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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is atherosclerosis?

A

Inflammatory process characterised by hardened plaques within the intima of a vessel wall. Eventually, plaque will either occlude vessel lumen resulting in a restriction of blood flow (angina) or rupture (thrombus formation - death).

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2
Q

Where do atherosclerotic plaques often occur?

A

Peripheral and Coronary arteries!

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3
Q

How are atherosclerotic plaques distributed in these arteries?

A

Focally distributed - governed by haemodynamic factors. For example, changes in flow/ turbulence (e.g. bifurcations)

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4
Q

What is neointima?

A

As the intima grows (new intima)

Changes in blood flow altering the phenotype of endothelial cells.

Altered gene expression in key; endothelial cells, smooth muscle cells, macrophages and fibroblasts

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5
Q

What makes up the structure of an atherosclerotic plaque?

A

Lipid
Necrotic core
Connective tissue
Fibrous cap
Lymphocytes

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6
Q

What are the 5 main stages of atherosclerosis progression over the course of the condition?

A

Fatty Streak
Intermediate Lesions
Fibrous Plaques (advanced lesions)
Plaque Rupture
Plaque Erosion

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7
Q

What is the fatty streak stage of atherosclerosis?

A

Earliest lesion of atherosclerosis < 10 years:

  • Scavenger receptors take up lipids in intima layer of vessel wall
  • Aggregations of lipid-laden macrophages (Foam Cells) and T lymphocytes within the intima layer of the vessel wall.
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8
Q

What is the intermediate lesion stage of atherosclerosis?

A

Lesion progresses to comprise layers of;

Foam cells
Vascular smooth muscle cells
T lymphocytes
Adhesion and aggregation of platelets to vessel walls
Extracellular Lipid Pools

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9
Q

What is the fibrous plaque stage of atherosclerosis?

A
  • Contains SMCs, macrophages, foam cell and T-lymphocytes
  • Covered by dense fibrous caps made of ECM proteins including; collagen (strength), elastin (flexibility) - these are laid down by SMCs
  • Impedes blood flow and prone to rupture
  • Often calcified
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10
Q

What is the plaque rupture stage of atherosclerosis?
Why might atherosclerotic plaques Rupture?

A
  • Plaque is constantly growing and receding - fibrous cap has to be resorbed and redeposited in order to be maintained
  • If balance shifted in favour inflammatory conditions (e.g. increased enzyme activity) the cap becomes weak and plaque ruptures.
  • Exposure of basement membrane, collagen, necrotic tissue and haemorrhage of vessels within plaque causes thrombus formation and vessel occlusion
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11
Q

What is the plaque erosion stage of atherosclerosis?

A
  • Small early lesions
  • Fibrous cap does not disrupt
  • Luminal surface underneath the clot may not have enough endothelium present but is smooth muscle rich
  • Prominent lipid core
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12
Q

What are the stages of atherosclerotic plaque formation?

A

1️⃣ Initiation of inflammation and endothelial cell dysfunction
2️⃣ Stimulus for adhesion of leukocytes - release of chemo-attractants
3️⃣ Dysfunctional endothelial cells allow the transmigration of LDLs into the tunica intima
4️⃣ Accumulation of LDLs tunica intima cause dysfuntional endothelial cells to release ROS and metalloproteases which function to oxidised the LDL → activated oxLDL
5️⃣ The activation of oxLDLs causes endothelial cells to express adhesion receptors for leukcocytes on their surface, leading to uptake of LDLs and monocytes
6️⃣ Surface of macrophages contain a scavenger receptor which facilitates the uptake of oxidised LDLs to form a foam cells
7️⃣ Foam cells have multiple pathophysiological functions:
- Release chemokines to attract more macrophages
- Release IGF-1 into tunica media to promote migration of SMCs (from media to intima) that increase collagen synthesis leading to the hardening of the atherosclerotic plaque
8️⃣ During this process, foam cells will die → releasing lipid content. This drives the growth of the plaque
9️⃣ Death of foam cells also causes release of contents which causes increased inflammation
🔟 T-cells also facilitate inflammation
🔟+ Excessive growth of the plaque causes it to rupture, leading to accumulation of the RBC, platelets and clotting factors → thrombosis

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13
Q

What initiates inflammation and leads to endothelial cell dysfunction in atherosclerosis?

A

Cholesterol/ high LDLs in the blood damages the endothelial cells
ROS from inflammation.

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14
Q

What chemo attractant is released by the endothelium and what does this lead to?

A

Selectins cause leukocyte rolling and firm adhesion to the blood vessel walls.

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15
Q

What are the pathological functions of a foam cell?

A

Release chemokines and attract further macrophages to the tunica intima

Release IGF-1 into the tunica media to promote migration of Smooth muscle cells from the tunica media into the tunica intima which increases the collagen synthesis and leads to the hardening of the atherosclerotic plaque.

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16
Q

What is a foam cell?

A

A macrophage that has been up take into the tunica intima that expresses scavenger receptors that will uptake oxidised LDLs

This uptake forms a foam cell.

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17
Q

What is a foam cell?

A

A macrophage that has been up take into the tunica intima that expresses scavenger receptors that will uptake oxidised LDLs

This uptake forms a foam cell.

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18
Q

What does the death of the foam cell release in atherosclerosis?

A

DNA material that attracts neutrophils
Proinflammatory cytokines
ROS
These all lead to increased inflammation.

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19
Q

What inflammatory cytokines are found in atherosclerotic plaques?

A
  • IL1, 6 and 8.
  • IFN-γ - strong proinflammatory cytokine
  • TGF-β - involves in wound healing
  • Chemokines (e.g. Monocyte Chemoattractant Protein-1)
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20
Q

How can Atherosclerosis (Coronary Heart Disease) be treated?

A

Percutaneous Coronary Intervention
Drugs

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21
Q

What is Percutaneous Coronary Intervention?

A

Non-surgical procedure that uses a catheter to place a stent into a narrowed blood vessel

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22
Q

What is Re-stenosis?

A

The recurrence of abnormal narrowing of an artery or valve after corrective therapy

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23
Q

What drugs are used to reduce restenosis in patients who have undergone corrective surgery?

A

Taxol and Sirolimus - work by reducing SMC proliferation after placement of stent. The stent is washed (eluted) with these drugs

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24
Q

How does Aspirin help to treat CHD?

A

Irreversible inhibitor of platelet cyclo-oxygenase to prevent Thromboxane A2 production and further platelet aggregation

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25
Q

How does Clopidogrel/ Ticagrelor help to treat CHD?

