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Cardiology Flashcards

1
Q

A negative risk factor for AAA - abdominal aortic aneurysm?

A

Diabetes but unknown reason

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2
Q

Risk factors for AAAs?

A

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

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3
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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4
Q

Inflammatory AAA-who affected, causes/associasions, symptoms?

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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5
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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6
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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7
Q

Primary diagnosis tool for AAA?

A

Abdominal ultrasound
-fast, cheap, reliable
-highly sensitive and specific

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8
Q

Treatment for an asymptomatic aneurysm <5.5cm?

A

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

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9
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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10
Q

Treatment for symptomatic AAA?

A

Urgent surgical repair (EVAR or open surgery)

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11
Q

Treatment for a ruptured AAA?

A

Stabilise ABCDE, fluids then urgent surgical repair

-Nice says EVAR (Endovascular Aneurysm Repair) 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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12
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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13
Q

Differential diagnosis for AAA?

A

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

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14
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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15
Q

Prevalence of AAA?

A

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

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16
Q

ECG changes and corrosponding coronary arteries: inferior : ll, lll, avf

A

right coronary

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17
Q

ECG changes and corrosponding coronary arteries: anterior: V3-V4

A

LAD

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18
Q

ECG changes and corrosponding coronary arteries: septal: V1-V2

A

LAD

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19
Q

ECG changes and corrosponding coronary arteries: lateral: l, V5-V6, AVL

A

Lateral circumflex

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20
Q

ECG changes and corrosponding coronary arteries: posterior: V1-V3 (reciprocal ST depression)

A

Posterior descending

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21
Q

Causes of ACS

A

Acute coronary syndrome

Rupture of atherosclerotic plaque and consequent arterial thrombosis is the main cause

Uncommon causes:
- stress induced cardiomyopathy
- coronary vasospasm without plaque rupture
- drug abuse

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22
Q

PCI (coronary artery bypass graft - with stent) and CABG (coronary artery bypass graft) use

A

STEMI : PCI= ++ CABG= -
NSTEMI : PCI = +++ CABG =+
Stable : PCI = ++ CABG = ++

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23
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

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24
Q

Examples of P2Y12 inhibitors

A

Clopidogrel
Prasugrel
Ticagelor

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25
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

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26
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

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27
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)

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28
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

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29
Q

Ticagrelor vs clopidogrel

A

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

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30
Q

What does acute coronary syndromes cover?

A

Umbrella term for unstable angina, NSTEMI and STEMI

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31
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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32
Q

Different acute coronary syndromes pathologies- unstable angina?
Occlusion, infarction, ECG, troponins and kinase test result?

A

Occlusion: partial of minor coronary artery

Infarction: no ischaemia only

ECG : normal. may show some ST depression/ T wave inversion

Troponins + Creatine Kinase MB : Normal

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33
Q

Different acute coronary syndromes pathologies- NSTEMI?

A

Occlusion: major partial/ total minor coronary artery

Infarction: sub endothelial infarction (area far away from c.a. occlusion dies)

ECG : ST depression + T wave inversion. NO Q waves!

Troponins + Creatine Kinase MB : Elevated (increased with infarction)

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34
Q

Different acute coronary syndromes pathologies- STEMI

A

Occlusion: total of major coronary artery

Infarction: transmural infarction

ECG : ST segment elevation in local leads (2+)
Q waves (pathological after some time)

Troponins + Creatine Kinase MB : Elevated (increased with infarction)

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35
Q

What does an ECG after MI look like?

A

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

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36
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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37
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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38
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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39
Q

Making a diagnosis of which 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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40
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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41
Q

Alternative causes of raised troponin?

A

Gram negative sepsis
Myocarditis
Aortic dissection
Pulmonary embolism
Arrhythmias

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42
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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43
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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44
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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45
Q

Treatment for low risk NSTEMI/unstable angina

A

Monitor

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46
Q

Treatment for high risk NSTEMI/ unstable angina?

A

Immediate angiogram and consider PCI

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47
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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48
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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49
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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50
Q

Other complications of ACS (2< weeks)

A

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

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50
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

embolism, valve disease, recurrence regurgitation, tamponade

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50
Q

Flow chart for treatment for NSTEMI or unstable angina

A

give aspirin 300mg and anticoagulant (fondaparinux or UFH if going for PCI)

clinically stable = immediate PCI+ second antiplatelet

Low risk = second antiplatelet

Intermediate/ high risk = PCI in 72 hours + second antiplatelet

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50
Q

Flowchart for STEMI treatment

A

STEMI diagnosed —> aspiring 300mg —>
symptom onset <12 h and PCI available in 2h?

No —> ticagrelor (clopdogrel if high bleeding risk)—-> fibrinolysis—-> failure of fibrinolysis = PCI

Yes —> Prasugrel (clopidogrel if on oral anticoagulent)—-> unfractionated heparin, GP IIb/ IIa inhibitor, Bivalirudin—-> PCI

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50
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

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51
Q

Risk factors for aortic dissection(AD)

A

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

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52
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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53
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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54
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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55
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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56
Q

Investigations for diagnosing aortic dissection?

A

ECG

Chest X-ray -may show widened mediastinum >8cm is suspicious

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

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57
Q

Investigation in an unstable patient? More for aortic dissection

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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57
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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57
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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57
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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57
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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58
Q

Complications of aortic dissections?

