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Haroon Phase 2A > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Break down the word atherosclerosis

A

Atheroma= fatty deposits in artery walls Sclerosis= process of hardening or stiffening of blood vessels

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2
Q

What is atherosclerosis caused by?

A

Chronic inflammation and activation of the immune system in the artery wall which causes deposition of lipids

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3
Q

What three things do fibrous atheromous plaques lead to?

A
  1. Stiffening - leads to hypertension and strain of heart pumping against resistance 2. Stenosis - leads to reduce blood flow (eg. Angina) 3. Plaque rupture- giving off a thrombus that blocks a distal vessel leading to ischaemia (eg. Acute conorary syndrome)
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4
Q

Atherosclerosis non-modifiable risk factors

A
  1. Older age 2. Family history 3. Male
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5
Q

Atherosclerosis modifiable risk factors

A
  1. Smoking 2. Alcohol consumption 3. Poor diet (High sugar and trans-fat and reduced fruit and vegetable and omega 3 consumption) 4. Low exercise 5. Obesity 6. Poor sleep 7. Stress
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6
Q

Medical co-morbidities that increase the risk of atherosclerosis

A
  1. Diabetes 2. Hypertension 3. Chronic kidney disease 4. Inflammatory conditions (rheumatoid arthritis) 5. Atypical antipsychotic medications
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7
Q

End result of atherosclerosis?

A
  1. Angina 2. Myocardial infarction 3. Transient ischaemic attacks 4. Stroke 5. Peripheral vascular disease 6. Messenteric ischaemia
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8
Q

Two types of prevention of cardiovascular disease?

A
  1. Primary prevention - for patients that have never had cardiovascular disease in the past 2. Secondary prevention - for patient that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease
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9
Q

How to optimise modifiable risk factors?

A
  1. Advice on diet, exercise and weight loss 2. Stop smoking 3. Stop drinking alcohol 4. Tightly treat co-morbities (diabetes)
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10
Q

Primary prevention of cardiovascular disease?

A
  1. Perform a Q-risk 3 score 2. Over 10% risk of having heart attack or stroke in the next ten years? Offer a statin (Current NICE = atorvastatin 20mg at night) 3. All patients with CKD or type 1 diabetes for more than ten years should also be offered atorvastatin 20mg
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11
Q

Nice guidelines to statin prescription?

A
  1. check lipids at 3 months- aim for increasing dose to aim for 40% reduction in non-HDL Cholesterol- always check adherence first! 2. Check LFTs within 3 months and at 12 months, don’t need to be checked again if normal 3. Statins can cause a transient and mild raise in ALT and AST in first few weeks of use and don’t need stopping if rise is less than 3 times the upper limit of normal
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12
Q

Secondary prevention of cardiovascular disease?

A

4 As: Aspirin (plus second anti platelet like clopidogrel for 12months) Atorvastatin 80mg Atenolol (or other beta-blocked - commonly bispropol - titrated to maximum tolerated dose) ACE inhibitor (commonly ramipril) (tritated to max tolerated dose)

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13
Q

Notable side effects of statins

A
  1. Myopathy (check creative kinase in patients with muscle pain or weakness) 2. T2DM 3. Haemorrhagic strokes (very rarely) Usually benefits far outweigh risks and newer statins are mostly very wel tolerated
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14
Q

What’s a Q-risk 3 score?

A

-Predicts risk of CVD in 10 upcoming years -Factors include: Age SBP BMI Socieconomic status Ethnicity -Score of ten plus (10% + risk in the next ten years) is an indication to start 1° lipid lowering therapy (statins)

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15
Q

What is atorvastatin an example of?

A

Lipid lowering therapy

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16
Q

Which arteries does atherogenesis affect most commonly?

A

LAD Circumflex RCA

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17
Q

Risk factors for IHD

A

Age Smoking Obesity, high serum cholesterol Diabetes Hypertension Family history M>F Cocaine use Stress Physical inactivity

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18
Q

Symptoms of stable angina pain?

A
  1. Central crushing chest pain radiating to neck/jaw 2. Brought on with exertion 3. Relieved with 5mins rest or GTN spray
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19
Q

Four types of angina?

A
  1. Stable - normal three point definition 2. Unstable - pain at rest, not relieved by inactivity or GTN spray + no ECG CHANGES 3. Prinzmetal’s - due to coronary vasospasm (not due to cv vessel atherogenesis) Seen increasingly in cocaine users ECG shows ST elevation 4. Decubitus - induced when lying flat (usually complication of cardiac failure)
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20
Q

Patholophysiology of ischaemic heart disease?

A

Atherogenesis: Endothelial injury attracts cells to site via chemokines (IL1, IL6, IFN-Y) 1. Fatty streak = Foam cells (lipid laden macrophages) and T-cells 2. Intermediate lesions = foam cells (bigger as taken up more lipid), t- cells and smooth muscle cells Platelets also aggregate and adhere to site inside vessel lumen 3. Fibrous plaques (advanced) = large lesions (foam cells, t-cells, smooth muscle, fibroblasts, lipids with a necrotic core) Develops a fibrous cap over lesion

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21
Q

Fibrous cap in stable angina?

A

Fibrous cap is strong and less rupture prone

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22
Q

What happens if plaque is prone to rupture?

A

Prothrombotic state, platelet adhesion and accumulation leads to progressive luminal narrowing

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23
Q

Difference between ischaemia and infarction?

A

Ischaemia= blood flow restricted Infarction= lumen fully occluded

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24
Q

When do symptoms for stable angina start?

A

When 70 to 80% lumen occluded Due to poiseulle’s law, nothing much happens until the diameter stenosis reaches 70% and then there is rapid decline

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25
Q

Symptoms of IHD?

A

Central crushing chest pain radiating to jaw/neck, worsens with time (doesn’t peak straight away ) NSFD: Nausea Sweating Fatigue Dyspnoeic weak breathing + hypotensive/tachycardic in ACS and “impending sense of doom” and palpitations

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26
Q

How to diagnose stable angina?

A

1st line= ECG- resting and with exercise (to induce ischaemia) Coronary angiography- looks for stenoses and atherosclerotic arteries (~70-80% occluded) Gold standard but invasive so not first line

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27
Q

Treatment for stable angina?

A

-Symptomatic= GTN sublingual spray -Lifestyle modifying (decrease weight, stop smoking, exercise, diet etc) -Pharmacological (all patients=1st line) 1. CCB (CI heart failure) or B-b (CI Asthma) Switch if either is not tolerated If both are contraindicated or not tolerated, other drugs to consider as monotherapy: - a long acting nitrate (isorbide monitrate) - nicorandil - ivabradine - ranolazine Secondary anti platelet treatment is recommended (75mg aspirin) (eg if they have a stent but not necessarily for stable angina) Potentially Revascularisation: PCI/CABG with an MDT meeting or coronary angiogram if symptoms not controlled

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28
Q

What does acute coronary syndromes cover?

A

Umbrella term for unstable angina, NSTEMI and STEMI

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29
Q

How to define different acute coronary syndromes?

A

Unstable angina- severe ischaemia NSTEMI- partial infarction + Q wave infarction STEMI- transmural infarct and ST elevation in local ECG leads +Non-Q infarction

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30
Q

Different acute coronary syndromes pathologies? (Chart)

A

img

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31
Q

What does an ECG after MI look like?

A

hyperacute t wave -pathologically deep q waves - ST segment elevation

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32
Q

What’s the difference between types of MI?

A

T1 = traditional MI due to an acute coronary event (athermatous plaque rupture) T2 = secondary to ischaemia due to either increased oxygen demand or decreased supply (vasopasm, anaemia and sepsis)

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33
Q

Is troponin or creatine kinase mb a better indicator of cardiac damage long term?

A

Troponin has a shorter half life so CKMB is a better biomarker after a few days

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34
Q

Pathophysiology of ACS (angina)?

A

ACS is usually the result of a thrombus—> atherosclerotic plaque formation due to damage to arterial walls causing myocardial ischaemia When a thrombus forms in a fast flowing artery it is made up mostly of platelets. - why anti-platelet medications= key

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35
Q

Making a diagnosis of ACS? (Step by step) (primary investigations)

A

1) when patient presents with symptoms (eg chest pain) perform ECG 2) ST elevation or new left bundle branch block = STEMI 3) no ST elevation—-> troponin blood tests: - increased troponin + changes (ST depression, t wave inversion or path Q waves) = NSTEMI -normal troponin + no ECG changes then unstable angina or another cause (musculoskeletal chest pain)

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36
Q

Symptoms of ACS?

A

Same as stable angina but pain @ rest prolonged with no relief “impending doom” palpitations and Symptoms more severe

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37
Q

Alternative causes of raised troponin?

A

Gram negative sepsis Myocarditis Aortic dissection Pulmonary embolism Arrhythmias

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38
Q

Other investigations when considering ACS?

A

Those normally arranged for stable angina: - physical examination (heart sounds, signs of heart failure, BMI) - FBC (anaemia) - U&Es (check for electrolyte imbalances prior to ACEi and other meds) -LFTs (prior to statins) -Lipid profile -Thyroid function tests (hypo/hyperthyroid) -HbA1c and fasting glucose (for diabetes) Plus: -chest x ray to investigate other causes of chest pain and pulmonary oedema -Echocardiogram after event to assess for functional damage -Ct coronary angiogram to assess for coronary artery disease

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39
Q

Acute management of ACS generally?

A

MONAC Morphine + anti-emetic (metoclopramide) O2 (if stats <94% or 88-92% if COPD) Nitrates (GTN) Aspirin (300mg) Clopidogrel/Ticagrelor (75mg dual antiplatelet) or pasugrel if undergoing PCI (PY12 inhibitor) Anticoagulant: fondaparinux or heparin *not all patients require oxygen

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40
Q

What does GRACE score assess?

A

Mortality risk of patients with ACS from MI within the next 6 months to 3 years

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41
Q

Treatment for low risk NSTEMI/unstable angina

A

Monitor

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42
Q

Treatment for high risk NSTEMI/ unstable angina?

A

Immediate angiogram and consider PCI

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43
Q

Treatment for STEMI if presenting <12h of Sx and <2h of first medical contact?

A

PCI (percutaneous intervention) (Insertion of a catheter via radial or femoral artery to open up blocked vessels using an inflated balloon (angioplasty) and a stent may also be inserted) -unfractionated heparin and glycoprotein IIb/IIIa inhibitor

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44
Q

Treatment for STEMI if presenting <12h Sx and more than 2h of first management?