A

Inhibitors of the stimulatory P2Y12 ADP receptor on platelets preventing platelet response amplification

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26
Q

How does Statins help to treat CHD?

A

Inhibit HMG CoA reductase - reduces cholesterol synthesis

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27
Q

What inflammation-causing cytokine is targeted using drugs alongside statin therapy?

A

IL-1

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28
Q

What drug therapy is used as an alternative to statins if ineffective or not tolerated?

A

PCSK9 inhibitors

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29
Q

Give some Non-modifiable risk factors for CVD and atherosclerosis?

A

Increased Age
Family Hx
Male

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30
Q

Give 5 Modifiable risk factors for atherosclerosis.

A
  1. Smoking.
  2. High levels of LDL’s.
  3. Obesity.
  4. Low exercise
  5. Diabetes.
  6. Hypertension.
  7. Alcohol consumption
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31
Q

Which histological layer of the artery may be thinned by an atheromatous plaque?

A

Tunica Media

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32
Q

What is the precursor for atherosclerosis.

A

Fatty streaks.

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33
Q

What are the functions of chemoattractants?

A

Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!

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34
Q

Describe the process of leukocyte recruitment.

A
  1. Capture.
  2. Rolling.
  3. Slow rolling.
  4. Adhesion.
  5. Trans-migration.
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35
Q

Define atherogenesis.

A

The development of an atherosclerotic plaque.

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36
Q

What are some end results of Atherosclerosis?

A

Angina
Myocardial Infarction
Transient Ischaemic Attacks
Stroke
Peripheral Vascular Disease
Mesenteric Ischaemia

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37
Q

What is the key principle behind the pathogenesis of atherosclerosis?

A

It is an inflammatory process!

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38
Q

What is Primary and Secondary Prevention of CVD?

A

Primary Prevention – for patients that have never had cardiovascular disease in the past.

Secondary Prevention – for patients that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease.

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39
Q

What is some advice for Primary and Secondary prevention of CVD?

A

Advice on diet, exercise and weight loss
Stop smoking
Stop drinking alcohol
Tightly treat co-morbidities (such as diabetes)

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40
Q

What is the management for secondary prevention of CVD?

A

4 As:
A – Aspirin (plus a second antiplatelet such as clopidogrel for 12 months)
A – Atorvastatin 80mg
A – Atenolol (or other beta-blocker – commonly bisoprolol)
A – ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose

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41
Q

What are Acute Coronary Syndromes?

A

Spectrum of acute cardiac conditions ranging from unstable angina to varying degrees of MI

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42
Q

What is the most common causes of Acute Coronary Syndromes?

A

Atherosclerotic rupture and consequential arterial thrombosis!

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43
Q

What is the mainstay treatment for ACS? why is this?

A

Anti-platelet medications:
Aspirin
Clopidogrel
Ticagrelor

Since a thrombus formed in a fast flowing artery are mostly made up of platelets.

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44
Q

Name some less common causes of Acute Coronary Syndromes?

A

Coronary vasospasm without plaque rupture

Drug abuse (amphetamines, cocaine)

Spontaneous Coronary Artery Dissection

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45
Q

What are the types of Acute Coronary Syndrome (ACS)?

A

Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)

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46
Q

Explain how Spontaneous Coronary Artery Dissection can lead to Acute Coronary Syndrome?

A

tear in lining, lining comes away from the wall of the artery and blocks vessel.

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47
Q

Briefly describe the pathophysiology of ACS?

A

Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation ->

ischaemia -> hypoxia of cells -> angina

infarction -> necrosis of cells -> permanent heart muscle damage and ACS.(MI)

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48
Q

How would you Diagnose someone presenting with ACS symptoms such as Chest pain?

A

ECG:
If there is ST elevation or new left bundle branch block the diagnosis is STEMI.

If there is no ST elevation then perform troponin blood tests:

If there are raised troponin levels and other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI

If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either:
unstable angina
Another cause such as musculoskeletal chest pain

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49
Q

What is Cardiac Troponin?

A

Protein complex functioning to regulate actin and myosin contraction

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50
Q

What would a rise in Troponin suggest?

A

Consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle.

However they are non specific so a raised troponin does not automatically mean ACS

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51
Q

Why is Cardiac Troponin relevant in diagnosing ACS?

A

Highly sensitive marker for cardiac muscle injury - increased levels is very indicative of myocardial cause

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52
Q

What is important to remember about Cardiac Troponin when being used for diagnosis?

A

not specific for ACS → also increases in conditions that causes stress in myocardium (e.g. PE, gram negative sepsis, myocarditis)

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53
Q

Give some other potential causes of raised troponins?

A

Chronic renal failure
Sepsis
Myocarditis
Aortic dissection
Pulmonary Embolism

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54
Q

What umbrella term does Stable Angina come under?
What umbrella Term does Unstable Angina come under?

A

Ischaemic Heart Disease (IHD)
Acute Coronary Syndrome (ACS)

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55
Q

Define angina.

A

Angina is a type of Ischaemic Heart Disease (IHD) characterised by chest pain

It is an imbalance of O2 supply/demand mismatch to the heart due to reduced blood flow from a blockage

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56
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis.

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57
Q

What are the different types of Angina Pectoris?

A

Stable
Unstable
Decubitus
Crescendo Angina
Prinzmetals’s Vasospastic
Microvascular Angina

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58
Q

What is Crescendo Angina?

A

patients present with angina over a period of months that gets progressively worse

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59
Q

What type of angina is associated with ACS?

A

Unstable Angina

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60
Q

Give 5 possible causes of angina.

A
  1. Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
  2. Increased distal resistance = LV hypertrophy.
  3. Reduced O2 carrying capacity e.g. anaemia.
  4. Coronary artery spasm.
  5. Thrombosis.
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61
Q

What is the prevalence of Angina in men and women?

A

Men - 5% (5000/100,000)
Women - 4% (4000/100,000)

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62
Q

Give 5 modifiable risk factors for angina.

A
  1. Smoking.
  2. Diabetes.
  3. High cholesterol (LDL).
  4. Obesity/sedentary lifestyle.
  5. Hypertension.
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63
Q

Give 3 non-modifiable risk factors for angina.

A
  1. Increasing age.
  2. Gender - Males
  3. Family history/genetics.
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64
Q

What are the symptoms associated with ACS?

A

Central, Crushing chest pain associated with:

Nausea and vomiting
Sweating and clamminess
Feeling of impending doom
Shortness of breath
Palpitations
Pain radiating to jaw or arms

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65
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis.

A

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.