A

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

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58
Q

Types of bradycardia

A

1) RBBB/LBBB (Right bundle branch block )
2) 1°/2°/3° heart block
3) Sinus bradycardia

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58
Q

Two major groups of tachycardia’s

A

Supraventricular tachycardias
AND
Ventricular tachycardias

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58
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

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59
Q

Transmission pathway for heartbeats

A

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

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59
Q

Tachycardia vs bradycardia?

A

Tachycardia = 100< bpm
Bradycardia = 60> bpm

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60
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

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60
Q

Causes of atrial fibrillation

A

Heart failure
Hypertension
2° to mitral stenosis
Sometimes idiopathic

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60
Q

What is atrial fibrillation

A

Irregularly irregular atrial firing rhythm

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60
Q

What is the most common cardiac arrhythmia?

A

Atrial Fibrillation

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61
Q

Risk factors for atrial fibrillation

A

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

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62
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

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63
Q

What does atrial blood pooling cause

A

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

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64
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

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65
Q

Pathophysiology pathways of atrial fibrillation

A

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

triggering event (sepsis and hyperthyroidism) —-> pre - excitation of the atria

structural abnormalities (heart failure, valvular abnormalities)—-> RAAS activation (increased left atrial pressure) —-> atrial dilation and fibrosis (differences in refractory periods causes electrical re-entry and ectopic foci)

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66
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 rate control and anticoagulation

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67
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)

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68
Q

Investigations to diagnose Atrial fibrillation

A

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

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69
Q

Treatment of atrial fibrillation

A

Determine if rate or rythm control is more appropriate

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70
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

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71
Q

What is rhythm control

A

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

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72
Q

When is rate control recommended for atrial fibrillation

A

Onset > 48 hours or unknown

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73
Q

When is rhythm 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
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74
Q

Treatment for atrial fibrillation if patient is haemodynamically unstable

A

Emergency electrical synchronised DC cardioversion

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75
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

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76
Q

First line drugs for rate control

A

Beta-blocker OR rate limiting CCB (Calcium channel blockers)

Bispropolol OR diltiazen or verapamil

Second line is to combine drugs

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77
Q

Pharmacological treatments for rhythm control

A
  • Flecainide or amiodarone
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78
Q

Electrical treatments for rhythm control

A

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

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79
Q

Pathway for atrial fibrillation treatment

A

< 48 hours onset = rate or rhythm control

> 48 hours onset or unknown = rate control and anticoag for 3 weeks (minimum)—> then consider rhythm control

Adverse features = rhythm control : electrical cardioversion —> rhythm control: pharmacological cardioversion

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80
Q

What does the CHA2DS2-VASc assess?

A

Assess stroke risk (once you’ve already had AF) and therefore the anticoagulation need for Atrial fibrillation

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81
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: 1 unless female then 2=< then oral coagulation required

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82
Q

Complications of atrial fibrillation

A

Heart failure
Ischaemic stroke
Mesenteric ischeamia

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83
Q

What is an atrial flutter

A

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

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84
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

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85
Q

Symptoms of atrial flutter

A

Dyspnoea
Palpitations

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86
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)

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87
Q

Treatment of acutely unstable atrial flutter

A

DC synchronised cardioversion

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88
Q

Treatment of stable atrial flutter

A

Rythm/rate control with oral anticoagulation (prevent thromboemboli)

Also radiofreq ablation

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89
Q

What the most common supraventricular tachycardia?

A

AVNRT (functional)

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90
Q

Pathophysiology of AVNRT

A

Re-entrant pathway goes through AVN

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91
Q

Treatment for AVNRT

A

Same as AVRT (WPW)

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92
Q

What is an AVRT?

A

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

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93
Q

Most common example of an AVRT

A

Wolff-Parkinson White syndrome (WPW)

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94
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)

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95
Q

Symptoms of WPW

A

Palpitation
Dizziness
Dyspnoea

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96
Q

Investigations to diagnose WPW

A

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

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97
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 nerves 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

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98
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+

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99
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)

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100
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 unsynchronised as patient is pulseless

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101
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

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102
Q

Heart sound S2?

A

Aortic + Pulmonary close

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103
Q

Heart sound S3?

A

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

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104
Q

Heart sound S4?

A

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

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105
Q

What does P represent on a normal ECG?

A

Atrial depolarisation

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106
Q

What does PR interval represent on a normal ECG?

A

AVN conduction delay

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107
Q

Average length of PR interval?

A

0.12-0.2s

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108
Q

What does QRS interval represent?

A

Ventricle depolarisation + atrial repolarisation

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109
Q

Average length of a QRS interval?

A

0.08-0.1s
0.12=< is abnormal

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110
Q

Why does ST segment represent on a normal ECG?

A

Isovolemic ventricular relaxation

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111
Q

What does T represent on a normal ECG?

A

Ventricular repolarisation

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112
Q

What are ECGs useful in diagnosing?

A

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

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113
Q

Scale for ECG paper?

A

0.5 mV for 1 big square amplitude and 0.2 seconds time

small square = 0.1mV and 0.04 s

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114
Q

ECG leads for RCA

A

aVF + II + III
(Inferior)

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115
Q

ECG leads for LAD

A

V1-V4
(Anterior + septal)

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116
Q

ECG leads for LCx

A

V5 + V6 + aVL + I
(Lateral)

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117
Q

Heart sound S1?

A

Mitral + Tricuspid close

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118
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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119
Q

Cause of Cardiac tamponade

A

Typically pericarditis
Hence risk factors are all pericarditis related

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120
Q

Symptoms of cardiac tamponade

A

Related to pericarditis

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121
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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122
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 - chest x ray : big globular heart

ECHO: diagnostic tool

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123
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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124
Q

Main symptom of arrhythmogenic cardiomyopathy

A

Arrhythmia

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125
Q

What do all cardiomyopathies carry a risk of?