A

Ineligible for PCI:-Fibrinolysis/ thrombolysis - IV administered alteplase or tenecteplase -antithrombin agent eg unfractionated heparin (bivalirudin and/or glycoproteins IIB/IIIa may also be considered) Offer ECG 60-90 mins after If shows residual ST elevation offer immediate angiography and PCI

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45
Q

Why are diabetics major culprits of Silent MIs?

A

diabetic neuropathy -don’t feel the anginal pain and therefore may miss diagnosis and die from sudden collapse

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46
Q

Long term and secondary prevention after ACS?

A

6 As -Atenolol (or other Beta blocker titrated to toleration) (life) -Aspirin (initial dose 300mg -> 75mg life) -Atorvastatin (80mg life) -ACEi (eg ramipril titrated to 10mg) (life) -Another antiplatelet (eg. clopidogrel (75mg for 12months) -Aldosterone antagonist for those with clinical heart failure (ie eplerenone titrated to 50mg once daily) Can add an opiate or GTN spray for pain relief Dual antiplatelet duration will vary following PCI procedures (due to higher risk of thrombus formation in diff stents)

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47
Q

Acute complications of ACS (2 >= wk)

A

Heart failure due to vent fibrillation Mitral incompetence Left ventricle free wall rupture Cardiogenic Shock

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48
Q

Other complications of ACS (2< weeks)

A

Dressler syndrome (autoimmune pericarditis) Heart failure LV aneurysm-heart literally becomes saggy :(

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49
Q

How to interpret GRACE score

A

<5% low risk 5-10% medium risk >10% high risk

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50
Q

Complications of MI

A

DREAD -Death -Rupture of heart septum or Papillary muscles -Edema (Heart failure) -Arrhythmia and Aneurysm -Dressler syndrome

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51
Q

Define heart failure

A

Inability for heart to deliver O2 blood to tissues at a satisfactory rate for the tissues metabolic requirements * a syndrome not a diagnosis

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52
Q

Cause of heart failure?

A

IHD Cardiomyopathy Valvular disease Cor pulmonale Anything that increases cardiac work: -obesity -htn -pregnancy -hyperthyroid -arrhythmias

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53
Q

Risk factors for heart failure

A

Age (65+) Smoking Obesity Previous MI Male

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54
Q

Pathophysiology for Cor pulmonale?

A

RH failure due to disease of lungs +/ pulmonary vessels Increased pressure and resistance in pulmonary arteries results in right ventricle being unable to pump blood out Leads to back pressure of blood into right atrium, the vena cava and the systemic venous system

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55
Q

Pathophysiology of heart failure

A

-Failing hearts = decreased CO due to dysfunctional frank starling law 1- compensatory mechanism activation —Raas + sns initially works (=increase BP) Increases aldosterone + ADH Increases ADR / NaD 2- soon compensation fails and heart undergoes cardiac remodelling (decreased CO) in response to compensation * heart less adapted to function so increase in RAAS + SNS will exacerbate fluid overload * heart failure affecting both L+R circuits = congestive heart failure

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56
Q

Normal physiology of heart

A

Normally- increased preload= increased afterload= increased cardiac output (frank starling law)

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57
Q

Three ways heart failure can be classified?

A

1) Time classified 2) Acute or chronic 3) Ejection fraction classified

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58
Q

How is heart failure ejection fraction classified?

A

Normal = 50–70% > 50% = preserved Diastolic failure (filling issues) Eg. Hypertrophic cardiomyopathy, LVH (aortic stenosis) < 40% = reduced Systolic failure (pump issues) Eg. IHD - ischaemic tissue

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59
Q

What does LHS failure result in?

A

Pulmonary vessel backlog —> pulmonary oedema

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60
Q

What does RHS failure result in?

A

Systemic venous backlog —> peripheral oedema

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61
Q

3 cardinal non specific symptoms of heart failure

A

SOBASFAT 1 Shortness of breath 2 Ankle swelling 3 Fatigue

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62
Q

Other symptoms of heart failure

A

orthopnoea (dyspnoea worse lying flat) -increased JVP -bibasal crackles (pul oedema) -hypotensive -tachycardic

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63
Q

NY heart association class 1-4 of HF severity

A

1 no limit on physical activity 2 slight limit on moderate activity 3 marked limit on moderate + gentle activity 4 symptoms even at rest

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64
Q

Methods of diagnosing of heart failure?

A

Bloods ECG Chest X-ray ECHOcardiogram - gold standard

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65
Q

Blood results with heart failure?

A

BNP (brain natriuretic peptide) = key marker High >400ug/ml Level correlates with extent of damage So more severe heart failure = higher bnp It is released from stressed ventricles in response to increase mechanical stress *might also measure NT ProBNP (inactive BNP) and levels are 5x higher so increase of >2000 ug/ml

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66
Q

ECG results with heart failure?

A

Abnormal Eg evidence of LVH

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67
Q

Chest x ray results with heart failure

A

ABCDE Alveolar bat wing oedema B-lines Cardiomegaly Dilated upper lobe vessels Effusion (pleural)

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68
Q

Purpose of echocardiogram?

A

Assess heart chamber dimensions

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69
Q

Conservative treatment for heart failure

A

Lifestyle changes: Decrease bmi Exercise Stop smoking + alcohol

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70
Q

First line treatment for chronic heart failure

A

ABAL First line: -ACEi (eg ramipril titrated up to tolerated dose of 10mg) -Beta blocker (eg bisoprolol titrated up to 10mg) Add in: -Aldosterone antagonist when symptoms not controlled with A and B (eg spironactone or eplerenone) -Loop diuretic improves symptoms (eg. Furosemide 40mg once daily) *consider desynchronisation therapy (improves A-V coordination) - low dose and slow uptitration is key with ACEi and Bb

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71
Q

Surgical treatments for heart failure?

A

Revascularisation Valve surgery Heart transplant (last resort)

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72
Q

What if ace inhibitors are not tolerated?

A

ARB like candersartan titrated go 32mg can be used instead

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73
Q

What should patients have monitored when on diuretics, ace inhibitors and aldosterone antagonists?

A

U&E All three medications cause electrolyte disturbances

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74
Q

Patients with valvular heart disease should avoid which drug?

A

Ace inhibitors unless indicated by a specialist

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75
Q

Respiratory causes of cor pulmonale?

A

COPD is most common cause -pulmonary embolism -interstitial lung disease -cystic fibrosis -primary pulmonary hypertension

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76
Q

Presentation of Cor Pulmonale

A

Patients often asymptomatic Main presenting complaint is shortness of breath (Also caused by chronic lung disease) May also present with peripheral oedema, increased breathlessness of exertion, syncope or chest pain

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77
Q

Signs of Cor Pulmonale

A

-Hypoxia -cyanosis -raised JVP (due to backlog of blood in jugular veins) -peripheral oedema -third heart sound -murmurs (eg pan-systolic in tricuspid regurgitation) -hepatomegaly due back pressure in the hepatic vein

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78
Q

Management of cor pulmonale?

A

Management involves treating the symptoms and underlying cause Long term oxygen therapy often used Prognosis is poor unless reversible underlying cause

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79
Q

Define hypertensive heart disease?

A

Heart failure and conduction arrhythmias due to unmanaged high blood pressure

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80
Q

Define abdominal aortic aneurysm? (AAA)

A

Permanent aortic dilation exceeding 50% where diameter >3cm Typically infrarenal (below renal arteries), in elderly men

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81
Q

ECG changes and corrosponding coronary arteries

A

img

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82
Q

Flow chart for treatment for NSTEMI or unstable angina

A

img

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83
Q

Flowchart for STEMI treatment

A

img

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84
Q

Prevalence of AAA?

A

1.3 to 12.7% in the uk, most commonly affecting elderly men Often inherited

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85
Q

A negative risk factor for AAA?

A

Diabetes but unknown reason

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86
Q

Risk factors for AAAs?

A

Smoking = biggest risk factor Increasing age Make Hypertension Connective tissue disorders - Ehlers Danos and Marfan syndrome (changes in balance of collagen and elastic fibres) Family history

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87
Q

Pathophysiology for AAA?

A

Smooth muscle, elastic + structural degredation in all 3 layers of vasuclar tunic (intima, media, adventitia) All 3 layers = true aneurysm Not all 3 = pseudoaneurysm (usually due to trauma ) Dilation in AAA typically 3cm+ A dilation that is 5.5cm+ has an increased rupture risk Rupture = surgical emergency

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88
Q

Inflammatory AAA?

A

Type that usually affects younger patients and is associated with smoking, atherosclerosis and vasculitis 5-10% of AAAs Same symptoms + pyrexia (fever)

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89
Q

Symptoms of AAA?

A

Mostly asymptomatic and discovered incidentally Symptoms generally when ruptured/impending rupture -sudden epigastric pain radiating to flank -pulsatile abdominal mass - tachycardia and hypertension

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90
Q

Surface potential signs of AAA?

A

Grey-Turner’s sign = flank bruising secondary to retroperitneal haemorrhage (also potentially haemorrhagic pancreatitis) Cullen’a sign = pre-umbilical bruising more associated with acute pancreatitis and ectopic pregnancy but also linked with AAA

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91
Q

Primary diagnosis tool for AAA?

A

Abdominal ultrasound -fast, cheap, reliable -highly sensitive and specific (Axial plane at level of the navel)

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92
Q

Treatment for an asymptomatic aneurysm <5.5cm?

A

Surveillance + offer advice to manage risk factors (decrease smoking, BMI, BP and satins)

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93
Q

Treatment for asymptomatic AAA and >= 5.5cm or >4.0cm and expanded more than 1cm per year?

A

Elective surgery Either: 1) EVAR (Endovascular aortic repair) - stent inserted through femoral/iliac artery -Less invasive but more post op complications 2) open surgery (favoured by nice unless sig comorbidities) -more invasive but fewer complications Survival for both=equivalent (EVAR)

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94
Q

Treatment for symptomatic AAA?

A

Urgent surgical repair (EVAR or open surgery)

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95
Q

Treatment for a ruptured AAA?

A

Stabilise ABCDE, fluids then urgent surgical repair -Nice says EVAR preferred in all women, and men over 70 otherwise open surgery preferred -Do not offer complex EVAR (eg BEVAR) if open surgery is suitable 20% of AAAs rupture anteriorly into peritoneal cavity= poor prognosis 80% rupture posteriorly = better prognosis 100% mortality for ruptured AAA if not treated immediately

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96
Q

Cause and treatment for rare AAA in thoracic aorta?

A

main cause = marfans/ehlers danos +atherogenesis - treatment = monitor with CT/MRI or if symptomatic—> surgery immediately

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97
Q

Pathophysiology of aortic dissection?