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66
Q

Briefly describe the pathophysiology of angina that results from anaemia.

A

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.

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67
Q

How do blood vessels try and compensate for increased myocardial demand during exercise.

A

When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!

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68
Q

Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?

A

In CV disease:
Epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest.

When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!

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69
Q

What determines if Angina is stable?

A

Angina is stable if symptoms are always relieved by rest or GTN (glyceryl Trinitrate) spray.

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70
Q

What percentage of stenosis is associated with stable angina?

A

70% occlusion of the artery.
This still allows enough blood flow through the artery at rest.

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71
Q

What is Stable angina?

A

Occlusion of an artery (70%) leading to ischaemia of the myocardial tissue resulting in chest pain.

At rest enough blood can still flow through the artery to meet the demands of the tissue.

Upon exercise or exertion, the tissue requires more oxygen and therefore a greater blood flow at which point the flow through the stenosed artery is not adequate enough and hence results in chest pain upon exertion.

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72
Q

what is the most common type of angina?

A

Stable angina

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73
Q

What is the most commonly affected region of the heart in stable angina?

A

Subendocardium.
The coronary arteries struggle to perfuse the deeper layers of the myocardium either due to coronary artery stenosis or LV hypertrophy resulting in ischaemia to this portion of the tissue.

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74
Q

What are the Symptoms of angina?

A

Central Crushing chest Pain on exertion/rest /emotion/cold/heavy meals.

May radiate to one or both arms, neck, jaws or teeth.
Worsens with time

Other Symptoms: Dyspnoea, nausea, sweatiness, faintness

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75
Q

What is the difference between symptoms of angina in Stable, unstable and decubitus types?

A

Stable angina occurs in periods of roughly 20 mins upon exertion or exercise.

Unstable angina can be continuously painful at rest or even minimal exertion.

Decubitus angina causes pain when lying down flat.

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76
Q

What is the difference pathophysiologically between stable and unstable angina?

A

Both are commonly caused by atherosclerotic plaque causing obstruction of a coronary artery.

In unstable angina, the plaque may rupture causing blood to leak out and a secondary thrombus to form which occludes the artery further creating an even narrower lumen for blood to flow through.

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77
Q

What is a key distinction between angina and MI?

A

Angina results in pain due to myocardial ischaemia where the heart tissue is starved of oxygen but is still alive.

MI is when the ischaemia has resulted in infarction that has led to the death of the heart tissue.

Angina is therefore reversible and MI is not.

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78
Q

What is Prinzmetals Vasospastic angina?

A

angina where patients may or may not have atherosclerosis of the coronary vessels.

instead ischaemia occurs due to vasospasms of the coronary arteries where they constrict so much they can cause ischaemia.

These can occur at any time not just on rest or on exertion.

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79
Q

What is the mechanism that causes prinzmetals angina?

A

Not clearly understood but likely due to vasoconstriction factors such as Thromboxane A2 release

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80
Q

What layers of the heart are affected in Prinzmetals angina?

A

Transmural Ischaemia

All layers of the heart wall supplied by the coronary arteries are affected.

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81
Q

What ECG reading would be shown on stable angina?

A

AT rest: Normal

On exertion:
ST segment depression due to subendocardium ischaemia.

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82
Q

What ECG reading would be shown in prinzmetals angina?

A

ST segment elevation due to transmural ischaemia.

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83
Q

How can symptoms of stable angina be relieved?

A

Relieved upon rest (after approx 5 mins)
OR
Symptoms relieved by GTN spray

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84
Q

Are troponin levels elevated in angina?

A

Often they are normal since the ischaemia has not killed the cells and thus the troponin have not been released

sometimes they may be elevated

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85
Q

Describe the primary prevention of angina.

A
  1. Risk factor modification.
  2. Low dose aspirin.
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86
Q

Describe the secondary prevention of angina.

A
  1. Risk factor modification.
  2. Pharmacological therapies for symptom relief and to reduce the risk of CV events.
  3. Interventional therapies e.g. PCI.
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87
Q

Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.

A
  1. Beta blockers.
  2. Nitrates e.g. GTN spray.
  3. Calcium channel blockers.
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88
Q

Describe the action of beta blockers.

A

Beta blockers are beta 1 specific.

They antagonise sympathetic activation and so are negatively chronotropic and inotropic.
Myocardial work is reduced and so is myocardial demand = symptom relief.

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89
Q

Give 4 side effects of beta blockers.

A
  1. Bradycardia.
  2. Tiredness.
  3. Erectile dysfunction.
  4. Cold peripheries.
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90
Q

When might beta blockers be contraindicated?

A

They might be contraindicated in someone with asthma or in someone who is bradycardic.

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91
Q

Give an example of a cardio-specific beta blocker

A

Atenolol

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92
Q

Describe the action of nitrates in GTN spray

A

Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.

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93
Q

What is a common side effect of nitrates in GTN?

A

headache due to vasodilation

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94
Q

Describe the action of Ca2+ channel blockers.

A

Ca2+ blockers are arterodilators and negative Chronotropic/ionotropic agents:

Reduced O2 demand -> reduced BP -> reduced afterload -> reduced myocardial demand.

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95
Q

What are some side effects of Calcium channel blockers?

A

postural hypotension
Swollen ankles
Flushing

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96
Q

Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.

A
  1. Aspirin.
  2. Statins.
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97
Q

How does aspirin work?

A

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!

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98
Q

What are statins used for?

A

They reduce the amount of LDL in the blood.

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99
Q

What ECG reading would be shown on unstable angina?

A

May be normal

May have some ST depression/T wave inversion

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100
Q

What ECG reading would be shown on unstable angina?

A

May be normal

May have some ST depression/T wave inversion

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101
Q

What is the treatment for Stable angina?

A

Immediate Symptomatic Relief - GTN sublingual stray

Long Term Symptomatic Relief - Beta Blocker (Atenolol) or Calcium Channel Blocker (Amlodipine)

Secondary Prevention of CVD:
Aspirin
Atorvastatin
ACE inhibitor
Already on a beta blocker

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102
Q

What is the gold standard diagnostic investigation for Stable Angina?

A

CT Coronary Angiography

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103
Q

What is the diagnosis of stable angina?

A

ECG :
Rest - normal
Exertion - ST depression/Flat T waves

CT Angiography - Stenosed atherosclerotic artery

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104
Q

What treatment should be considered for angina if pharmacology is unsuccessful?

A

Referral for revascularisation
Through PCI or CABG

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105
Q

What is revascularisation?

A

Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.

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106
Q

Name 2 types of revascularisation.