A

Arrhythmias

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126
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

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127
Q

Cause of arrhythmogenic hypertrophy

A

Desmosome gene mutations

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128
Q

What is the most common cardiomyopathy in general

A

Dilated cardiomyopathy

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129
Q

Cause of dilated cardiomyopathy

A

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

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130
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

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131
Q

Symptoms of dilated cardiomyopathy

A

-Shortness Of Breath
-heart failure (usually)
-atrial fibrillation
-thromboemboli

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132
Q

Investigations to diagnose dilated cardiomyopathy

A

ECG
ECHO

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133
Q

Treatment for dilated cardiomyopathy

A

Treat underlying condition
Eg Atrial fibrillation, heart failure

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134
Q

Epidemiology of hypertrophic cardiomyopathy

A

Affects 1 in 500 people

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135
Q

What is LVOT?

A

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

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136
Q

Three types of cardiomyopathy?

A

1) Hypertrophic
2) Restrictive
3) Dilated

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137
Q

What are cardiomyopathies?

A

Diseases of the myocardium
(Muscular/conduction defects)

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138
Q

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

A

Hypertrophic cardiomyopathy

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139
Q

Causes of hypertrophic cardiomyopathy

A

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

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140
Q

Pathophysiology of of hypertrophic cardiomyopathy

A

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

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141
Q

Symptoms of hypertrophic cardiomyopathy

A

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

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142
Q

Investigations to diagnose hypertrophic cardiomyopathy

A

Confirm with abnormal ECG
ECHO (diagnostic)
Genetic testing

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143
Q

Treatment for hypertrophic cardiomyopathy

A

Beta blocker
CCB
Amiodarone (anti-arrhythmic)

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144
Q

What is the cause of inherited arrhythmia? (Channelopothy)

A

Caused by ion channel protein gene mutations

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145
Q

Which ions do cardiac channelopathies relate to?

A

Potassium
Sodium
Calcium

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146
Q

Examples of cardiac channelopothies?

A

Long QT
Short QT
Brugada
CPVT

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147
Q

Cardiac channelopothies effect on heart structure?

A

No effect- have a structurally normal heart

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148
Q

Symptom of cardiac channelopothy?

A

Syncope

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149
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

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150
Q

SADS sudden arrhythmic death syndrome?

A

Usually refers to normal heart/arrhythmia

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151
Q

Familial hypercholesterolaemia (FH)?

A

Inherited abnormality of cholesterol metabolism

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152
Q

What does familial hypercholesterolaemia lead to?

A

Serious premature coronary and other vascular diseases

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153
Q

Aortavascular syndromes

A

Marfan
Loeys-Dietz
Vascular Ehler Danos

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154
Q

What type of inheritance are inherited cardiac conditions usually?

A

Dominantly inherited
Offspring have a 50% chance of inheritance

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155
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

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156
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

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157
Q

What investigations need to be done as part of a hypertension screening?

A

Urine dipstick (kidneys = end organ damage)
ECG (LVH)
HBA1c
Renal function
Fundosocopy (eyes)
Lipid profile
Qrisk

Only check cortisol if there’s a secondary cause of hypertension

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158
Q

What do you need to calculate Qrisk?

A

Lipid profile

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159
Q

What changes in the arteries are likely to be seen due to angina?

A

-Smooth muscle proliferation and migration from the tunica media to the intima
-decreased release of nitric oxide
- infiltration of Subendothelial space by low-density lipoprotein (LDL) particles
- formation of foam cells from macrophages

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160
Q

Which blood test is the most accurate marker for acute cardiac damage?

A

Troponin T - short term, released by cardiac myocytes

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161
Q

Blood marker for heart failure?

A

Brain natriuretic peptide

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162
Q

Inflammatory blood marker?

A

C reactive protein (CRP)

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163
Q

Which investigation is diagnostic for heart failure?

A

Echocardiogram- allows you to see ventricles and valves (valves cause murmurs)

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164
Q

Which medication can be prescribed to relieve symptoms (swollen ankles) of heart failure?

A

Oral digoxin (cardiac glycoside)

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165
Q

Which two medications can cause postural hypertension?

A

Bisproplol
Amlodipine

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166
Q

Non pharmacological treatment to help with postural hypertension?

A

Increase salt intake
Increase oral fluid intake
Compression stockings
Sit + stand slowly

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167
Q

What is postural hypertension?

A

Sustained reduction of systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within 3 minutes of standing

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168
Q

Causes of postural hypersensitivity?

A

Disorders affecting autonomic nervous system (eg. Parkinson’s disease) reduced blood volume, or iatrogenic causes eg. Antihypertensives

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169
Q

Pharmovological treatment options of postural hypertension?

A

Oral fludrocortisone

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170
Q

Prevalence of postural hypertension?

A

Affects 5% to 30% of people aged over 65 years and up to 60% of people with Parkinson’s disease

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171
Q

5 investigations to assess for infective endocarditis?

A

Bedside- ECG, urinalysis
Bloods - FBC, CRP, blood cultures
Imaging - Echo

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172
Q

Low amplitude p wave possible causes?

A

Atrial fibrosis
Obesity
Hyperkalemia

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173
Q

High amplitude p waves possible cause?

A

Right atrial enlargement

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174
Q

Broad notched ‘bifid’ p wave possible causes?