A

Surgical emergency!! Tear in intima resulting in blood dissecting through media and separating layers apart -due to mechanical wall stress Creates a false lumen (can propagate forwards and backwards) Abnormal flow can occlude flow through branches of aorta Decreased perfusion to end organs = shock/failure

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98
Q

Risk factors for aortic dissection(AD)

A

Hypertension = most key Connective tissue disorders (ED,Marafan) Family history of AAA/AD Truma Smoking

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99
Q

Most common location for aortic dissection

A

Sinotubular junction = where aortic root becomes tubular aorta, near aortic valve (Stanford A)

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100
Q

Stanford classification for aortic dissection

A

A = proximal to left subclavian artery (ascending + arch) (2/3=most common) B = distal to left subclavian artery (descending thoracic) (1/3=less common)

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101
Q

Debakey classification of aortic dissection

A

Type I = originates in ascending aorta and involves at least the aortic arch, but can extend distally Type II = originates and confined to the ascending aorta Type III = originates in the descending aorta and extends distally, but can extend proximally

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102
Q

Signs and symptoms of aortic dissection

A

Symptoms: -Sudden onset ripping/tearing chest pain that may radiate to the back -Syncope (fainting) red flag Signs: -Radio-radial and/or radio-femoral delay -Diastolic murmer due to aortic regurgitation -diff in blood pressure between two arms >10mmHg -hypertension -tachycardia and hypotension (commonly type A)

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103
Q

Differential diagnosis for AAA?

A

Acute pancreatitis Typically non pulsatile + more associated with grey-turner/Cullen signs

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104
Q

Investigations for diagnosing aortic dissection?

A

ECG Chest X-ray -may show widened mediastinum >8cm is suspicious (1= widened mediastinum and 2= enlarged aortic knuckle) Contrast-enhanced CT angiogram (gold standard) -v specific and sensitive and used if patient is hemodynamically stable -shows intima flap, false lumen, dilation of aorta and rupture (Type a aortic dissection)

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105
Q

Investigation in an unstable patient?

A

Transthoracic (TTE) or transoesphageal (TOE) echo TOE is more invasive but more specific for AD and v sensitive -shows intima flap and false lumen -Allows classification of AD as type A or B

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106
Q

Treatment for type A aortic dissection

A
  • Blood transfusion - IV labetol (aim for systolic bp 100-120) - Urgent open surgical repair to replace ascending aorta
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107
Q

Treatment for type B aortic dissection

A
  • conservative management: analgesia and bed rest - IV lavetol (aim for 100-120 systolic bp) - thoracic endovascular aortic repair (TEVAR) may be performed to reduce risk of further dissection yet not standard practice
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108
Q

Complications of aortic dissections?

A

cardio tampenade -aortic insufficiency (regurgitation) -pre renal AKI -stroke (ischemic)

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109
Q

Mortality rate for untreated aortic dissection?

A

Will result in a false channel rupture and fatal haemorrhage in 50-60% if patients within 24hrs Estimated 20% of patients die before reaching hospital and 30% die before reaching theatre 5 yr survival rate after surgery is 80%

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110
Q

Limits for diagnosing hypertension

A

> = 140/90 mmHg in clinic >= 135/85 mmHg at home (ambulatory blood pressure monitoring)

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111
Q

Primary vs secondary hypertension

A

1° = Essential hypertension (idiopathic/no known cause) 95% cases 2° = known underlying cause 5% cases

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112
Q

Causes of secondary hypertension

A
  • Renal disease (CKD-most common cause due to diabetic nephropathy) - Endocrine disorders (phaeochromocytoma, conn’s, cushing’s) - Medication/iatrogenic : glucocorticoids, ciclosporin, atypical antipsychotics, combined oral contraceptive pill -pregnancy
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113
Q

Non modifiable risk factors for hypertension

A

Age African heritage Family history

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114
Q

Modifiable risk factors for hypertension

A

Obesity Sedentary lifestyle Alcohol excess Smoking High sodium intake (>1.5g a day) Stress

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115
Q

Define the limits for stages of hypertension

A

(H) = clinic reading (A) = ambulatory Discrepancy of >= 20/10mmHg between clinic and ambulatory suggests “white-coat hypertension

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116
Q

Malignant (accelerated) hypertension?

A

Severe increase in blood pressure >=180/120 mmHg (stage 3) with signs of retinal haemorrhage and/or pailloedema, associated with target organ damage = emergency assessment and treatment

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117
Q

Pathophysiology of hypertension

A

Ultimately all mechanisms will increase RAAS and SNS activity (CO) and TPR => increase in BP as BP=COxTPR

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118
Q

Signs of malignant hypertension

A

Hypertensive retinopathy Visual disturbances Cardiac symptoms eg chest pain Oliguira or polyuria Overall rare but scary and unrelated to cancer just very severe symptoms

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119
Q

Symptoms of hypertension

A

Mostly asymptomatic and found in screening May have pulsatile headache, classically occipital and worse in the morning

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120
Q

Signs of hypertension to consider

A

Signs of the underlying cause of secondary hypertension Eg phaeochromocytoma, hyperthyroidism or Cushing’s

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121
Q

How to diagnose hypertension

A

If bp reading in hospital is between 140/90 and 180/120 mmHg then offer ABPM to confirm diagnosis -bp is measured for 24h with at least 2 measurements per hour during waking hours -overall at least 14 measurements are required

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122
Q

Other investigations for hypertension?

A

Assess end organ damage (more damage = worse prognosis) : - Fundoscopy: assess for hypertensive retinopathy - 12- lead ECG: assess for LVH - Urinalysis and ACR: assess for renal dysfunction + diabetes risk - Bloods: HbA1c, U&Es, total cholesterol, HDL cholesterol

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123
Q

Treatment guidelines for hypertension

A

img

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124
Q

If a patient has T2DM and is black or 55+, would they take CCB or ACEi?

A

T2DM takes precedence and they should take ACEi BUT ARBs are preferred for black patients so that might be preferable

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125
Q

Complications for hypertension?

A

Heart failure Increased IHD risk CKD/Renal failure PVD Dementia Increased risk of cerebrovascular incident

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126
Q

Pathophysiology of types of deep vain thrombosis (DVT)?

A

Formation of thrombus in a deep leg vein -around\below calf = minor veins (eg. Anterior and posterior tibial) => less concerning and more common -above calf (in thigh) = major veins (eg. Superficial femoral) occlusion may impede distal flow => life threatening and less common

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127
Q

Risk factors for DVT?

A

Dependant on Virchow’s triad: 1. Hypercoagulability 2. Venous stasis 3. Endothelial damage (abnormality in any component can result in thrombus)

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128
Q

Hypercoagulabilty and causes? (Virchow’s triad)

A

= increased platelet adhesion and clotting tendency Hereditary: - Factor V Leiden - protein C and S deficiency - antiphospholipid syndrome Acquired: - malignancy - chemotherapy - COCP/HRT - Pregnancy - Obesity

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129
Q

Venous stasis and cause? (Virchow’s triad)

A

blood flow is normally laminar to spread out platelets and clotting factors without activation Stasis —> aggregation of clotting factors = thrombus formation cause = immobility (long flights, after surgery)

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130
Q

Endothelial damage and causes? (virchow’s triad)

A

=endothelial cells normally prevent thrombosis by secreting anticoagulants, as well as blocking exposure to pro-thrombotic collagen - damaged endothelial cells cannot!! Causes: — endothelial dysfunction: - smoking — endothelial damage: - surgery - catheter (PICC lines) - Lower limb trauma

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131
Q

Symptom and signs of DVT?

A

Symptom: Unliateral calf pain, redness and swelling Signs: -unliateral swelling -oedema -tender and erythematous -distension of superficial veins Right leg = swollen and erythematous

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132
Q

What is phlegmasia cerulea dolens?

A

Occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). => ischemia and a blue, painful leg

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133
Q

What is a Wells score?

A

Calculates the risk of DVT and determines investigations + management >= 2 DVT likely =< 1 DVT unlikely (Don’t learn all but know a few)

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134
Q

Gold standard for diagnosis of DVT

A

Duplex ultrasound of leg (Duplex USS) -if unavailable, alternative is D-dimer

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135
Q

Flow chart of investigations when considering DVT

A

img

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136
Q

Positive d-dimer and negative duplex USS? (In patient with suspect DVT)

A

-stop interim anticoagulation -offer repeat ultrasound 6 to 8 days later +ve= restart anticoagulation -ve= alternative diagnosis

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137
Q

Treatment for DVT?

A

Offer DOACs: apixaban or rivaroxaban If there’s a CI eg patient is renally impaired offer one of: -LMWH -Unfractionated heparin Treatment for at least 3 months or 3 to 6 months if they’re a cancer patient +mobilisation and compression stockings

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138
Q

Complications of DVT

A

Pulmonary embolism Post thrombotic syndrome Increased risk of bleeding (as on anticoagulants)

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139
Q

Risk of recurrence with DVT?

A

30% in the next five years

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140
Q

Differential diagnosis to DVT?

A

Cellulitis Skin infection-typically staph aureus + strep pyogenes -tender, inflamed swollen calf with pronounced demarcation will show leukocytosis on FBC while DVT will have normal levels

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141
Q

Pathophysiology of pulmonary embolism (PE)

A

Most commonly DVT embolises and lodges in oil on art after circulation (Could be any embolus) Can cause strain on right ventricle due to increased pulmonary vascular resistance

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142
Q

What can a PE cause?

A

img

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143
Q

Risk factors for PE?

A

Virchow’s triad (Mentioned in detail in DVT)

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144
Q

Symptoms of PE

A

Pleuritic chest pain (present in only 10% of patients) Dyspnoea Cough or haemoptysis Fever Syncope 🚩

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145
Q

Signs of PE?

A

Tachypnoea and tachycardia Hypoxia DVT (swollen tender calf) Pyrexia Hypotension (SBP <90 mmHg suggests massive PE) Elevated JVP (suggest cod Pulmonale)

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146
Q

Wells two level score?

A

Used to determine probability of PE >4: high probability =<4: low probability (Don’t learn all just a few examples)

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147
Q

Process for investigating PE?

A

D-dimer is NOT diagnostic but CTPA is -CXR should be normal -ECG: Often find sinus tachycardia S1Q3T3 (classic finding but only in 20% px) RBBB and right axis deviation suggest right heart strain

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148
Q

Why is D-dimer not diagnostic?

A

Measure of clot burden; a small protein relaxers into blood when blood clot fibronlysed Is sensitive (rules PE in) Not specific (doesn’t rule out other conditions)

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149
Q

What’s massive PE?

A

Hypotensive patient with <90 systolic bp Less common that non massive

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150
Q

Treatment for massive PE?

A

Thrombolysis => alteplase (“clot buster”)

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151
Q

Treatment for non massive PE?

