lead to right ventricle hypertrophy and pulmonary hypertension

280
Q

what is eisenmengers complex

A

Eisenmengers complex - occurs in VSD or ASD
Reversal of the L too R shunt due to pulmonary hypertension leading to left hypertension
Causes deoxygenated blood to travel around the body and the only cure is a transplant

281
Q

atrial septal defect - what is Pulmonary artery banding

A

Pulmonary artery banding - band reduces the flow to the lungs wihc reduces pulmoanry hypertensino and eisenmengers syndrom

282
Q

atrial septal defect key oresintations

A

Pulmonary flow murmur
Split second heart sound
Dyspnea
Exercise intolerance
Atrial arrhythmias

283
Q

atrial septal defect treatmetn

A

Surgical closure done via keyhole

284
Q

Patent ductus arteriosus defornition

A

A connection between the pulmnary artery and the aorta still exists

285
Q

Patent ductus arteriosus epidemiology

A

Females more than males

286
Q

Patent ductus arteriosus pathophysiology

A

t sould have closed within a few ours of birth but it remins open

It can cuases a left to right shunt and eventulal leads ot plmonary hypertension and eisenmengers sundrome and RS heart faiure due to hypertrophy

287
Q

Patent ductus arteriosus key presintations

A

Murmur
Breathlessness
Eisemengers syndrome (differentila cyanosis - clubbed toes which are blue)

288
Q

Patent ductus arteriosus tests

A

CXR - large shunts may be preominent
ECG - lA abnormality and LV hypertrophy
Echocardiogram - dialated LA and LV

289
Q

Patent ductus arteriosus treatmetns

A

urgical closing
Venous approach has lower complications
Indomethacin (prostoglandin inhibitor can stimulae the duct to close)

290
Q

what are two conditions that will cuases a systoic murmur

A

mitral regurgitatoin
aortic stenosis

291
Q

what are two conditions that will causes a diastoil murmur

A

aortic regurgitation
mitral stenosis

292
Q

what is hypohidrosis

A

A rare condition in which the sweat glands make little or no sweat.

293
Q

what is atropine used for

A

tropine is a prescription medicine used to treat the symptoms of low heart rate (bradycardia), reduce salivation and bronchial secretions before surgery or as an antidote for overdose of cholinergic drugs or mushroom poisoning.

294
Q

what is teh mechanism of atropine

A

its is an ACTH antagonist so block teh parasympathetic signals allowing the heart rate to increase via teh sympathetic pathway

295
Q

where is b type natritic peptide secreted form

A

ventricle myocardium

296
Q

what do high livels of Btype natriuetic peptide indicate

A

heart faliure

297
Q

what are teh two drug classes prescried for heart faliure

A

beta blocker
ace inhibitors

298
Q

define ejection fraction

A

jection fraction (EF) is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction.

299
Q

what are teh bacteria most likely to causes rheumatic fever

A

Strep grouop A - staphylococcus pyogenes

these are teh bacteria whihc cuases strep throat

300
Q

what infections in teh rest of the body will heart faliure incrase the risk of

A

chest infections and ulcerated cellulitic legs - due ot teh excess fluid collecing

301
Q

what are teh two types of peripheral vascular disease

A
  • Functional - when your vessels open in exaggeration and thre is no actuall damage to the structure, for example in raynards and tempriture
    Organic, meaning that there is a change in structure of your blood vessels,
302
Q

what are teh three medications to give for peripheral vascular disease

A

Naftidrofuryl oxylate - peripheral vasodilator
Cilostazol - relax blood vesse and prevent platelets from sticking together
anticoagulation

303
Q

what is teh treatment algorhythem for hypertension

A

diabetic - ace inhibitor

304
Q

what is teh treatment algorhythem for hypertension

A

non diabetic under 55 or any diabetic type 2 - ace, thn add on ccb or thiazide, then all three togther if still not controlled

diabetic over 55 or afro-caribean - CCB, then ccb and ace, then ccb ace and thiazide like diuretic

305
Q

what is an easy test to do for aortic dissection

A

do teh blood pressure on both of teh arms and one arm should be >20mmhg higher than the other.

306
Q

what is teh diagnostic test for aortic dissection

A

CT angiogram with contrast dye!

307
Q

what are teh shockable and non shockabel rhythems

A

shockable:
ventricular fibrillation
ventricular tachycardia

non shockable:
pulseless electircal activity
asystole

308
Q

what is pericardiocentisis

A

Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the heart (pericardium). It’s done using a needle and small catheter to drain excess fluid. A fibrous sac known as the pericardium surrounds the heart.

Pericardiocentesis typically begins with a needle inserted at a 15-degree angle between in the xiphoid process and left costal margin. The needle is then carefully lowered to a horizontal level with the chest and gradually moved towards the point of the left shoulder blade, with the aspiration of fluids.

309
Q

what is teh way of working out if a person with AF needs anticoagulents

A

CHADVASC - A scoring system to see if anticoagulets are recommended or not for atrial fibrillation. each is worth 1 point unless stated otherwise. If they score 2 or more give DOAC.

Congestive heart falire
Hypertension
Age over 75
Diabetes
Stroke (this is worth 2 points)
Vascular disease
Age over 65
Sex

310
Q

what is pulsus paridoxus

A
  • Pulsus parixods is when you’re bp drops more than 20mmgh on inspiration. The normal levels is 8-12mmhg.
    It is caused by cardiac tamponade, constrictive pericarditis, atria septal defect, aortic regurgitation.
311
Q

what is kussmals sign

A
  • Kussmals sign - a paridoxical rise in JVP on inspiraion
    • Due to increased volue in thr rhght ventricle
      Caused y contrictive pericarditi, restirctive cardiomyopathy, pericardial effusion, severe right sidede heart faliure
312
Q

what is teh difference between pericadial effusion, cardiac tamponade and constrictive pericarditis

A
  • Pericardial effusion happns ver time and cuases a slow stretching of the sack, it has kussmals sign
    • Tamponade is a sudden accumulation of fluid that constricts the heart, it has becks triad - muffles heart sounds, hypotension and distentin of the juglar viens. This is when there is an anctual pressure on the heart muscle which prevents it from working properly. A sign of it is pulsus paridoxusdue to the large drp in systolic blood pressure during inspiration
    • Constrictive pericarditis is when the sack has become all fiberous which cuases kussmals sign, it is a chronic condition and it is caused by viruses, surgery and radiaiton therapy.
313
Q

what is teh duke criteria

A

There are two main diagnostic criteria -
* bugs grown form cultures
* evidence of endocarditis on an echo or new valve leak

There are 5 minor ones:
1. Fever > 38 oC
2. Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor)
3. Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjuntival hemorrhage, Janeway lesions)
4. Echocardiography findings (suggestive but not definitive)
5. Predisposition (heart condition or IV drug user)
6. Microbiologic evidence (Positive blood culture but not meeting major criteria)

This is the duke criteria. Definitive Diagnosis requires 2 Major or 3 Minor + 1 Major or 5 Minor
Use the mnumonic of BE FIVE PM ot remember the criteria

314
Q

what percentage of people wth DVT will deveop PE

A

10%

315
Q

what are teh 3 main symptms of DVT

A

SOD
coughing up blood
pleuric chest pain - pain on breathing in

Phase 2a (18 decks)

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