A

Left atrial enlargement

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175
Q

Broad QRS possible causes?

A

Ventricular conduction delay/ branch bundle block
Pre-excitation

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176
Q

Small QRS complex possible causes?

A

Obese patient
Pericardial effusion
Infiltrative cardiac disease

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177
Q

What can T wave changes indicate?

A
  • ischeamia/infarction
  • myocardial strain (hypertrophy)
  • myocardial disease (cardiomyopathy)
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178
Q

Ecg for ischeamia?

A

T wave flattening inversion
ST segment depression

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179
Q

How common is restrictive cardiomyopathy

A

Rare

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180
Q

Causes of restrictive cardiomyopathy

A

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

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181
Q

Pathophysiology of restrictive cardiomyopathy

A

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

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182
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)

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183
Q

Investigations to diagnose restrictive cardiomyopathy

A

ECG
ECHO
cardiac catheterisation (diagnostic)

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184
Q

Treatment for restrictive cardiomyopathy

A

None
Consider transplant
Patients typically die within 1yr

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185
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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186
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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187
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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188
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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189
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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190
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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191
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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192
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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193
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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194
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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195
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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196
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 well tolerated

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197
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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198
Q

What is atorvastatin an example of?

A

Lipid lowering therapy

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199
Q

Two types of bundle branch block?(BBB)

A

RBBB right
LBBB left

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200
Q

Causes of RBBB

A

Pulmonary emboli
IHD
VSD

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201
Q

Causes of LBBB

A

IHD
Valvular Disease

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202
Q

Pathophysiology of RBBB?

A

RV later activation than LV

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203
Q

Pathophysiology of LBBB?

A

LV activation later than RV

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204
Q

Atherosclerosis non-modifiable risk factors

A
  1. Older age
  2. Family history
  3. Male
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205
Q

ECG presentation of RBBB?

A

MaRRoW
M in v1 (RSR wave)
W in v6 (seep S wave)
Wide: physiological S2 splitting (heart sound)

206
Q

ECG presentation of LBBB?

A

WiLLiaM
W in V1
M in V6
Reversed S2 splitting

207
Q

What is a bundle branch block?

A

Blocks of bundles of His

208
Q

What is a 1° AV block?

A

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

209
Q

Symptoms of 1° heart block?

A

Asymptomatic

210
Q

Treatment of 1° heart block

A

No treatment as it is mild

211
Q

Causes of 1° heart block

A

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

212
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

213
Q

What is 2° heart block?

A

When some p waves are conducted but others aren’t

214
Q

Two types of 2° heart block

A

Mobitz I (Weinkebach’s)
Mobitz II

215
Q

What is Mobitz I?

A

PR prolongation until a QRS is dropped (PR interval progressively elongates). Can eventually drop a beat occasionally.

216
Q

Causes of Mobitz I?

A

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

217
Q

Treatment of Mobitz I?

A

No treatment unless symptomatic eg syncope
Treatment—> pacemaker

218
Q

Symptoms of Mobitz I?

A

May have syncope

219
Q

What is Mobitz II?

A

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

220
Q

Causes of Mobitz II?

A

Drugs, Inferior MI, Rheumatic fever

221
Q

Symptoms of Mobitz II?

A

Syncope
SOB
Chest pain

222
Q

Treatment for Mobitz II?

A

Pacemaker

223
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)

224
Q

Causes of 3° heart block

A

Acute MI
Hypertension
Structural heart disease

225
Q

Treatment for 3° heart?

A

IV atropine + permanent pacemaker

226
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

227
Q

Define hypertensive heart disease?

A

Heart failure and conduction arrhythmias due to unmanaged high blood pressure

228
Q

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

A

Hydralazine/nitrate combination

229
Q

Main phenotypes of heart failure

A

HF with reduced ejection fraction (HFrEF)
HF with preserved ejection fraction (HFpEF)

HF due to severe valvular heart disease (HF-VHD)
HF with pulmonary hypertension (HF-PH)
HF due to right ventricular systolic dysfunction (HF-RVSD)

230
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

231
Q

Cause of heart failure?

A

IHD
Cardiomyopathy
Valvular disease
Cor pulmonale

Anything that increases cardiac work:
-obesity
-htn
-pregnancy
-hyperthyroid
-arrhythmias

232
Q

Risk factors for heart failure

A

Age (65+)
Smoking
Obesity
Previous MI
Male

233
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

234
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
235
Q

Normal physiology of heart

A

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

236
Q

Three ways heart failure can be classified?

A

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

237
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

238
Q

What does LHS failure result in?

A

Pulmonary vessel backlog —> pulmonary oedema

239
Q

What does RHS failure result in?

A

Systemic venous backlog —> peripheral oedema

240
Q

3 cardinal non specific symptoms of heart failure

A

SOBASFAT
1 Shortness of breath
2 Ankle swelling
3 Fatigue

241
Q

Other symptoms of heart failure

A

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

242
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

243
Q

Methods of diagnosing of heart failure?

A

Bloods
ECG
Chest X-ray
ECHOcardiogram - gold standard

244
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

245
Q

ECG results with heart failure?

A

Abnormal
Eg evidence of LVH

246
Q

Chest x ray results with heart failure

A

ABCDE

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

247
Q

Purpose of echocardiogram?

A

Assess heart chamber dimensions

248
Q

Conservative treatment for heart failure

A

Lifestyle changes:
Decrease bmi
Exercise
Stop smoking + alcohol

249
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

250
Q

Surgical treatments for heart failure?