A

Anticoagulation (DOAC) 3 to 6 month treatment 1st line = apixaban\riveroxaban *If there’s a CI due to renal impairment offer LMWH or UFH

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152
Q

Another name for peripheral vascular disease? (PVD)

A

Peripheral arterial disease (PAD)

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153
Q

What is PVD?

A

Peripheral vascular disease is essentially reduced blood supply and ischaemia in the lower limbs due to atherosclerosis and thrombosis in the arteries

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154
Q

Risk factors for PVD?

A

Smoking = singke greatest risk factor T2DM Ageing Males affected at younger age Obesity Hypertension CKD

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155
Q

Three main patterns of presentation of PVD?

A
  1. Intermittent claudication (least severe) 2. Critical limb ischaemia 3. Acute limb-threatening ischaemia (most severe)
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156
Q

Intermittent claudication?

A

Reflects an inadequate increase in skeletal muscle perfusion during exercise - atherosclerotic partial lumen occlusion - pain on exertion

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157
Q

Critical limb ischaemia?

A

Advanced form of chronic limb ischaemia - big occlusion and blood supply barely adequate to meet metabolic demand - pain at rest - risk of gangrene/infection

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158
Q

Acute limb-threatening ischeamia?

A

Most commonly caused by emboli, usually cardiac origin, resulting in sudden decrease in limb perfusion - total vessel occlusion - emboli tend to lodge at bifurcations or sudden narrowing

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159
Q

Symptoms of acute limb-threatening ischeamia

A

6Ps Pulselessness Pallor Pain Perishingly cold Paralysis Paresthesia - present in chronic limb ischemia too but more you have=more limb threatening - all 6 = deadly!!

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160
Q

What happens when BV supplying region is occluded?

A

1) irreversible nerve damage (within 6h) 2) irreversible muscle damage (6-10h) 3) skin changes are last to appear =>likely gangrenous

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161
Q

Fontaine classifications of PVD

A

I) asymptomatic II) intermittent claudication- aching or burning of leg muscles -stage IIa = after 200m walking -stage IIb = after less than 200m walking Relieved within minutes of rest III) critical limb ischaemia - pain at rest + night IV) tissue loss: ulceration or gangrene

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162
Q

Why might symptoms be masked in PVD?

A

Inability to walk (eg severe heart failure) Pain insensitivity (eg diabetic neuropathy)

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163
Q

Signs to look for in PVD?

A

-Low ABPI (<0.9) or lack of lower leg pulse -Skin changes on leg (ulceration, thin, shiny, discolouration -Buerger’s test +ve -Bruits: pulsatile regions due to turbulent blood flow (aortic, femoral, carotid) -Some of 6Ps

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164
Q

Buerger’s test?

A

1) lie patient flat 2) elevate leg to 45° for 1 min 3) positive = pallor then reactive hyperaemia

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165
Q

Primary investigations for PVD?

A

1) ABPI (ankle-brachial blood pressure index) 0.8-1.3 normal 0.5-0.8 intermediate claudication <0.5 critical limb ischaemia Pulse absent = acute limb-threatening ischaemia 2) duplex ultrasound imaging- assess location and severity of stenosis 3) ECG, U+E, FBC, HbA1c - assess cardiovascular risk Ct angiography if surgery considered, not routine as more invasive

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166
Q

Treatment of intermittent claudication

A

RF management: -Supervised exercise programme if available (2 hrs per week for three months) -or if not then unsupervised exercise training -smoking cessation -bp control -diet and weight management -statins -HbA1c control -antilplatelets If 3 months exercise doesn’t improve quality of life then consider Revascularisation surgery

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167
Q

Treatment of chronic limb ischaemia

A

Revascularisation surgery (PCI if small, bypass if larger) Amputation if severe

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168
Q

Treatment for acute limb threatening ischeamia

A

Surgical emergency Revascularisation within 4-6hrs otherwise increased amputation risk

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169
Q

Complications of PVD

A

Amputation Ulceration + gangrene Permanent limb weakness Infection and poor tissue healing Increased risk of cerebrovascular accidents + CVD

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170
Q

What is pericarditis?

A

Typically acute (can be chronic); inflammation of pericardium +/- effusion -pericardium has two layers and innervated by phrenic hence inflammation results in pain

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171
Q

Epidemiology of pericarditis?

A
  • males - 20-50yrs
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172
Q

Causes of pericarditis

A

1) Usually idiopathic 2) Or caused by a virus: - most common cause = coxsackievirus - mumps - EBV - VZV - HIV Less common causes: - bacterial - TB - systemic autoimmune disorders - malignancy - trauma

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173
Q

Pathophysiology of pericarditis

A
  • inflamed pericardial layers rub against each other = more inflammation -cause exudate and adhesions within pericardial sac 1) may stay dry (no extra fluid needed to compensate for friction) 2) develop pericardial effusion (extra fluid) - if it becomes large enough to affect heart function = cardiac tamponade
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174
Q

Symptoms of pericarditis

A

Sudden onset sharp, pleuritic chest pain which can spread to left shoulder tip (phrenic) - Relieved by sitting up or leaning forward - Worse laying flat *may have signs of rhs failure due to constructive pericarditis -> SOB, peripheral oedema and tachycardia

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175
Q

Sign of pericarditis

A

Pericardial friction rub on auscultation - heard at left sternal edge as patient leans forward - squeaky leather “to and fro” sound

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176
Q

Differential diagnosis of pericarditis

A

Most key to rule out MI - central crushing chest pain not related to lying down - no pericardial rub

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177
Q

What is constructive pericarditis

A

granulation tissue formation in pericardium means impaired diastolic filling as it becomes thickened and hardened - late complication of pericarditis - sign of poor prognosis—> congestive heart failure - commonly associated with TB

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178
Q

Primary investigations to diagnose pericarditis

A

ECG: widespread saddle shaped ST-elevation (sensitive) and PR depression (specific) Eg. CXR: may show “water bottle” heart = pericardial effusion - pneumonia commonly seen in bacterial pericarditis Transthoracic ecg: to exclude pericardial effusion or tamponade ESR and CRP: might increase due to inflammation Troponin will be daisies if there’s an element of concomitant myocarditis

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179
Q

Treatment for idiopathic or viral pericarditis

A

1st line: NSAIDs + Colchine 2nd line: NSAIDs + Colchine + low-dose prednisolone

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180
Q

Treatment for bacterial pericarditis

A

IV antibiotics and pericardiocentesis with washout, culture and sensitivities

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181
Q

Treatment for cardiac tamponade

A

Urgent therapeutic pericardiocentesis - needle inserted between xiphisternum and left costal margin and directed towards left shoulder -sometimes done under ultrasound guidance -pericardial fluid aspirated to relieve intrapericardial presure

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182
Q

Compilcations of pericarditis

A

1) Pericardial effusion—> cardiac tamponade 2) Myocarditis 3) Constrictive pericarditis

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183
Q

What is cardiac tamponade

A

Accumulation of a large vol of fluid in the pericardial space (pericardial effusion) that begins to impair ventricle filling

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184
Q

Cause of Cardiac tamponade

A

Typically pericarditis Hence risk factors are all pericarditis related

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185
Q

Symptoms of cardiac tamponade

A

Related to pericarditis

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186
Q

Signs of cardiac tamponade

A

Beck’s triad: - hypotension (reduced cardiac output) - raised JVP (heart failure) - muffled heart sounds Pulses paradoxes: systolic bp reduction of >10mmHg on inspiration

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187
Q

Primary investigations to diagnose cardiac tamponade

A

ECG: may show electrical alternations - varying QRS amplitudes due to heart bouncing back and forth in pericardial fluid CXR: big globular heart ECHO: diagnostic tool

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188
Q

What is infective endocarditis

A

Infection of endocardium: - an abnormal endocardium - bacterial source —> vegetation

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189
Q

Two most common causes of infective endocarditis

A

1) S.aureus- most common overall + associated with IV drug use and prosthetic heart valves => increased virulence, Sx onset in days-weeks = ACUTE 2) S.viridans- second most common + usually affects a native valve and associated with poor dental hygiene => decreased virulence, Sx onset in weeks-months = SUBACUTE

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190
Q

Catergorisations of endocarditis

A

1) Acute 2) Subacute 3) Non- bacterial thrombotic ‘marantic’ - non-infective cause of endocarditis secondary to thrombus formation on the valvular surface - associated with malignancy or SLE (Libman-Sacks endocarditis)

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191
Q

Other less common causes of infective endocarditis

A

S. Bovis (associated with colon cancer) S. Epidermis (associated with in dwelling lines and prosthetic valves) HACEK organsisms (usually culture -ve) - Haemophilus - Aggregatibacter - Cardiobacterium - Eikenella - Kingella

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192
Q

Risk factors for infective endocarditis

A

Male 2.5x Elderly with prosthetic valve Young IV drug user Young with congenital heart defect Rheumatic heart disease

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193
Q

Which valves are more commonly affected by Infective endocarditis

A

Mitral valve most commonly affected overall Tricuspid valve is most associated with IV drug use (Mitral valve)

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194
Q

Pathophysiology of infective endocarditis

A
  • any cause of abnormal endocardium —> turbulent blood flow and thrombus formation (platelets) - thrombus can get infected due to bacterial source - bacterial colonisation of the thrombus —> formation of vegetations —> valvular damage -typically happens around valves -causing regurgitation => aortic and mitral insufficiency and increase risk of heart failure
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195
Q

Symptoms of infection endocarditis

A

Rather vague -Fever or chills -headache -SOB -night sweats, fatigue, weight loss -joint pain (might be due to septic emboli)

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196
Q

Signs of infective endocarditis

A

1) Osler nodes (painful nodules on fingers\toes) 2) Janeway lesions (painless placques on palms and soles) 3) splinter haemmorrhages (red plum lines under nails) 4) Roth’s spots: white centred retinal haemorrhages heart murmer +- signs of heart failure

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197
Q

Primary investigations for infective endocarditis

A

-ECG (prolonged PR interval=aortic root abscess) -Blood cultures - 3 sets in 24 hours BEFORE ANTIBIOTICS -Inflammatory markers (CRP) - eg raised ESR\CRP + neutrophillia -FBC -ECHO: TOE more invasive than TTE but much more sensitive and specific = gold standard -Urinalysis

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198
Q

What is the modified Duke Criteria

A

Requires 2 major criteria, or 1 major and 3 minor, or 5 minor criteria for diagnosis of infective endocarditis

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199
Q

Major Duke Criteria for infactive endocarditis

A
  • 2 positive blood cultures - ECHO TOE shows endocardia’s involvement Eg. Vegetations , abscess or regurgitation
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200
Q

Minor Duke criteria for infective endocarditis

A

-predisposing heart condition -IVDU -Fever >38°C -1 +ve blood culture -immunological phenomenon (Osler’a nodes, Roth’s spots or rheumatoid factor) -vascular abnormalities (eg. Septic/arterial emboli, pulmonary infarct)

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201
Q

First line treatment for infective endocarditis

A

IV antibiotics for 4 weeks following nice guidelines, extended to 6 weeks for prosthetic valves -local guidelines should be followed with nice antibiotic guidance below (Idk if you need to know all these but have a rough idea)

202
Q

Second line treatment for infective endocarditis

A

Surgery: aim to remove infected tissue and repair it replace affected valves

203
Q

Complications of infective endocarditis

A

Congestive heart failure Septic embolisation Valvular rupture or fistula Aortic root abscess

204
Q

What does regurgitation cause?