A
  1. PCI.
  2. CABG.
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107
Q

What procedures may be involved in PCI?

A

Balloon Stent
Angioplasty with Stent

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108
Q

Give 2 advantages and 1 disadvantage of PCI.

A
  1. Less invasive.
  2. Convenient and acceptable.
  3. High risk of restenosis.
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109
Q

Give 1 advantage and 2 disadvantages of CABG.

A
  1. Good prognosis after surgery.
  2. Very invasive.
  3. Long recovery time.
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110
Q

How is unstable angina diagnosed?

A

History

ECG - may present as ST-segment depression, transient ST-segment elevation, or T-wave inversion

No elevation in troponin - unstable angina not associated with damage to the heart

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111
Q

What is the Clinical Classification of Unstable Angina?

A
  • Cardiac chest pain at rest or during minimal exertion
  • Severe and of new onset cardiac chest pain
  • Cardiac chest pain with crescendo pattern (distinctly more severe, prolonged, or frequent than before)
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112
Q

What are the types of MI?

A

Non-ST Elevated Myocardial Infarction (NSTEMI)

ST Elevated Myocardial Infarction (STEMI)

Silent MI

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113
Q

What would the ECG for a STEMI look like?

A

ST segment elevation in local leads

May have Q waves (Pathological after some time)

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114
Q

What would the ECG for a NSTEMI look like?

A

ST depression
T wave inversion

No Q waves

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115
Q

What is the difference in an NSTEMI and STEMI when caused by atherosclerosis?

A

NSTEMI occurs after a partial occlusion of major Coronary artery

STEMI occurs after complete occlusion of a major Coronary artery.

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116
Q

What is the acute treatment for ACS?

A

MONAC:
Morphine
Oxygen (if Sats < 94%)
Nitrates (GTN)
Aspirin (300mg)
Clopidogrel (dual antiplatelet)

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117
Q

What is the treatment for an NSTEMI following acute treatment of ACS?

A

GRACE score:

low risk - monitor

Med-High risk - angiogram / PCI

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118
Q

What is the treatment of choice for STEMI?

A

PCI

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119
Q

What is the long term treatment/Secondary prevention management following ACS?

A

6 As
Aspirin (75g once daily)
Another antiplatelet - Ticagrelor/Clopidogrel
Atorvastatin (80mg once dail)
ACE inhibitors (ramipril)
Atenolol (or another bB)
Aldosterone antagonist (spironolactone) in those with clinical heart failure

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120
Q

What is Dressler’s Syndrome?

A

Post myocardial infarction syndrome.

Localised immune response causing pericarditis.

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121
Q

What are the complications of MI?

A

DREAD:
Death
Rupture of the heart septum/papillary muscles
Edema (causing heart failure)
Arrythmia and Aneurysm
Dressler’s Syndrome

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122
Q

What heart area and ECG leads correspond to:
Left Coronary Artery

LAD

Circumflex

Right Coronary Artery

A

Left Coronary Artery:
Heart area - Anterolateral
ECG leads - I, aVL, V3-V6

LAD:
Heart area - Anterior
ECG leads - V1-4

Circumflex:
Heart area - Lateral
ECG leads - I aVL, V5-6

Right Coronary Artery:
Heart area - Inferior
ECG leads - II, III, aVF

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123
Q

What is the Epidemiology for an MI?

A

600/100,000 for men.

200/100,000 for women

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124
Q

Name some of the function of platelets during arterial thrombosis

A
  • Procoagulant activity; release of thrombin
  • Dense granule secretion; contributes to platelet activation
  • Alpha granule secretion; contributes to coagulation and inflammation
  • Platelet-fibrin clot; fibrin acts as glue that keeps the thrombus growing and allow it block of arteries to cause MI.
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125
Q

Give a brief overview of the process by which platelets cause the platelet plug?

A

(1) Shear flow

(2) Initial adhesion GPIb/VWF

(3) Rolling GPIb/VWF/α2β1/collagen

(4) Stable adhesion activation/aggregation GPVI, GPIIb/IIIa

(5) Platelets are activated by ADP (vai P2Y12R), causing them to change shape, aggregate and seal off the endothelial breach

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126
Q

What combined therapy is used to manage patients with ACS?

A

Aspirin, P2Y12 Inhibitors and GPIIb/IIIa antagonists

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127
Q

Give some examples of P2Y12 inhibitors?

A

Clopidogrel
Ticagrelor
Prasugrel

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128
Q

What is a major side effect of P2Y12 inhibitors?

A

Increases risk of bleeding!
Serious bleeding must subside prior to administration and risk of thrombosis vs. risk of bleeding must be monitored throughout use.

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129
Q

Why are GPIIb/IIIa Antagonists very useful in STEMI pateints undergoing PCI?

A

Cover for delayed absorption of oral P2Y12 Inhibitors occuring due to opiates delaying gastric emptying

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130
Q

What is the role of anticoagulants used in the treatment of ACS?

A

Targets formation and/or activity of thrombin; inhibiting both fibrin formation and platelet activation

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131
Q

What anticoagulant is commony used during Non-STEMI ACS?

A

Fondaparinux (a pentasaccharide) is used prior to coronary angiography

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132
Q

What anticoagulants are used during PCI?

A

Full Dose:
Heparin (unfractionated or LMWH)
Bivalirudin

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133
Q

What is a Silent MI?

A

When a diabetic patient may not experience typical chest pain during an acute coronary syndrome

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134
Q

Name some causes of oxygen supply reduction associated with IHD?

A
  • Common: anaemia and hypoxaemia
  • Uncommon: polycythemia, hypothermia, hypovolaemia, hypervolaemia
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135
Q

Name some causes of oxygen demand increase associated with IHD?

A
  • Common: hypertension, tachyarrhythmia, valvular heart disease
  • Uncommon: hyperthyroidism, hypertrophic cardiomyopathy
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136
Q

Name some environmental causes of Angina?

A

Emotional stress
Large meals
Cold weather

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137
Q

Give some predisposing factors associated with IHD?

A
  • Age
  • Smoking
  • Family history
  • Diabetes mellitus
  • Hyperlipidemia
  • Hypertension
  • Kidney disease
  • Obesity
  • Physical inactivity
  • Stress
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138
Q

What are the three major physiological factors lending to oxygen mismatch associated with IHD?

A
  • Impairment of blood flow by proximal arterial stenosis (e.g. atherosclerosis)
  • Increased distal resistance (e.g. left ventricular hypertrophy)
  • Reduced oxygen carrying capacity of blood (e.g. anaemia)
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139
Q

What is Ohms Law?