A

Revascularisation
Valve surgery
Heart transplant (last resort)

251
Q

What if ace inhibitors are not tolerated?

A

ARB like candersartan titrated go 32mg can be used instead

252
Q

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

A

U&E
All three medications cause electrolyte disturbances

253
Q

Patients with valvular heart disease should avoid which drug?

A

Ace inhibitors unless indicated by a specialist

254
Q

Respiratory causes of cor pulmonale?

A

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

255
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

256
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

257
Q

Primary vs secondary hypertension

A

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

2° = known underlying cause 5% cases

258
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

259
Q

Non modifiable risk factors for hypertension

A

Non modifiable risk factors for hypertension

260
Q

Modifiable risk factors for hypertension

A

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

261
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

1 = 140/90 (H), 135/85 (A)

2= 160/100 (H), 150/95 (A)

3 = 180 and/ or 110 <

262
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

263
Q

Pathophysiology of hypertension

A

Ultimately all mechanisms will increase RAAS and SNS activity (CO) and TPR

=> increase in BP as BP=COxTPR

264
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

265
Q

Symptoms of hypertension

A

Mostly asymptomatic and found in screening

May have pulsatile headache, classically occipital and worse in the morning

266
Q

Signs of hypertension to consider

A

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

267
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

<135/85 = not hypertensive

> 135/ 85 = stage 1 hypertension - treat if < 80 years and any of:
target organ damage, diabetes, established CVD, renal disease, Qrisk > 10%
-then other medication to treat hypertension

> 150/95 = stage 2 hypertension - treat all patients regardless of age
-then other medication to treat hypertension

268
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

269
Q

Treatment guidelines for hypertension

A

If age <55 years or T2 diabetes —> ACE in (or ARB if intolerant)
then offer ACE in + CCB or ACE in + thiazide like diuretic—->
then all three if needed.
if k+ > 4.5 add alpha or beta blocker
if K+ < 4.5 add spironolactone

If age >55 years or Afro Caribbean then CCB —> then offer ACE in + CCB or ACE in + thiazide like diuretic—->
then all three if needed.
if k+ > 4.5 add alpha or beta blocker
if K+ < 4.5 add spironolactone

if <80 aim for <140/90
> 80 years aim for <150/90

CKD: aim for <140/90
CKD and DM <130/80

270
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

271
Q

Complications for hypertension?

A

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

272
Q

What reduction do you expect with a full dose of any single drug?

A

Systolic: 8-10mmHg
Diastolic: 4-6mmHg

273
Q

Thresholds for treatment for hypertension?

A

Low CVD risk 160/100mmHg
High CVD risk 140/90mmHg
(Clinic thresholds)

274
Q

Targets for blood pressure after treatment?

A
  • Routine <140/90 mmHg
  • Previous stroke < 130/80mmHg
  • Heavy proteinuria <130/80mmHg
  • CKD and Diabetes <130/80mmHg
  • older patients <150/90mmHg
275
Q

How many drugs are generally needed to control blood pressure?

A

Mostly one or two

276
Q

Can you lower blood pressure with lifestyle changes?

A

Yes:
-Weight loss
-Salt restriction
-Exercise
-Alcohol

277
Q

Why would blood pressure treatment be withheld?

A

During general anaesthesia hypotension can be a problem and anyihypertensives block attempts to increase BP
==> ACEi + ARBs temporarily stopped

278
Q

Limits for diagnosing hypertension

A

> = 140/90 mmHg in clinic

> = 135/85 mmHg at home (ambulatory blood pressure monitoring)

279
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

280
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)

281
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

282
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

283
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

284
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
285
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)

286
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

287
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

288
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

289
Q

Major Duke Criteria for infactive endocarditis

A
  • 2 positive blood cultures
  • ECHO TOE shows endocardia’s involvement Eg. Vegetations , abscess or regurgitation
290
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)

291
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.

General antibiotic ideas?

General: Amoxycillin, gentamicin, vancomyocin and rifampicin

Staphylococci: flucloxacillin, vancomyocin, rifampicin, gentamicin

Streptococci: benzylpenicillin
Enterococci: amoxicillin
HACEK : cefrtriaxone

292
Q

Second line treatment for infective endocarditis

A

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

293
Q

Complications of infective endocarditis

A

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

294
Q

What is infective endocarditis

A

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

295
Q

Environmental exacerbating factors for IHD

A

Exercise
Cold weather
Heavy metals
Emotional stress

296
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

297
Q

What is microvascular angina (syndrome X)

A

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

298
Q

Which risk factor drastically increases incidence of IHD

A

Age

299
Q

Symptoms that don’t associate with angina

A

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

300
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

301
Q

Differential diagnosis for myocardial ischemia

A

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

302
Q

Treatment for myocardial ischemia

A

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

303
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

304
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)

305
Q

Side effects of beta blockers

A

Tiredness, nightmares
Erectile dysfunction
Bradycardia
Cold hands and feet

306
Q

Contraindication for beta blockers?

A

Asthma- do not give

307
Q

Side effect of aspirin

A

Gastric ulceration

308
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

309
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

310
Q

Which veins can a CABG use?

A

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

311
Q

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

A

Very low probability

312
Q

Side effect of GTN spray?

A

Excruciating headache

313
Q

Reasons for imperfect blood supply to the heart?

A
  • Atherosclerosis
  • Thrombosis
  • Thromboemboli
  • Artery spasm
  • collateral blood vessels
  • blood pressure/ cardiac output/ heart rate
  • Arteritis
314
Q

Which arteries does atherogenesis affect most commonly?