A

Insufficiency + proximal chamber dilation -loss of structural chamber integrity and strength

205
Q

What does stenosis cause?

A

Increase in upstream pressure + proximal chamber dilation+hypertrophy - heart becomes huge and rigid; poorly compliant

206
Q

Main valve disorders?

A

Aortic regurgitation and stenosis Mitral regurgitation and stenosis

207
Q

What do the main valve disorders cause?

A

Murmers

208
Q

How are murmers best heard?

A

Using RILE Right side defects (tricuspid /pulmonary) heard on Inspiration Left sided defects (mitral\aortic) heard on Expiration

209
Q

Normal size of mitral bicuspid lumen and after undergoing stenosis?

A

Mitral bicuspid lumen = 4-6cm2 Symptoms of stenosis start at <2cm

210
Q

Causes of mitral stenosis

A

Most common = rheumatic fever (Post strep pyogenes infection) Also valve calcification in older patients + infective endocarditis

211
Q

Pathophysiology of mitral stenosis

A

RHD causes mitral reactive inflammation, after years exacerbated with calcification => LA hypertrophy and chamber dilation

212
Q

Symptoms and signs of mitral stenosis

A

malar cheek flush (due to CO2 retention) - association with Atrial Fibrillation (due to Stasis in LA and hypertrophy of LA) -dyspnoea - a wave on JVP

213
Q

Mitral stenosis murmur?

A

Low pitched Mid diastolic murmer Loudest at apex Best heard on expiration with patient lying on left hand side

214
Q

Investigations to diagnose mitral stenosis

A

CXR (LA enlarged) EVG (AFib, P mitrale= bifid “m” shale P waves when LA enlarged) ECHO -assess valve area, gradient, mobility (gold standard)

215
Q

Treatment for mitral stenosis

A

Surgical Percutaneous balloon valvotomy (stent open mitral valve opening) Mitral valve replacement

216
Q

Why is mitral stenosis more atrial fibrillation associated?

A

Mitral stenosis causes left atrium hypertrophy - more chances of embolisation as blood actively pumped harder

217
Q

Causes of mitral regurgitation

A

Myxomatous mitral valve (most common valve disease) = mass of cells in valve connective tissue makes leaflets heavier + prolapse

218
Q

What is mitral regurgitation

A

Heart valve disease in which the valve between the left heart chambers doesn’t close completely, allowing blood to leak backward across the valve

219
Q

Risk factors for mitral regurgitation

A

Females Older Decreased BMI Prior MI Connective tissue disorder (marfan, ehlers danos)

220
Q

Symptoms of mitral regurgitation

A

Exertion dyspnoea (due to pulmonary hypertension from back logging of blood)

221
Q

Mitral regurgitation murmer?

A

Pan systolic blowing murmur radiating to axila (at apex) soft S1, prominent S3 in heart failure (severe cases)

222
Q

Investigations for diagnosing mitral regurgitation

A

ECG CXR ECHO (gold standard) - check left atrium size and left ventricle function analysis Also assess valve structure to decide treatment

223
Q

Treatment for mitral regurgitation

A

ACEi, Bb + serial ECHO monitoring If severe - (symptoms at rest) = valve repair\replacement

224
Q

What is aortic stenosis

A

Pathological narrowing or aortic valve -decrease in flow Normal area 3-4cm Symptoms at 1/4 lumen size Most common valve disorder- results in LV dilation + hypertrophy

225
Q

Symptoms of aortic stenosis

A

SAD Syncope (exertional) Angina Dyspnoea (relates to heart failure)

226
Q

Aortic stenosis murmur

A

Ejection systolic crescendo decrescendo, radiating to carotids heard at right sternal border, second IC space -prominent S4 seen in LVH - narrow pulse pressure + slow rising pulse (not collapsing corrigan’s pulse)

227
Q

Investigations to diagnose aortic stenosis

A

ECG CXR ECHO = gold standard for LV size and function + aortic valve area

228
Q

Treatment for Aortic stenosis

A

General: Fastidious dental care to prevent IE As it is a mechanical problem-drugs are not effective Surgical if symptomatic: - in a healthy patient -> open repair\valve replaced (definitive) - more at risk (eg 75+) ->TAVI (transcutaneous aortic valve implant) less invasive and stents valve open

229
Q

Differential diagnosis for aortic stenosis

A

Hypertrophic cardiomyopathy may also cause S4 - associated with sudden death in young men

230
Q

What is aortic regurgitation

A

Leaky aortic valve which makes it insufficient

231
Q

Causes of aortic regurgitation

A

Congenital bicuspid valve RHD Connective tissue disorders (Marfan/ehlers danos) Infective endocarditis

232
Q

Symptoms and signs of aortic regurgitation

A

Collapsing carrigon’s pulse with wide pulse pressure -Quincke’s sign (nailed pulses when pressed) -De Musset sign (head bobbing in time with arterial pulsation)

233
Q

Aortic regurgitation murmur

A

Early diastolic blowing murmer at right sternal border 2nd intercostal space - Austin fling murmer (severe) - mid diastolic low pitched rumble - heard when regurgitation is so severe blood bounces if mitral valve cusps and makes sound

234
Q

Investigations to diagnose aortic regurgitation

A

ECG CXR ECHO gold standard, evaluates aortic valve, root, dimensions

235
Q

Treatment for aortic regurgitation

A

Consider IE prophylaxysis (consider as differential diagnosis) Surgical valve replacement if symptoms

236
Q

Epidemiology of rheumatic fever

A

Almost exclusively in developing countries only In young people

237
Q

Cause of rheumatic fever

A

Systemic response to B haemolytic group A strep (Strep pyogenes) Typically pharyngitis

238
Q

Rheumatic heart disease?

A

In 50% of cases of rheumatic fever it goes on to affect the heart

239
Q

Histological appearance of rheumatic fever

A

Valves affected show Aschoff Bodies (Seen on the right)

240
Q

Pathophysiology of rheumatic fever

A

M protein from S. pyogenes reacts with valve tissue of the heart Antibodies vs this “cross-link” results ins auto-antibody mediated destruction +- inflammation Molecular Mimicry!! * mostly affects the mitral valve (70% just mitral and 25% mitral and aortic) Typically thickens leaflets causing mitral stenosis

241
Q

Symptoms of rheumatic fever

A

New murmur (esp mitral stenosis) - Syadenham’s chorea (neurological disorder that results in uncoordinated jerky movements) - arthritis - Erythema nodosum (swollen fat causing red patches\bumps) - pyrexia - evidence of strep a infection

242
Q

Investigations to diagnose rheumatic fever

A

CXR= cardiomegaly/ heart failure (signs of mitral stenosis) ECHO= details extent of valvular damage

243
Q

Jone’s criteria for diagnosis of rheumatic fever

A

1) recent S. pyogenes infection AND 2) 2 major signs (new murmur, arthritis, erythema nodosum, syndham chorea) OR 3) 1 major + 2 minor (pyrexia, increased ESR/CRP, arythalgia)

244
Q

Treatment for rheumatic fever

A

Antibiotics- IV benzyloenicillin STAT, then phenoxypenicillin for 10days

245
Q

Treatment for Sydenham’s chorea

A

Haloperidol

246
Q

Most common congenital heart defect?

A

Bicuspid aortic valve 1-2% of the population M>F

247
Q

Is the aortic valve bicuspid or tricuspid?

A

Typically tricuspid

248
Q

Disadvantage of bicuspid aortic valve?

A

Bicuspid degenerates quicker than normal and will become regurgitative earlier Are also associated with coarction and dilation of ascending aorta Can be severely stenotic in infancy or childhood

249
Q

Another name for atrial septal defect

A

Patent foramen ovale

250
Q

Pathophysiology of atrial septal defect

A

Shunt of blood L->R and therefore not cyanotic (blue skin inducing) - increased flow to right side of heart and lungs - may overload RHS circulation causing RVH

251
Q

Investigations to diagnose an atrial septal defect

A

Using an ECHO

252
Q

Treatment for atrial septal defect

A

Sometimes there is spontaneous closure Otherwise treatment is surgical Percutaneous (key hole technique)

253
Q

What is a ventricular septal defect

A

L->R non cyanotic shunt (not blue) Blood flows from high pressure to low pressure chamber Increased blood flow through the lungs (more in larger defects) Risk of Eisenmengers syndrome and RVH later

254
Q

Symptoms of small ventricular septal defect

A

Typically asymptomatic Normal heart rate/size Loud systolic murmur

255
Q

Symptoms of a large ventricular septal defect

A

Exercise intolerance Failure to thrive Murmur varies in instensity Tachycardia + increased respiratory rate Small skinny breathless baby :(

256
Q

Investigation used to diagnose ventricular septal defect?

A

ECHO

257
Q

Treatment for ventricular septal defect

A

Spontaneous or surgical closure in infancy if big No need for intervention if small and asymptomatic

258
Q

What is an atrioventricular septal defect?