A

Flow = Change in pressure / Resistance

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140
Q

What is Poiseuille’s Equation?

A

Q = R^4

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141
Q

What is Poiseuille’s Law?

A

Change in pressure = 8luQ/pi r^4

l - length of vessel
U - viscosity
Q - flow
R - radius of vessel

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142
Q

How does Poiseuille’s Law relate to CCS?

A

Relationship between flow, pressure and resistance; combination of Ohm’s law and vessel resistance equation. Radius has to fall below 75% before symptoms

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143
Q

How would you discuss a patients pain when taking a history for IHD?

A

OPQRST:
- Onset
- Position (site)
- Quality (nature/ character) - heavy, central, tight
- Relationship - associated with SOB, exertion, posture, meals
- Radiation - to arms, jaw, neck
- Relieving/ aggravating factors
- Severity
- Timing
- Treatment - if use GTN spray, ascertain if it helps!

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144
Q

What characteristics of chest pain suggest ischaemic cardiac pain?

A
  • Heavy, tight pain
  • Located centrally
  • Provoked by cold weather, big meals, exertion
  • Relieved by rest, GTN spray
  • Associated SOB
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145
Q

What is exercise testing?

A

Patient undertakes mild exercise on a treadmill and ECG is run simultaneously - any abnormailites, refer patient to catheterisation lab

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146
Q

What is a Perfusion/ Myoview scan?

A

IV radio-labelled agent travels to the coronary arteries - areas of darkness signify a blockage.

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147
Q

What are Psychosocial factors?

A

Factors influencing psychological responses (cognitive; behavioural; emotional) to the social environment and pathophysiological changes

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148
Q

What is a Coronary Prone Behaviour Pattern?

A

Coronary prone behaviour is the collection of behaviours and attitudes associated with heart disorders especially coronary heart disease and cardiovascular disorders.

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149
Q

Give some examples of personality trains associated with Coronary Prone Behaviour Patterns?

A
  • Aggressiveness/Anger (biggest risk factor)
  • Ambition
  • Competitiveness
  • Hostility (biggest risk factor)
  • Impatience
  • Sense of time urgency
  • Need for achievement
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150
Q

What causes the first and Second Heart Sound?

A

First - Mitral Valve closure

Second - Aortic Valve Closure

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151
Q

What is the cause for the 3rd heart sound?

A

early-diastolic rapid distension of the left ventricle that accompanies rapid ventricular filling and abrupt deceleration of the atrioventricular blood flow

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152
Q

What is the cause for the 4th Heart Sound?

A

the result of vibrations generated within the ventricle.

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153
Q

Give some psychosocial factors that increase the risk for CHD?

A

Depression and Anxiety
Low quantity and quality of social support
High demanding jobs/low control of jobs

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154
Q

What are the layers of the pericardium?

A

Outer Fibrous layer - Continuous with the central tendon of the Diaphragm
Serous layer:
Outer Parietal - lines the inner surface of the fibrous pericardium
Inner Visceral - forms the outer layer of the heart (Epicardium)

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155
Q

What is found between the parietal and Visceral pericardium?
What is the Function of this?

A

Pericardial cavity:
Contains 50ml of serous fluid to minimise the friction generated when the heart contracts

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156
Q

Which great vessels are Contained within the pericardium?

A

Roots of the great vessels:
Aortal
Pulmonary Artery
Pulmonary Veins
SVC
IVC

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157
Q

What are the main functions of the pericardium?

A
  • Fixes the heartin the mediastinum and limits its motion.
  • Prevents overfillingof the heart. The relatively inextensible fibrous layer of the pericardium limits the filling pressure and volume of the heart
  • Lubrication. A thin film of fluid between the two layers of the serous pericardium reduces the friction generated by the heart as it moves within the thoracic cavity
  • Protection from infection. The fibrous pericardium serves as a physical barrier between the muscular body of the heart and adjacent organs prone to infection, such as the lungs.
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158
Q

What is the purpose of the small reserve volume associated with the pericardial sac?

A

Volume of pericardial fluid changes based on the physiological state of the heart.

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159
Q

What is Cardiac Tamponade?

A

Reduction in cardiac output due to a raised intrapericardial pressure secondary to a pericardial effusion.
As there is a greater pressure, the heart chambers cannot expand during diastole reducing SV and CO

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160
Q

What is Beck’s Triad?

A

Three clinical signs associated with pericardial tamponade:
- Hypotension (weak pulse or narrow pulse pressure)
- Muffled heart sounds
- Raised jugular venous pressure.

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161
Q

What are some signs associated with cardiac tamponade?

A

Beck’s Triad
Pulsus Paradoxus
Tachycardia

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162
Q

What is Pulsus Paradoxus?

A

An inspiratory decrease in systolic BP >10mmHg.
(not a paradox but exaggeration of normal physiology)

Paradox:
On physical exam, beats are detected on cardiac auscultation during inspiration which cannot be palpated at the radial pulse. This is associated with increased JVP (kussmauls sign)

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163
Q

How is cardiac tamponade diagnosed?

A

ECHO - diagnostic
ECG - varying QRS peaks
CXR - big globular heart

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164
Q

How is Cardiac Tamponade treated?

A

Urgent pericardiocentesis

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165
Q

Define Pericardial Effusion?

A

Accumulation of excess fluid in the pericardial cavity; the pericardial fluid contains blood components such as fibrin, RBCs and WBCs

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166
Q

What is the main cause of pericardial effusion?

A

Typically pericarditis

RF are all factors related to pericarditis

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167
Q

How is Pericardial Effusion treated?

A

treat underlying cause
NSAIDS
Colchicine

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168
Q

What is Chronic pericardial effusion?

A

Slow accumulation of fluid allowing for adaptation of the parietal pericardium

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169
Q

Why does Chronic Pericardial Effusion rarely cause Cardiac Tamponade?

A

Increased compliance reduces the effect on diastolic filling and therefore slow accumulating effusion does not often cause tamponade.

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170
Q

Define Acute Pericarditis?

A

Inflammation of the pericardium commonly due to viral infection.

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171
Q

What are the different types of Pericarditis?

A

Acute
Chronic effusive
Chronic Constrictive

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172
Q

What is Constrictive Pericarditis?

A

Calcification thickens the pericardium and affects cardiac function

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173
Q

Who is typically affected by pericarditis?

A

Males - 20-50yrs

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174
Q

What is the Pathology of Pericarditis?

A

inflammation narrows the pericardial space causing the inflamed layers to rub against each other and cause further inflammation.