A

LAD
Circumflex
RCA

315
Q

Risk factors for IHD

A

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

316
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
317
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)
318
Q

Fibrous cap in stable angina?

A

Fibrous cap is strong and less rupture prone

318
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
319
Q

What happens if plaque is prone to rupture?

A

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

320
Q

Difference between ischaemia and infarction?

A

Ischaemia= blood flow restricted
Infarction= lumen fully occluded

321
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

322
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

323
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

324
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

325
Q

Exacerbating factors for IHD

A

Supply:
-Anemia
-hypoxemia

Demand:
-hypertension
-tachycardia
-valvular heart disease

326
Q

Epidemiology of pericarditis?

A
  • males
  • 20-50yrs
327
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

328
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

329
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

330
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

331
Q

Differential diagnosis of pericarditis

A

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

332
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
333
Q

Primary investigations to diagnose pericarditis

A

ECG: widespread saddle shaped ST-elevation (sensitive) and PR depression (specific)

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

334
Q

Treatment for idiopathic or viral pericarditis

A

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

335
Q

Treatment for bacterial pericarditis

A

IV antibiotics and pericardiocentesis with washout, culture and sensitivities

336
Q

Complications of pericarditis

A

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

337
Q

Prognosis of pericarditis

A

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

338
Q

Another name for pericarditis?

A

Dressler syndrome

339
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

340
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

341
Q

Risk factors for PVD?

A

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

342
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)
343
Q

Intermittent claudication?

A

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

344
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

345
Q

Acute limb-threatening ischemia?

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

346
Q

Symptoms of acute limb-threatening ischemia

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!!
347
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

348
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

349
Q

Why might symptoms be masked in PVD?

A

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

350
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

351
Q

Buerger’s test?

A

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

352
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

353
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

354
Q

Treatment of chronic limb ischaemia

A

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

355
Q

Treatment for acute limb threatening ischeamia

A

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

356
Q

Complications of PVD

A

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

357
Q

Another name for peripheral vascular disease? (PVD)

A

Peripheral arterial disease (PAD)

358
Q

The main indications for ACEi?

A

Hypertension
Heart failure
Diabetic neuropathy

359
Q

Examples of ACEi?

A

Ramipril
Enalapril
Perindopril
Trandolapril

(Largely do the same job but vary in price)

360
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

361
Q

Main clinical indications for ARBs?

A

-Hypertenison
-Diabetic Neuropathy
-Heart failure (when ACEi contraindicated)

362
Q

Examples of ARBs?

A

Cadersartan (most common)
Losartan
Val sar tan
Irbesartan
Telmisartan

363
Q

Main side effects of ARBs?

A

Symptomatic hypotension
Hyperkalemia
Potential for renal function
Rash
Angioedema

Generally very well tolerated

364
Q

Contraindication of ARBs?

A

Pregnancy

365
Q

Main clinical indications of CCBs?

A

Hypertension
ischaemic heart disease - angina
Arrrhythmia (tachycardia)

366
Q

Examples of CCBs?

A

Amlodipine
Diltiazem
Verapamil
Felodipine
Lacidipine
Nifedipine

367
Q

Dihydropyridines CCBs?

A

Nifedipine
Amlodipine
Felodipine
Lacidipine

Preferentially affect vascular smooth muscle
= peripheral arterial vasodilators

368
Q

Phenylyalkylamines CCBs?

A

Verapamil

Main effects in the heart
= negatively chronotropic and inotropic

369
Q

Benzothiazepines CCBs?

A

Diltiazem

= immediate heart/peripheral vascular effects

370
Q

Main side effects of peripheral vasodilation? (CCBs)

A

Flushing
Headache
Oedema
Palpitations

371
Q

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

A

Bradycardia
Atrioventricular block

372
Q

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

A

Worsening of cardiac failure

373
Q

Side effect of verapamil?

A

Constipation

374
Q

Main clinical indications for Bb?

A

Ischaemic heart disease - angina
Heart failure
Arrhythmia
Hypertension

375
Q

Examples of B1 selective Bb?

A

Metoprolol
Bisoprolol

376
Q

An example of a less selective B1 Bb?

A

Atenolol

377
Q

B1/B2 (non-selective) Bb examples?

A

Propranolol
Nadolol
Carvedilol

378
Q

Are beta 1 selective blockers absolute?

A

Selectivity is relative rather than absolute

379
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

380
Q

Main side effects of Bb?

A

Fatigue
Headache
Sleep disturbance/ night mares

Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction

381
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

382
Q

Main clinical indications of Diuretics?

A

Hypertension
Heart failure

383
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

384
Q

Examples of thiazide and related diuretics?

A

Bendroflumethiazide
Hydroclorothiazide
Chlorthalidone

385
Q

Examples of loop diuretics?

A

Furosemide
Bumetanide

386
Q

Examples of potassium-sparing diuretics

A

Spironalactone
Eplerenone
Amiloride
Triamterine

387
Q

Main side effects of loop diuretics

A

Hypovolemia
Hypotension

388
Q

General side effects of diuretics?

A

Hypokalemia
Hyponatremia
Hypomagnesaemia
Hypocalcemia

Hyperuricaemia- gout

389
Q

Side effects of thiazides?

A

Erectile dysfunction
Impaired glucose tolerance

390
Q

Other anti hypertensives?