A

Essentially a hole down the middle of heart (no atrial or IV septum!) Can be complete or partial

259
Q

What is atrioventricular septal defect associated with

A

Massively associated with Downs Syndrome

260
Q

Symptoms of atrioventricular septal defect

A

Dyspnoea Exercise intolerance Complete defect: - breathless new pats with poor weight gain and feeding and needs repair wishing is surgically challenging Partial defect: Can present late in adulthood band can be left alone if no right heart dilation

261
Q

Prognosis of atrioventricular septal defect

A

Progresses to eventually Eisenmenger’s and hard to treat

262
Q

What is patent ductus arteriosus

A

When ductus arteriosus fails to close post birth = unusual

263
Q

Pathophysiology of patent ductus arteriosus

A

Blood shunt from aorta to pulmonary trunk -risk of pulmonary overload and Eisenmengar’s

264
Q

Symptoms of patent ductus arteriosus

A

Dyspnoea Failure to thrive Machine like murmur Risk of infective endocarditis

265
Q

Investigations to diagnose patent ductus arteriosus

A

CXR ECG ECHO

266
Q

Treatment for patent ductus arteriosus

A

Prostaglandin inhibitor (indomethacin) may induce closure Otherwise consider surgery by catheters

267
Q

What is tetralogy of fallot

A

Cyanotic! Ventricular septal defect with right ventricular outflow obstruction - therefore O2 deficient blood is systemically shunted = blue blood passes from RV to LV

268
Q

Most common congenital cyanotic heart disease

A

Tetralogy of Fallot 10% of all congenital birth defects

269
Q

Four congenital abnormalities present in Tetralogy of Fallot

A

PROV Pulmonary stenosis: RV outflow obstruction Right ventricular hypertrophy Overriding aorta (over top of VSD) Ventricular septal defect (VSD)

270
Q

Symptoms of tetralogy of fallot

A

Infants are often seen bringing their knees up to their chest as if squatting which partially occluded femoral arteries, this increases systemic vascular resistance and left ventricular pressure => relives cyanosis by reducing right to left shunt *cyanosis often exacerbated when cring or feeding

271
Q

How to diagnose tetralogy of fallot

A

ECHO CXR - presents as boot shaped heart

272
Q

Treatment of tetralogy of fallot

A

Full surgical repair within 2y of life and good prognosis if done Normally at 3-6months👩🏻‍🍼

273
Q

Pathophysiology of coarction of aorta

A

Aorta narrows at or just distal to ductus arteriosus => blood diverted massively through aortic arch branches = increased perfusion in upper body vs lower body

274
Q

Symptoms of coarction of aorta

A

Scapular bruits from collateral vessels Hypertension in collaterals (right arm) Murmur

275
Q

Investigations to diagnose coarction of aorta

A

CXR: “notched ribs” dilated intercostal vessels CT angiogram

276
Q

Treatment of coarction of aorta

A

Surgical repair or stenting of stenoses segment, even when mild to prevent long term problems

277
Q

Three types of cardiomyopathy?

A

1) Hypertrophic 2) Restrictive 3) Dilated

278
Q

What are cardiomyopathies?

A

Diseases of the myocardium (Muscular/conduction defects)

279
Q

What is the most common cause of death in young people?

A

Hypertrophic cardiomyopathy

280
Q

Causes of hypertrophic cardiomyopathy

A

Familial -inherited mutation of sarcomere proteins — troponin T and Myosin B

281
Q

Pathophysiology of of hypertrophic cardiomyopathy

A

Thick non compliant heart = impaired diastolic filling => decrease in CO

282
Q

Symptoms of hypertrophic cardiomyopathy

A

May present with sudden death Chest pain/angina Palpitations SOB Syncope/dizzy spells

283
Q

Investigations to diagnose hypertrophic cardiomyopathy

A

Confirm with abnormal ECG ECHO (diagnostic) Genetic testing

284
Q

Treatment for hypertrophic cardiomyopathy

A

Bb CCB Amiodarone (anti-arrhythmic)

285
Q

What is the most common cardiomyopathy in general

A

Dilated cardiomyopathy

286
Q

Cause of dilated cardiomyopathy

A

Autosomal dominant familial inheritance (cytoskeleton gene mutation) -IHD -Alcohol

287
Q

Pathophysiology of dilated cardiomyopathy

A

Thin cardiac walls poorly contract leading to a decrease in CO LV/RV or 4 chamber dilation and dysfunction

288
Q

Symptoms of dilated cardiomyopathy

A

SOB -heart failure (usually) -Atrial Fibrillation -thromboemboli

289
Q

Investigations to diagnose dilated cardiomyopathy

A

ECG ECHO

290
Q

Treatment for dilated cardiomyopathy

A

Treat underlying condition Eg Atrial fibrillation, heart failure

291
Q

How common is restrictive cardiomyopathy

A

Rare

292
Q

Causes of restrictive cardiomyopathy

A

Granulomatous disease (sarcoidosis,amyloidodis) -idiopathic -post MI-fibrotic

293
Q

Pathophysiology of restrictive cardiomyopathy

A

Rigid fibrotic nyocardium fills poorly and contracts poorly => decreased CO

294
Q

Symptoms of restrictive cardiomyopathy

A

Severe: -dyspnoea -S3 + S4 sounds -oedema -congestive heart failure -narrow pulse pressure ( normally 120/80 but here it’s 105/95 and consequently blood stasis due to the decreased gradient)

295
Q

Investigations to diagnose restrictive cardiomyopathy

A

ECG ECHO cardiac catheterisation (diagnostic)

296
Q

Treatment for restrictive cardiomyopathy

A

None Consider transplant Patients typically die within 1yr

297
Q

What is shock

A

A medical emergency- life threatening -hypoperfusion -due to acute circulation failure -leads to tissue hypoxia and risk of organ dysfunction

298
Q

What are the five different types of shock?

A
  • Cardiogenic (heart pump failure) - Distributive (arterial supply to tissues): 1) septic 2) neurogenic 3) anaphylactic - Hypovolemic (affects venous return to heart and therefore preload)
299
Q

Presentation of shock

A

1) decreased urine output 2) reduced GCS (Glasgow coma scale) 3) Skin - pale , cold, sweaty, vasoconstriction - increased capillary refill time = earliest, most accurate indicator - takes 3+ seconds for hand to turn pink after pressed for 5seconds 4) confusion 5) pulse- weak + rapid 6) prolonged hypotension = can lead to life threatening organ failure AFTER acute emergency recovery

300
Q

Causes of hypovolemic shock

A

1) Blood loss - trauma, GI bleed 2) Fluid loss- dehydration

301
Q

Symptoms of hypovolemeic shock

A

Clammy pale skin Confusion Hypotension Tachycardia

302
Q

Treatment of hypovolemic shock

A

ABCDE Airways Breathing (give O2) Circulation (IV fluids)

303
Q

Cause of anaphylactic shock

A

Due to IgE mediated Type 1 hypersensitivity vs allergen -Histamine release causes construction -causes excess vasodilation and bronchoconstriction Hypoxic!

304
Q

Symptoms of anaphylactic

A

Hypotension Tachycardia Urticaria Puffy face flushing of cheeks

305
Q

Treatment of anaphylactic shock

A

ABCDE IM adrenaline (SNS activation=stress response)

306
Q

Key organs at risk of failure from shock?

A

Kidneys Lungs Heart Brain

307
Q

Cause of neurogenic shock

A

Due to spinal cord trauma eg RTA Results in disrupted SNS, but intact PSNS

308
Q

Symptoms of neurogenic shock

A

Hypotension Bradycardia Confused Hypothermic

309
Q

Treatment for neurogenic shock

A

ABCDE IV Atropine (Blocks vagal tone: allows more psns inhibition, more chance for SNS to work)

310
Q

Cause of cardiogenic shock

A

Due to heart pump failure; MI, cardiac tamponade, pulmonary emboli

311
Q

Symptoms of cardiogenic shock

A

Heart failure signs (oedema) Increased JVP S4

312
Q

Treatment of cardiogenic shock

A

ABCDE Treat underlying cause

313
Q

Cause of septic shock

A

Due to uncontrolled bacterial infection

314
Q

Symptoms of septic shock

A

Pyrexia warm peripheries Tachycardic

315
Q

Treatment for septic shock

A

ABCDE Broad spectrum antibiotic

316
Q

Tachycardia vs bradycardia?

A

Tachycardia = 100< bpm Bradycardia = 60> bpm

317
Q

Types of bradycardia

A

1) RBBB/LBBB 2) 1°/2°/3° heart block 3) Sinus bradycardia

318
Q

Two major groups of tachycardia’s

A

Supraventricular tachycardias AND Ventricular tachycardias

319
Q

Types of supraventricular tachycardias (SVT)

A

1) AVRT (including WPW) 2) Atrial: -Sinus Tachycardia- Regular -Atrial fibrillation - Irregular -Atrial Flutter - Regular 3) AVNRT (functional) = most common SVT

320
Q

Transmission pathway for heartbeats

A

SAN -> AVN -> Bundle of His -> Purkinje Fibres

321
Q

What is atrial fibrillation

A

Irregularly irregular atrial firing rhythm

322
Q

What is the most common cardiac arrhythmia?

A

Atrial Fibrillation

323
Q

Causes of atrial fibrillation

A

Heart failure Hypertension 2° to mitral stenosis Sometimes idiopathic

324
Q

Risk factors for atrial fibrillation

A

60+ T2DM Hypertension Valve defects (mitral stenosis) History of MI

325
Q

Pathophysiology of atrial fibrillation

A

Regular,physiological impulses produced in the sinoatrial node are overwhelmed by the presence of rapid, uncoordinated electrical discharges produced in the atria. -Causes atrial spasm -Atrial blood pools instead of being pumped efficiently to ventricles

326
Q

What does atrial blood pooling cause

A

Cause a decrease in cardiac output and increased risk of thromboembolic events (particularly stroke)

327
Q

Potential underlying causes of Atrial Fibrillation

A

Pirates Pulmonary: PE and COPD Ischaemic heart disease: including heart failure Rheumatic heart disease: any valvular abnormality Anaemia, Alcohol, Advancing age Thyroid disease:hyperthyroidism Electrolyte disturbances eg hyper/hypokalaemia Sepsis and sleep apnoea

328
Q

Pathophysiology pathway of atrial fibrillation

A

(In reality it’s an overlap of these two pathways)

329
Q

Types of atrial fibrillation

A

1) First episode 2) Paroxysmel : recurrent episodes that stop on their own <7days 3) Persistant: recurrent episodes >7days 4) Permanent: continuous and refractory to treatment so management is aimed at rat control and anticoagulation

330
Q

Symptoms and signs of atrial fibrillation

A

Symptoms: 1) Palpitations 2) Dyspnoea 3) Chest pain 🚩 4) Syncope 🚩 Signs: 1) irregularly irregular pulse 2) Hypotension 🚩 3) Evidence of heart failure 🚩(eg pulmonary oedema)

331
Q

Investigations to diagnose Atrial fibrillation

A

ECG: - irregularly irregular pulse - narrow QRS (<120ms) - absent p waves

332
Q

Treatment of atrial fibrillation

A

Determine if rate or rythm control is more appropriate

333
Q

What is rate control

A

Rate control accepts the fact that the patient is not in sinus rythm, but aims at controlling the rate to reduce long-term deleterious effects of AF on cardiac function = decrease in heart rate

334
Q

What is rythm control

A

Rythm control aims to restore normal sinus rythm, “cardioversion”, can be either electrical or pharmalogical =restore normal PQRS shape

335
Q

When is rate control recommended for atrial fibrillation

A

Onset > 48 hours or unknown

336
Q

When is rythm control recommended for atrial fibrillation?