Extra fluid may be produced to compensate causing effusive pericarditis

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175
Q

What is the Pathology of Pericarditis?

A

inflammation narrows the pericardial space causing the inflamed layers to rub against each other and cause further inflammation.
Extra fluid may be produced to compensate causing a pericardial effusion.
If this fluid accumlation impacts the hearts function this is cardiac tamponade

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176
Q

What is the most common cause of Pericarditis?

A

Viral infection

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177
Q

What is the Most common Infectious, Non infectious and Iatrogenic cause of pericarditis?

A

Infectious - Viral
Non infectious - Neoplastic (secondary metastatic tumours)
Iatrogenic - direct injury from PCI/radiofrequency ablation

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178
Q

What is the Most common Infectious, Non infectious and Iatrogenic cause of pericarditis?

A

Infectious - Viral
Non infectious - Neoplastic (secondary metastatic tumours)
Iatrogenic - direct injury from PCI/radiofrequency ablation

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179
Q

What are some of the main causes of pericarditis?

A

Infection - Coxsackie Virus
Dressler’s Syndrome
Autoimmune
Neoplastic
Metabolic
Traumatic
Iatrogenic - PCI

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180
Q

What are some infectious causes of pericarditis?

A

HEAP:
Herpes virus
Enterovirus (Coxsackie)
Adenovirus
Parovirus

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181
Q

What are some Autoimmune causes of Pericarditis?

A

Sjogren’s Syndrome
Rheumatoid Arthritis
Scleroderma
Systemic Vasculitides

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182
Q

How is Pericarditis diagnosed?

A

ECG:
Widespread saddle shaped ST elevation
PR depression

ECHO - exclude pericardial effusion/tamponade

FBC - increased WCC

Chest Pain

ESR/CRP - High ESR may suggest aetiology

Pericardial Rub

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183
Q

What is Pericardial Rub?

A

Extra heart sound heard upon auscultation
One systolic - Two diastolic
Sound resembles scratching.

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184
Q

What are the signs of effusion associated with pericarditis?

A

Pulsus paradoxus

Kussmaul’s Sign - rise in JVP on inspiration

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185
Q

What are the symptoms of pericarditis?

A

Severe pleuritic chest pain

Dyspnoea
Cough
Systemic disturbance - weight loss, joint pain

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186
Q

What is the nature of the chest pain associated with pericarditis?

A

Sharp severe pleuritic chest pain - radiate to left shoulder due to phrenic nerve

Pain is relieved when sitting forward
Pain is exacerbated when lying flat or on inspiration

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187
Q

What are some important differential diagnoses of pericarditis?

A

MI - has no pericardial rub/not related to lying down (ST elevation not saddle shaped)
pneumonia
Aortic Dissection
PE

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188
Q

What is the management for pericarditis?

A

Period of sedentary activity until resolution of inflammation

NSAIDS (2 weeks)
Cochicine (3 weeks)
Consider Abx for bacterial aetiology

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189
Q

What are some complications of pericarditis?

A

Pericardial effusion - cardiac tamponade
myocarditis
constrictive pericarditis

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190
Q

How is cardiac tamponade diagnosed?

A

ECHO - diagnostic
ECG - varying QRS peaks
CXR - big globular heart

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191
Q

What is cardiomyopathy?

A

A disease of the heart muscle tissue where there is impaired ability to contract and/or there is electrical conduction dysfunction.

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192
Q

What are the 3 major determinants of myocardial performance?

A

Preload - the volume of blood entering the ventricles that causes a greater stretch on the ventricles.

Afterload - The pressure that must be overcome in order to eject blood from the ventricles during systole.

Contractility

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193
Q

What are the main types of cardiomyopathy?

A

Hypertrophic Cardiomyopathy (HCM)
Dilated Cardiomyopathy (DCM)
Arrhythmogenic Right/Left ventricular Cardiomyopathy (ARVC/ALVC)
Restrictive Cardiomyopathy.

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194
Q

What is the most common type of Cardiomyopathy?

A

Dilated Cardiomyopathy

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195
Q

What is Primary Cardiomyopathy?

A

Occurs when genes encoding proteins involved in the Myocardial tissue are dysfunctional resulting in poor/altered function myocardial cells and further pathology.

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196
Q

What is Secondary Cardiomyopathy?

A

Where the Myocardial cells structure and function becomes damaged through:
Toxins
inflammation
infection
systemic disorders

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197
Q

How are cardiomyopathies diagnosed?

A

ECHO
Some with MRI
Troponins may be elevated.

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198
Q

What is Dilated Cardiomyopathy?

A

Dilation of the ventricles (chamber enlargement) causing weakness of the ventricular myocardial cells impairing their contractility and hence their systolic function leading to poorly ejected blood.

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199
Q

What are the Symptoms of Dilated Cardiomyopathy?

A

Can be Asymptomatic
May present as congestive heart failure.

Dyspnoea
Weakness
Fatigue
Oedema
Raised JVP
Pulmonary congestion
Cardiomegaly
3rd/4th Heart Sounds

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200
Q

What is the Aetiology of Dilated Cardiomyopathy?

A

Gene mutations often in cytoskeletal genes.

Ischaemia
Alcoholism
Thyrotoxicosis

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201
Q

What is the epidemiology of DCM?

A

More common in males
35/100,000
Median age - 50

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202
Q

How is DCM diagnosed?

A

ECHO - Marked Dilatation
CXR - Cardiomegaly, pulmonary oedema
ECG - May have tachycardia

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203
Q

What is the treatment for DCM?

A

Tx of underlying conditions - AF/ HF
Bed rest
Loop and Thiazide Diuretics for fluid overload
ACEi
Beta Blockers

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204
Q

What is Hypertrophic Cardiomyopathy (HCM)?

A

Unexplained primary cardiac hypertrophy (often on LV wall and interventricular septum) leading to impaired diastolic filling and a reduced stroke volume. due to thick heart and reduced compliance

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205
Q

What is the cause of HCM?

A

Autosomal Dominant mutation in Sarcomeric genes:
Beta-myosin heavy chain
Troponin T
alpha tropomyosin.

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206
Q

What are the symptoms of HCM?

A

Most may be asymptomatic

Variable dyspnoea
Chest pain / palpitations
Syncope
Sudden death

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207
Q

What are the main complications of DCM?

A

Progressive Heart Failure
Sudden Cardiac Death

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208
Q

What may be found upon examination of a patient with HCM?

A

Forceful Apex beat
Late ejection systolic Murmur
Jerky Carotid pulse
Alpha wave in JVP.