A

A-1 adrenoceptor blockers
(Doxazosin)

Centrally acting anti-hypersensitive
(Moxonidine + methyldopa)

Direct renin inhibitor
(Aliskeren)

391
Q

What do nitrates do?

A

Arterial and venous dilators
Reduction of preload and afterload
Lower BP

392
Q

Main clinical indications for nitrates?

A

Ischeamic heart disease - angina
Heart failure

393
Q

Main examples of nitrates

A

Isorbide mononitrate
GTN spray
GTN infusion

394
Q

Main side effects of nitrates

A

Headache due to GTN syncope (spray)

395
Q

Drug for antiplatelet therapy in angina if aspirin intolerant?

A

Clopidogrel

396
Q

Example of an antiarrhythmic drug?

A

Digoxin

397
Q

Drug class and mechanism of Digoxin?

A

Class: Cardiac glycoside

Inhibits Na/K pump and causes:
- bradycardia
- slows AVN conduction
- increased ectopic activity
- increased force of contraction

398
Q

Side effects of digoxin?

A

Narrow therapeutic range
Nausea
Vomiting
Diarrhoea
Confusion

399
Q

Main clinical indication of Digoxin?

A

Atrial fibrillation to reduce ventricular rate response
Severe heart failure as +vly ionotropic

400
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

401
Q

Cause of rheumatic fever

A

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

402
Q

Rheumatic heart disease?

A

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

403
Q

Histological appearance of rheumatic fever

A

Valves affected show Aschoff Bodies

404
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
405
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
406
Q

Investigations to diagnose rheumatic fever

A

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

407
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)

408
Q

Treatment for rheumatic fever

A

Antibiotics- IV benzyloenicillin STAT, then phenoxypenicillin for 10days

409
Q

Treatment for Sydenham’s chorea

A

Haloperidol

410
Q

Epidemiology of rheumatic fever

A

Almost exclusively in developing countries only
In young people

411
Q

Symptoms of anaphylactic

A

Hypotension
Tachycardia
Urticaria
Puffy face flushing of cheeks

412
Q

Treatment of anaphylactic shock

A

ABCDE
IM adrenaline (SNS activation=stress response)

413
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!

414
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

415
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)
416
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

417
Q

Key organs at risk of failure from shock?

A

Kidneys
Lungs
Heart
Brain

418
Q

Cause of cardiogenic shock

A

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

419
Q

Symptoms of cardiogenic shock

A

Heart failure signs (oedema)
Increased JVP
S4

420
Q

Treatment of cardiogenic shock

A

ABCDE
Treat underlying cause

421
Q

Causes of hypovolemic shock

A

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

422
Q

Symptoms of hypovolemeic shock

A

Clammy pale skin
Confusion
Hypotension
Tachycardia

423
Q

Treatment of hypovolemic shock

A

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

424
Q

Cause of neurogenic shock

A

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

425
Q

Symptoms of neurogenic shock

A

Hypotension
Bradycardia
Confused
Hypothermic

426
Q

Treatment for neurogenic shock

A

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

427
Q

Cause of septic shock

A

Due to uncontrolled bacterial infection

428
Q

Symptoms of septic shock

A

Pyrexia (high temp.)
warm peripheries
Tachycardic

429
Q

Treatment for septic shock

A

ABCDE
Broad spectrum antibiotic

430
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 - (Right ventricular hypertrophy (RVH) is a pathologic increase in muscle mass of the right ventricle in response to pressure overload,)
431
Q

Investigations to diagnose an atrial septal defect

A

ECHO

432
Q

Treatment for atrial septal defect

A

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

433
Q

Clinical signs of atrial septal defects

A

Pulmonary flow murmur
Big pulmonary arteries on CXR
Big heart on chest x ray

Risk of infective endocarditis

434
Q

Another name for atrial septal defect

A

Patent foramen ovale

435
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

436
Q

What is atrioventricular septal defect associated with

A

Massively associated with Downs Syndrome

437
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

438
Q

Prognosis of atrioventricular septal defect

A

Progresses to eventually Eisenmenger’s and hard to treat

439
Q

Most common congenital heart defect?

A

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

440
Q

Is the aortic valve bicuspid or tricuspid?

A

Typically tricuspid

441
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

442
Q

Pathophysiology of coarctation 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

443
Q

Symptoms of coarction of aorta

A

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

444
Q

Investigations to diagnose coarctation of aorta

A

CXR: “notched ribs” dilated intercostal vessels
CT angiogram

445
Q

Treatment of coarctation of aorta

A

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

446
Q

Long term problems of coarctation

A

-Re coarctation requiring repeat intervention
-Aneurysm formation at the site of repair
Hypertension leads to:
- early coronary artery disease/stroke
- sub arachnoid haemorrhage

447
Q

What is coarction of the aorta associated with?

A

Turner’s syndrome and Berry aneurysms of the brain

448
Q

Prevalence of patent ductus arteriosus

A

10-20%

449
Q

What is patent ductus arteriosus

A

When ductus arteriosus fails to close post birth = unusual

450
Q

Pathophysiology of patent ductus arteriosus

A

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

451
Q

Symptoms of patent ductus arteriosus

A

Dyspnoea
Failure to thrive
Machine like murmur

Risk of infective endocarditis

452
Q

Investigations to diagnose patent ductus arteriosus

A

CXR
ECG
ECHO

453
Q

Treatment for patent ductus arteriosus

A

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

454
Q

What is pulmonary stenosis?

A

Narrowing of the outflow of the right ventricle
can occur in different locations:
- Valvar
- Sub valvar
- Supra valvar
- in branches

455
Q

Severe pulmonary stenosis?