A
  • younger age - onset <48 hours - no underlying heart disease - reversible cause of AF - Failure of rate control - Haemodynamic instability acutely
337
Q

Treatment for atrial fibrillation if patient is haemodynamically unstable

A

Emergency electrical synchronised DC cardioversion

338
Q

Treatment of atrial fibrillation if patient is haemodynamically stable?

A

Onset of AF <48hrs: rate or rythm control Onset of AF >48hr/unknown: rate control and anticoagulation for at least three weeks Then offer rythm control if unsuccessful or still symptomatic

339
Q

First line drugs for rate control

A

Beta-blocker OR rate limiting CCB Bispropolol OR diltiazen or verapamil Second line is to combine drugs

340
Q

Pharmacological treatments for rythm control

A

Flecainide or amiodarone

341
Q

Electrical treatments for rythm control

A

Synchronised DC shock starting at 150J under shirt acting general anaesthesia

342
Q

Pathway for atrial fibrillation treatment

A

img

343
Q

What does a Has-bled score assess

A

Assess risk of major bleeds in AF patients on anticoagulants >= 3 (max 9) = regular reviews

344
Q

What does the CHA2DS2-VASc assess?

A

Assess stroke risk and therefore the anticoagulation need for Atrial fibrillation

345
Q

Scoring criteria for CHA2DS2-VASc score

A

Congestive heart failure Hypertension Age 75=< (2) DM Stoke (2) Vascular disease Age 65-74 Female Total: 2=< then oral coagulation required

346
Q

Complications of atrial fibrillation

A

Heart failure Ischaemic stroke Mesenteric ischeamia

347
Q

What is an atrial flutter

A

Irregular organisers atrial firing ~250-350bpm Less common and less severe than AF

348
Q

Pathophysiology of atrial flutter

A

Fast atrial ectopic firing (250-350bpm) causes atrial spasm, but not as uncoordinated as A-Fib. Pathway typically from opening of tricuspid valve

349
Q

Symptoms of atrial flutter

A

Dyspnoea Palpitations

350
Q

Investigations to diagnose atrial flutter

A

ECG : (diagnostic) f wave “saw tooth” pattern Often with a 2:1 block (2 p waves for every QRS)

351
Q

Treatment of acutely unstable atrial flutter

A

DC synchronised cardioversion

352
Q

Treatment of stable atrial flutter

A

Rythm/rate control with oral anticoagulation (prevent thromboemboli) Also radiofreq ablation

353
Q

What the most common supraventricular tachycardia?

A

AVNRT (functional)

354
Q

Pathophysiology of AVNRT

A

Re-entrant pathway goes through AVN

355
Q

Treatment for AVNRT

A

Same as AVRT (WPW)

356
Q

What is an AVRT?

A

AVRT ( Atrioventricular reciprocating tachycardia) -> an accessory pathway exists for impulse conduction, not re entry through AVN Often Hereditary

357
Q

Most common example of an AVRT

A

Wolff-Parkinson White syndrome (WPW)

358
Q

Pathophysiology of WPW

A

Accessory pathway for conduction= Bundle of Kent A pre excitation syndrome (excites ventricles earlier than typical pathway so that’s why you see delta waves)

359
Q

Symptoms of WPW

A

Palpitation Dizziness Dyspnoea

360
Q

Investigations to diagnose WPW

A

Ecg: 1) slurred delta waves 2) short PR interval 3) wide QRS

361
Q

Treatment for WPW

A

First line: Valsalva manoeuvre (Forceful exhalation against a closed airway.. close nose and mouth and breath hard like ur trying to pop ur ears) This triggers never to slow down electrical signals in the heart Carotid massage 2nd line: if 1st unsuccessful IV Adenosine (will temporarily cease conduction; when patient feels like dying) 6mg, then 12mg, then further 12mg (additional doses if 6mg is unsuccessful) Can also consider surgical radiofrequency ablation of bundle of Kent

362
Q

What is long QT syndrome?

A

Ventricular tachycardia Typically congenital channelopathy disorder where mutation affects cardiac ion channels and therefore heart conduction QT interval 480ms+

363
Q

Causes of long QT syndrome

A

-Romano ward syndrome (autosomal dominant) -Jervell - lang - Nielsen syndrome (autosomal recessive) -Hypokalemia + hypocalcemia (non-inherited) -Drugs (Amiodarone,magnesium)

364
Q

What is torsades de pointes?

A

-Polymorphic ventricular tachycardia in patients with prolonged QT -Rapid irregular QRS complexes which “twist” around baseline - can cease spontaneously or develop to ventricular fibrillation

365
Q

Initial management of MI

A

Get in to hospital quickly- 999 call Paramedics-if ST elevation, contact primary PCI centre for transfer Take 300g aspirin immediately Pain relief

366
Q

Causes of ACS

A

Rupture of atherosclerotic plaque and consequent arterial thrombosis is the main cause Uncommon causes: - stress induced cardiomyopathy - coronary vasospasm without plaque rupture - drug abuse

367
Q

What is troponin?

A

Protein complex regulates actin:myosin contraction Highly sensitive marker for cardiac muscle injury Not specific for acute coronary syndrome May not represent permanent muscle damage

368
Q

Examples of PY12 inhibitors

A

Clopidogrel Prasugrel Ticagelor

369
Q

Why are GPIIb//IIa antagonists used selectively?

A

Increase risk of major bleeding But still used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS

370
Q

Alternative treatment to PCI for NSTE ACS

A

CABG used in about 10% of patients But uncommonly, patients may have severe CAD not amenable to revascularisation

371
Q

Pain relief used in ACS management?

A

Opiates (can delay absorption of P2Y12 inhibitor so only if necessary) Nitrates for unstable angina/coronary vasospasm (GTN spray) (may be ineffective for MI)

372
Q

Clopidogrel vs pasugrel

A

Pasugrel is much more reliable and useful because it has a direct liver breakdown pathway while clopidogrel effectiveness relies on genetics alongside other factors

373
Q

Ticagrelor vs clopidogrel

A

Ticagrelor decreases risk of myocardial infarction and cardiovascular death in comparison to clopidogrel

374
Q

What is ventricular fibrillation?

A

Shapeless rapid auscultations on ECG Patient becomes pulseless + goes into cardiac arrest (no effective cardiac output) 1st line treatment-> electrical defibrillation But jinn synchronised as patient is pulseless

375
Q

Is rate control or rythm control preferred?

A

Rate control is generally preferred and first line for all patients unless they meet specific criteria

376
Q

Most common congenital heart disease?

A

Ventricular septal defect 25-30%

377
Q

Prevalence of patent ductus arteriosus

A

10-20%

378
Q

Prevalence of tetralogy of fallot

A

4-10%

379
Q

Exacerbating factors for IHD

A

Supply: -Anemia -hypoxemia Demand: -hypertension -tachycardia -valvular heart disease

380
Q

Environmental exacerbating factors for IHD

A

Exercise Cold weather Heavy metals Emotional stress

381
Q

Physiology of IHD

A

Myocardial ischemia occurs when there is an imbalance between heart’a oxygen demand and supply, usually from an increase in demand accompanied by limitation of supply: 1) impairment of blood flow by proximal arterial stenosis 2) increased distal resistance eg. Left ventricular hypertrophy 3) reduced oxygen-carrying capacity of blood eg. Anaemia

382
Q

What is microvascular angina (syndrome X)

A

‘ANOCA’ Angina with apparently normal (main) coronary arteries Females mostly Cause unknown

383
Q

Which risk factor drastically increases incidence of IHD

A

Age

384
Q

Symptoms that don’t associate with angina

A

No fluid retention (unlike heart failure) Palpitation (not usually) Syncope or pre-syncope (very rare)

385
Q

How to assess chest pain?

A

OPQRST Onset Position (site) Quality (nature/character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing Treatment

386
Q

Differential diagnosis for myocardial ischemia

A

Pericarditis/myocarditis Pulmonary embolism/pleurisy Chest infection/ pleurisy Gastro-oesophageal (reflux/spasm/ulceration) Musculoskeletal Physcological

387
Q

Treatment for myocardial ischemia

A

Reassure Lifestyle - smoking - weight - exercise - diet Advice for emergency Medication Revascularisation

388
Q

Advantages and limitations of CT angiography (fuzzier than normal angiography)

A

Good diagnostic test and at spotting severe disease Not so good at moderate disease Anatomical, not functional

389
Q

Advantages and drawbacks to exercise testing

A

Good functional test Relies on patients ability to walk on a treadmill (useless for elederly, obese, arthritis etc)

390
Q

Side effects of beta blockers

A

Tiredness, nightmares Erectile dysfunction Bradycardia Cold hands and feet

391
Q

Contraindication for beta blockers?

A

Asthma- do not give

392
Q

Side effect of aspirin

A

Gastric ulceration

393
Q

Pros and cons of PCI

A

Pro: - less invasive - convenient - repeatable - acceptable Cons: - risk stent thrombosis - can’t deal with complex disease - dual antiplatelet therapy

394
Q

Pros and cons of CABG

A

Pros: - prognosis - deals with complex disease Cons: - invasive - risk of stroke - can’t do if frail - one time treatment -time for recovery

395
Q

Which veins can a CABG use?

A

Internal mammary artery (from chest) Saphenous vein (from leg)

396
Q

PCI and CABG use

A

img

397
Q

If you don’t get chest pain when you run.. how likely is IHD?

A

Very low probability

398
Q

Prognosis of pericarditis

A

Majority of cases (viral and Idiopathic) are self limiting, whereas bacterial (purulent) pericarditis can be fatal if untreated.

399
Q

Heart sound S1?

A

Mitral + Tricuspid close

400
Q

Heart sound S2?

A

Aortic + Pulmonary close

401
Q

Heart sound S3?

A

Shows RAPID VENTRICULAR FILLING in early diastole * normal in young/pregnant * pathological in mitral regurgitation + heart failure

402
Q

Heart sound S4?

A

Pathological “gallop” * due to blood forced in to stiff hypertrophic ventricle (LVH + aortic stenosis)

403
Q

What does P represent on a normal ECG?

A

Atrial depolarisation

404
Q

What does PR interval represent on a normal ECG?

A

AVN conduction delay

405
Q

Average length of PR interval?

A

0.12-0.2s

406
Q

What does QRS interval represent?

A

Ventricle depolarisation + atrial repolarisation

407
Q

Average length of a QRS interval?

A

0.08-0.1s 0.12=< is abnormal

408
Q

Why does ST segment represent on a normal ECG?

A

Isovolemic ventricular relaxation

409
Q

What does T represent on a normal ECG?