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209
Q

What is the Epidemiology of HCM?

A

1/500
Men and black people more likely

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210
Q

What is the most common form of sudden cardiac death in the young population and atheletes?

A

Hypertrophic Cardiomyopathy

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211
Q

How is HCM diagnosed?

A

ECG - LVH, ST segment changes, T wave inversion

CXR - variable, left atrial enlargement

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212
Q

What is the treatment of HCM?

A

Amiodarone - reduce risk of arrythmias and sudden death

Treat chest pain:
Beta blockers and CCB - Verapamil

Implantable cardioverter defibrillator

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213
Q

What is a severe complication of HCM?

A

Sudden Death

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214
Q

What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

A

Associated with Desmosome gene mutations
Fibro-fatty replacement of the RV myocytes leading to impaired ability of RV muscle to contract due to muscle cell loss.

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215
Q

What is Naxos disease?

A

A autosomal recessive genetic condition associated with ARVC and diffuse palmoplantar keratoderma and woolly hair

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216
Q

What are the symptoms of ARVC?

A

Palpitations
Presyncope/syncope
Death possible on first presentation

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217
Q

What is the most common sustained arrythmia in HCM?

A

Atrial Fibrillation

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218
Q

What is the cause of ARVC?

A

Unknown but may be due to apoptosis, inflammation or genetics

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219
Q

What is the Epidemiology of ARVC?

A

1/2000
Mainly affects males
30-50% of cases have autosomal dominant genetic predisposition

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220
Q

How is ARVC diagnosed?

A

ECHO - RV wall Dimensions and abnormalities

RV angiography

MRI - fatty infiltration and fibrosis on RV wall.

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221
Q

How is ARVC treated?

A

Standard heart failure medication.
Beta blockers in asymptomatic patients.
Heart transplant/

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222
Q

What is the most frequent cause of heart transplants?

A

Dilated cardiomyopathy.

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223
Q

What is Restrictive cardiomyopathy?

A

Rigid Fibrotic Myocardium
Increased myocardial stiffness despite normal LV cavity size and function.
Increased stiffness restricts diastolic filling as the ventricle is incompliant.

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224
Q

What are the causes of Restrictive cardiomyopathy?

A

infiltrative myocardial disease
Granulomatous disease - Amyloid heart disease, Sarcoidosis.

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225
Q

What is the epidemiology of Restrictive cardiomyopathy?

A

between 1/1000 to 1/1500
5% of all cardiomyopathies
Mainly affects the elderly, tropical Africa

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226
Q

What are the symptoms of restrictive cardiomyopathy?

A

Heart failure with normal systolic function
Dyspnoea
Fatigue
S3 and S4 heart sound
pulmonary oedema
Murmurs
Features of RV failure

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227
Q

What is the diagnosis of restrictive cardiomyopathy?

A

ECHO - thickened ventricular walls, valves and atrial septum.

MRI - to distinguish between cardiomyopathies.

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228
Q

What is the Treatment for restrictive cardiomyopathy?

A

None
Consider transplant

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229
Q

What are the complications of restrictive cardiomyopathy?

A

Heart failure
sudden death
Poor prognosis.

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230
Q

What is the main feature of ARVC?

A

Arrhythmia

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231
Q

What do all cardiomyopathies carry a risk of?

A

Developing arrythmia

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232
Q

What is a channelopathy?

A

Gene mutations in genes that are involved in ion channel proteins resulting in channelopathies.

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233
Q

What can be a cardiovascular sign of channelopathies?

A

Arrythmias

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234
Q

Give some examples of cardiac Channelopathies

A

Long QT
Short QT
Brugada
Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)

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235
Q

What is the major clinical sign of ARVC?

A

Ventricular Tachycardia

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236
Q

What is the commonest symptoms of channelopathies?

A

Recurrent Syncope

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237
Q

What is Brugada Syndrome?

A

A channelopathy caused by a mutation in the cardiac sodium channel gene

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238
Q

What are the symptoms of Brugada Syndrome?

A

Asymptomatic
May have syncope
Can cause sudden death

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239
Q

What are the common rhythmic abnormalities associated with Brugada Syndrome?

A

Ventricular fibrillation
Polymorphic Ventricular Tachycardia

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240
Q

What would the ECG look like with a patient with Brugada?

A

Characteristic ST elevation in chest leads.

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241
Q

What is sudden cardiac death in young people often due to?

A

Inherited condition likely a cardiomyopathy or channelopathy

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242
Q

What conditions are included in Aortovascular syndromes?

A

Marfans
Vascular Ehler Danlos (EDS)
Loeys-Dietz

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243
Q

What is Diastolic Distensibility?

A

The pressure required to fill the ventricle to the same diastolic volume

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244
Q

What are the Consequences of Hypertension?

A

Stroke (ischaemic and haemorrhagic)

Myocardial Infarction

Heart failure

Chronic renal disease

Cognitive decline

Premature death

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245
Q

What are the different stages of clinical Hypertension?

A
  • Define Stage 1 Hypertension.
    Clinical = 140/90
    Ambulatory = 135/85
  • Define Stage 2 Hypertension
    Clinical = 160/100
    Ambulatory = 150/95
  • Define severe Hypertension.
    Clinical = 180/110
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246
Q

How is Hypertension treated?

A

Lifestyle modification

Antihypertensive drug therapy

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247
Q

Who should be offered antihypertensive drug treatment for hypertension?

A

Individuals aged 80 or below and individuals who have one or more of the following:
- Target organ damage
- Established CVD
- Renal disease
- Diabetes
- 10-year CVD risk of >20%

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248
Q

Describe mechanisms of BP control - targets for therapy

A
  • Cardiac output and peripheral resistance
  • Interplay between the RAAS and sympathetic nervous system (NA)
  • Local vascular vasoconstrictor and vasodilator mediators
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249
Q

Describe the renin angiotensin-aldosterone system.

A
  1. Kidneys sense low BP and renin is released from juxtaglomerular cells.
  2. Renin converts angiotensinogen to angiotensin I
  3. ACE from the lungs converts angiotensin I to angiotensin II
  4. Angiotensin II (extremely potent vasoconstrictor) stimulates aldosterone release resulting in increased Na+ and thus water reabsorption which leads to increased blood volume and thus blood pressure
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250
Q

Describe the Sympathetic nervous system response to a drop in BP?

A

Drop in BP results in the release of noradrenaline,
leading to vasoconstriction and increased contractility of the heart
thus increasing peripheral resistance and cardiac output and thus BP.
Also results in renin release which further augments RAAS

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251
Q

What is the MOA of ACE inhibitors?