A

-Right ventricular failure as a neonate
-Collapse
-Poor pulmonary blood flow
-RV hypertrophy
-Tricuspid regurgitation

456
Q

Moderate/mild pulmonary stenosis?

A

-well tolerated for many years
-right ventricular hypertrophy

457
Q

Treatment of pulmonary stenosis?

A

Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass blockage)

458
Q

Prevalence of tetralogy of fallot

A

4-10%

459
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

460
Q

Most common congenital cyanotic heart disease

A

Tetralogy of Fallot
10% of all congenital birth defects

461
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)

462
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 crying or feeding

463
Q

How to diagnose tetralogy of fallot

A

ECHO
CXR - presents as boot shaped heart

464
Q

Treatment of tetralogy of fallot

A

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

465
Q

Most common congenital heart disease?

A

Ventricular septal defect
25-30%

466
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

467
Q

Symptoms of small ventricular septal defect

A

Typically asymptomatic
Normal heart rate/size
Loud systolic murmur

468
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 :(

469
Q

Investigation used to diagnose ventricular septal defect?

A

ECHO

470
Q

Treatment for ventricular septal defect

A

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

471
Q

Eisenmenger’s syndrome?

A

High pressure pulmonary flow
Damages to delicate pulmonary vasculature
The resistance to blood flow through lungs increases
RV pressure increases
Shunt direction reverses
Patient becomes BLUE

472
Q

Causes of aortic regurgitation

A

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

473
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)

474
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
475
Q

Investigations to diagnose aortic regurgitation

A

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

476
Q

Treatment for aortic regurgitation

A

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

477
Q

What is aortic regurgitation

A

Leaky aortic valve which makes it insufficient

478
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

479
Q

Symptoms of aortic stenosis

A

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

480
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)

481
Q

Investigations to diagnose aortic stenosis

A

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

482
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

483
Q

Differential diagnosis for aortic stenosis

A

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

484
Q

Pathophysiology of aortic stenosis

A

-A pressure gradient develops between left ventricle and aorta
- LV function initially maintained by compensatory pressure hypertrophy
- When compensatory mechanism exhausted, LV function declines

485
Q

What does regurgitation cause?

A

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

486
Q

What does stenosis cause?

A

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

487
Q

Main valve disorders?

A

Aortic regurgitation and stenosis
Mitral regurgitation and stenosis

488
Q

What do the main valve disorders cause?

A

Murmers

489
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

490
Q

Systolic murmurs?

A

ASMR
Aortic Stenosis
Mitral Regurgitation

491
Q

Diastolic Murmer?

A

ARMS
Aortic regurgitation
Mitral stenosis

492
Q

Causes of mitral regurgitation

A

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

493
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

494
Q

Risk factors for mitral regurgitation

A

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

495
Q

Symptoms of mitral regurgitation

A

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

496
Q

Mitral regurgitation murmer?

A

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

497
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

498
Q

Treatment for mitral regurgitation

A

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

499
Q

Normal size of mitral bicuspid lumen and after undergoing stenosis?

A

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

500
Q

Causes of mitral stenosis

A

Most common = rheumatic fever
(Post strep pyogenes infection)

Also valve calcification in older patients
+ infective endocarditis

501
Q

Pathophysiology of mitral stenosis

A

RHD (rheumatic heart disease) causes mitral reactive inflammation, after years exacerbated with calcification
=> LA hypertrophy and chamber dilation

502
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

503
Q

Mitral stenosis murmur?

A

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

504
Q

Investigations to diagnose mitral stenosis

A

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

505
Q

Treatment for mitral stenosis

A

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

506
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

507
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)

508
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

509
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)

510
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

511
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

512
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

513
Q

What is a Wells score?

A

Calculates the risk of DVT and determines investigations + management

> = 2 DVT likely
=< 1 DVT unlikely

actve cancer, major surgery, calf swelling >3 cm, superficial and tender veins present, pitting oedema in leg, previous dvt.

514
Q

Gold standard for diagnosis of DVT

A

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

515
Q

Flow chart of investigations when considering DVT

A

wells score likely—> is duplex uss available with 4 hour or not.
-yes and DVT = treatment, no and no = no treatment

if duplex not available—> D dimer with interim anticoagulation, duplex uss withing 24 hours to see if DVT.

unlikley wells—> d dimer if raised then try duplex uss.

516
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

517
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

518
Q

Risk of recurrence with DVT?

A

30% in the next five years

518
Q

Complications of DVT

A

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

519
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

520
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

521
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

522
Q

What can a PE cause?

A

PE—> increased pulmomnary vascular resistance—> right ventricular strain —-> cor pulmonale —> cardiac arrest

523
Q

Risk factors for PE?

A

Virchow’s triad
(Mentioned in detail in DVT)

524
Q

Symptoms of PE

A

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

525
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)

526
Q

Wells two level score?

A

Used to determine probability of PE
>4: high probability
=<4: low probability

signs and symptoms, tachycardia, immobilisation etc

527
Q

Process for investigating PE?

A

D-dimer is NOT diagnostic but CTPA (CT pulmonary angiogram) 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

high wells > 4 —> CTPA and then treat if needed

low wells —> D dimer if raised then CTPA if not then no treatment

528
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)

529
Q

What’s massive PE?

A

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

530
Q

Treatment for massive PE?

A

Thrombolysis => alteplase (“clot buster”)

531
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

532
Q
A

Haroon flashcards (10 decks)

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