A

Ventricular repolarisation

410
Q

What are ECGs useful in diagnosising?

A

-MI (STEMI, NSTEMI) -Arrhythmias -Electrolyte disturbance: K+, CA++ -Pericarditis -Chamber hypertrophy -Drug toxicity (eg. digoxin)

411
Q

Scale for ECG paper?

A

img

412
Q

ECG leads for RCA

A

aVF + II + III (Inferior)

413
Q

ECG leads for LAD

A

V1-V4 (Anterior + septal)

414
Q

ECG leads for LCx

A

V5 + V6 + aVL + I (Lateral)

415
Q

What is a 1° AV block?

A

PR interval prolongation (200ms+) Every P is followed by a QRS

416
Q

Symptoms of 1° heart block?

A

Asymptomatic

417
Q

Treatment of 1° heart block

A

No treatment as it is mild

418
Q

Causes of 1° heart block

A

Drugs (Bb, CCB, digoxin —> block AVN conduction)

419
Q

The difference between different degrees of heart block?

A

Severity 1° may not cause symptoms 2° sometimes troublesome symptoms 3° most serious = medical emergency

420
Q

What is 2° heart block?

A

When some p waves are conducted but others aren’t

421
Q

Two types of 2° heart block

A

Mobitz I (Weinkebach’s) Mobitz II

422
Q

What is Mobitz I?

A

PR prolongation until a QRS is dropped (PR interval progressively elongates)

423
Q

Causes of Mobitz I?

A

Same as 1° heart block (Bb, CCB, Digoxin) Inferior MI

424
Q

Treatment of Mobitz I?

A

No treatment unless symptomatic eg syncope Treatment—> pacemaker

425
Q

Symptoms of Mobitz I?

A

May have syncope

426
Q

What is Mobitz II?

A

PR interval consistently prolonged (not progressively enlarging) with random dropped QRS

427
Q

Causes of Mobitz II?

A

Drugs, Inferior MI, Rheumatic fever

428
Q

Symptoms of Mobitz II?

A

Syncope SOB Chest pain

429
Q

Treatment for Mobitz II?

A

Pacemaker

430
Q

What is 3° heart block?

A

AV dissociation (complete heart block; atria + ventricles beat independently of each other) * ventricular ESCAPE rythm is sustaining heartbeat —> SAN (best) if dysfunctional, AVN takes over —> if dysfunctional ventricle pacemakers take over (worst, firing rate 20-40bpm)

431
Q

Causes of 3° heart block

A

Acute MI Hypertension Structural heart disease

432
Q

Treatment for 3° heart?

A

IV atropine + permanent pacemaker

433
Q

What is a bundle branch block?

A

Blocks of bundles of His

434
Q

Two types of bundle branch block?(BBB)

A

RBBB right LBBB left

435
Q

Causes of RBBB

A

Pulmonary emboli IHD VSD

436
Q

Causes of LBBB

A

IHD Valvular Disease

437
Q

Pathophysiology of RBBB?

A

RV later activation than LV

438
Q

Pathophysiology of LBBB?

A

LV activation later than RV

439
Q

ECG presentation of RBBB?

A

img

440
Q

ECG presentation of LBBB?

A

img

441
Q

Epidemiology of hypertrophic cardiomyopathy

A

Affects 1 in 500 people

442
Q

What is LVOT?

A

Left ventricular outflow tract obstruction is a recognised feature of hypertrophic cardiomyopathy

443
Q

Cause of arrhythmogenic hypertrophy

A

Desmosome gene mutations

444
Q

Main symptom of arrhythmogenic cardiomyopathy

A

Arrhythmia

445
Q

What do all cardiomyopathies carry a risk of?

A

Arrhythmias

446
Q

Likely cause of sudden cardiac death in a young person?

A

Often due to an inherited condition Most likely a cardiomyopathy or ion channelopothy

447
Q

What is the cause of inherited arrhythmia? (Channelopothy)

A

Caused by ion channel protein gene mutations

448
Q

Which ions do cardiac channelopothies relate to?

A

Potassium Sodium Calcium

449
Q

Examples of cardiac channelopothies?

A

Long QT Short QT Brugada CPVT

450
Q

Cardiac channelopothies effect on heart structure?

A

No effect- have a structurally normal heart

451
Q

Symptom of cardiac channelopothy?

A

Syncope

452
Q

QT prolonging drugs?

A

Many drugs on this list that may be used to treat other conditions eg some antidepressants But they can kill people with long QT syndrome

453
Q

SADS sudden arrhythmic death syndrome?

A

Usually refers to normal heart/arrhythmia

454
Q

Familial hypercholesterolaemia (FH)?

A

Inherited abnormality of cholesterol metabolism

455
Q

What does familial hypercholesterolaemia lead to?

A

Serious premature coronary and other vascular diseases

456
Q

Aortavascular syndromes

A

Marfan Loeys-Dietz Vascular Ehler Danos

457
Q

What type of inheritance are inherited cardiac conditions usually?

A

Dominantly inherited Offspring have a 50% chance of inheritance

458
Q

Why is screening important for inherited cardiac conditions?

A

Genetic testing is available Risk (arrhythmic death, vascular dissection) needs to be assessed for each individual Life saving treatments are available (ICD, beta blockers, statins, vascular surgery) Lifestyle modifications can save lives

459
Q

Why is screening for inherited cardiac conditions highly contentious?

A

Because long QT has only a 1/5000 prevalence so it will very rarely be picked up and not a huge benefit to it in the normal population But for first degree relatives- 1/2 chance of it being passed on so highly recommended

460
Q

Why treat hypertension?

A

Important preventable cause of premature morbidity and mortality Major risk factors for: - stroke (ischaemic and haemorrhagic) - myocardial infarction - heart failure - cognitive decline - premature death Increases risk of Atrial fibrillation as well

461
Q

The main indications for ACEi?

A

Hypertension Heart failure Diabetic neuropathy

462
Q

Examples of ACEi?

A

Ramipril Enalapril Perindopril Trandolapril (Largely do the same job but vary in price)

463
Q

Main side effects of ACEi?

A

Due to reduced angiotensin II formation: - hypotension - acute renal failure - hyperkalemia - teratogenic effects in pregnancy Due to increased kinins: - cough - rash - anaphylactoid reactions

464
Q

Main clinical indications for ARBs?

A

Hypertenison -diabetic neuropathy -heart failure (when ACEi contraindicated)

465
Q

Examples of ARBs?

A

Cadersartan (most common) Losartan Val sat tan Irbesartan Telmisartan

466
Q

Main side effects of ARBs?

A

Symptomatic hypotension Hyperkalemia Potential for renal function Rash Angioedema Generally very well tolerated

467
Q

Contraindication of ARBs?

A

Pregnancy

468
Q

Main clinical indications of CCBs?

A

Hypertension ischaemic heart disease - angina Arrrhythmia (tachycardia)

469
Q

Examples of CCBs?

A

Amlodipine Diltiazem Verapamil Felodipine Lacidipine Nifedipine

470
Q

Dihydropyridines CCBs?

A

Nifedipine Amlodipine Felodipine Lacidipine Preferentially affect vascular smooth muscle = peripheral arterial vasodilators

471
Q

Phenylyalkylamines CCBs?

A

Verapamil Main effects in the heart = negatively chronotropic and inotropic

472
Q

Benzothiazepines CCBs?

A

Diltiazem = immediate heart/peripheral vascular effects

473
Q

Main side effects of peripheral vasodilation? (CCBs)

A

Flushing Headache Oedema Palpitations

474
Q

Main side effects due to negatively chronotropic effects? (CCBs)

A

Bradycardia Atrioventricular block

475
Q

Main side effects due to negatively ionotropic effects? (CCBs)

A

Worsening of cardiac failure

476
Q

Side effect of verapamil?

A

Constipation

477
Q

Main clinical indications for Bb?

A

Ischameic heart disease - angina Heart failure Arrhythmia Hypertension

478
Q

Examples of B1 selective Bb?

A

Metoprolol Bisoprolol

479
Q

An example of a less selective B1 Bb?

A

Atenolol

480
Q

B1/B2 (non-selective) Bb examples?

A

Propranolol Nadolol Carvedilol

481
Q

Are beta 1 selective blockers absolute?

A

Selectivity is relative rather than absolute

482
Q

What percentage of beta adrenoreceptors in the heart are actually B1?

A

Only 60% 40% are B2 =hence you can’t use the term cardioselective to describe B1 selective beta blockers

483
Q

Main side effects of Bb?

A

Fatigue Headache Sleep disturbance/ night mares Bradycardia Hypotension Cold peripheries Erectile dysfunction

484
Q

Contraindications of Bb?

A

Worsening of : - asthma (can be severe) or COPD - PVD - claudication or raynauds - Heart failure - if given in standard dose or acutely

485
Q

Main clinical indications of Diuretics?

A

Hypertension Heart failure

486
Q

4 classes of diuretics?

A

1) thiazides and related drugs (distal tubule) 2) loop diuretics (loop of henle) 3) potassium-sparing diuretics 4) aldosterone antagonists

487
Q

Examples of thuazide and related diuretics?

A

Bendroflumethiazide Hydroclorothiazide Chlorthalidone

488
Q

Examples of loop diuretics?

A

Furosemide Bumetanide

489
Q

Examples of potassium-sparing diuretics

A

Spironalactone Eplerenone Amiloride Triamterine

490
Q

Main side effects of loop diuretics

A

Hypovolemia Hypotension

491
Q

General side effects of diuretics?

A

Hypokalemia Hyponatremia Hypomagnesaemia Hypocalcemia Hyperuricaemia- gout

492
Q

Side effects of thiazides?

A

Erectile dysfunction Impaired glucose tolerance

493
Q

Other anti hypertensives?

A

A-1 adrenoceptor blockers (Doxazosin) Centrally acting anti-hypersensitive (Moxonidine + methyldopa) Direct renin inhibitor (Aliskeren)

494
Q

What if patients are intolerant to ACEi and ARB? (Heart failure)

A

Hydralazine/nitrate combination

495
Q

What do nitrates do?

A

Arterial and venous dilators Reduction of preload and afterload Lower BP

496
Q

Main clinical indications for nitrates?

A

Ischeamic heart disease - angina Heart failure

497
Q

Main examples of nitrates

A

Isorbide mononitrate GTN spray GTN infusion

498
Q

Main side effects of nitrates

A

Headache due to GTN syncope (spray)

499
Q

Drug for antiplatelet therapy in angina if aspirin intolerant?

A

Clopidogrel

500
Q

Example of an antiarrhythmic drug?

A

Digoxin

Haroon Phase 2A (14 decks)

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