A

Prevent ACE converting angiotensin I to Angiotensin II and therefore inhibiting the CVS effects of Angiotensin II

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252
Q

Give examples of ACEis?

A
  • Ramipril
  • Enalapril
  • Perindopril
  • Trandolapril
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253
Q

What are the indications for ACE Inhibitors?

A
  • Hypertension
  • Heart Failure
  • Diabetic nephropathy
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254
Q

What are the main Adverse effects of ACEi?

A

Related to reduced Angiotensin II:

Hypotension
Acute renal failure
Hyperkalaemia
Teratogenic effects in pregnancy

Related to increased Kinin Production:
Cough
Rash
Anaphylactoid reactions

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255
Q

Why are there side effects such as cough when using ACEi?

A

ACE breaks down bradykinin.
If ACE is inhibited then bradykinin levels increase
This can cause a persistent dry cough

256
Q

What are Angiotensin II Receptor Blockers (ARBs)?

A

They block the receptors of angiotensin II preventing its binding and it inducing effects.

257
Q

Give examples of ARBs?

A
  • Candesartan
  • Losartan
  • Valsartan
  • Telmisartan
258
Q

What are the indications for ARBs?

A
  • Hypertension (and when ACEi is contradicted due to cough)
  • Diabetic nephropathy
  • Heart failure (when ACEi contraindicated - acts on AT-1 receptor)
259
Q

What are the ADRs associated with ARBs?

A
  • Symptomatic hypotension (esp. in volume depleted patients)
  • Hyperkalaemia
  • Potential renal dysfunction
  • Rash
  • Angiooedema
  • Teratogenic in pregnancy
260
Q

What are Calcium Channel Blockers (CCBs)?

A

These block the calcium channels from allowing Ca entry into cardiomyocytes.

261
Q

What are the indications for CCBs?

A
  • Hypertension
  • IHD (angina)
  • Arrhythmias
262
Q

Give examples of CCBs.

A
  • Dihydropyridines (e.g.amlodopine, nifedipine, felodipine)
  • Phenylalkylamines(e.g. verapamil)
  • Benzothiozepines(e.g. diltiazem)
263
Q

Give an example and explain the actions of Dihydropyridines?

A

Amlodipine:

Preferentially affect Vascular smooth muscle and act as peripheral arterial vasodilators

264
Q

Give an example and explain the actions of Phenylalkylamines?

A

Verapamil:

Directly affects the heart - negatively chronotropic, negatively ionotropic

265
Q

Give an example and explain the actions of Benzothiozepines?

A

Diltiazem:

Intermediate heart and peripheral vascular effects

266
Q

What are the ADRs associated with CCBs?

A

Due to peripheral vasodilation (Dihydropyridines):
- Flushing
- Headache
- Peripheral oedema
- Palpitations

Due to negative chrontropic effect (Phenylalkylamines and Benzothiozepines):
- Bradycardia
- Atrioventricular block
- Postural hypotension

Due to negative ionotropic effect (Benzothiozepines)
- Worsening of HF

Verapamil causes constipation

267
Q

What are Beta Blockers?

A

Beta adrenoceptor blockers that prevent the effects of adrenaline and noradrenaline in the sympathetic nervous system.
They work on B1 and B2 receptors.

268
Q

Give examples of Beta Blockers?

A
  • Bisoprolol
  • Propranolol
  • Atenolol
  • Carvedilol
269
Q

What are the indications for beta blockers?

A
  • IHD - angina
  • HF
  • Arrhythmia
  • Hypertension
270
Q

Which beta blockers are B-1 selective?

A

Metoprolol
Bisoprolol
(Atenolol is mostly B1 but not entirely cardioselective)

271
Q

Which beta blockers are non-selective?

A

Propranolol
Nadolol
Carvedilol

272
Q

What condition is contraindicative for beta blockers?

A

Asthma

273
Q

What are the ADRS associated with Beta blockers?

A
  • Fatigue
  • Headache
  • Sleep disturbance
  • Bradycardia
  • Hypotension
  • Cold peripheries
  • Erectile dysfunction
274
Q

What conditions can Beta blockers cause exacerbations of

A

Asthma
PVD - Claudication or Raynauds
Heart Failure - when given in standard doses or acutely

275
Q

How do Diuretics reduce blood pressure?

A

Increased excretion of water, salt and metabolites in urine

276
Q

What are the indictations for Diuretics?

A
  • Hypertension
  • Heart failure
277
Q

What are the different classes of Diuretics?

A

Thiazide diuretics - act on distal tubule blocking Na/Cl exchanger
Loop diuretics - act on ascending loop of henle, blocks Na/K/2Cl (NKCC2) transporter
Potassium-sparing diuretics(Aldosterone antagonists) - Retain Potassium

278
Q

Give examples of Diuretics of each class?

A
  • Thiazide diuretics: bendroflumethiazide, hydrochlorothiazide
  • Loop diuretics: furosemide, bumetanide
  • Potassium-sparing diuretics: spironolactone, eplerenone
279
Q

What are the ADRs associated with Diuretic?

A
  • Hypovolaemia (mainly loop)
  • Hypotension (mainly loop)
  • Hypokalaemia
  • Hyponatraemia
  • Hypomagnesaemia
  • Hypocalcaemia
  • Hyperuricaemia (gout)
  • Erectile dysfunction (thiazides)
  • Impaired glucose tolerance (thiazides)
280
Q

Give an alpha 1 adrenoceptor blocker used as an anti-hypertensive?

A

Doxazosin

281
Q

Give examples of centrally acting antihypertensives?

A

Act on the CNS:
Moxonidine
Methyldopa

282
Q

When may Methyldopa be used?

A

During pregnancy for gestational hypertension

283
Q

Give an example of a direct Renin Inhibitor?

A

Aliskiren

284
Q

Outline the treatment programme for hypertension of someone under the age of 55yrs?

A

First line: ACEi or ARB

Second Line: ACEi/ARB + CCB

Third Line: ACEi/ARB + CCB + Thiazide

Fourth line (Resistance HTN): Consider addition of Spironolactone, alpha blocker, beta blocker

285
Q

Outline the treatment programme for hypertension of someone over the age of 55yrs or afro-caribbean ?

A

First line: CCB

Second Line: ACEi/ARB + CCB

Third Line: ACEi/ARB + CCB + Thiazide

Fourth line (Resistance HTN): Consider addition of Spironolactone, alpha blocker, beta blocker

286
Q

Define Heart Failure?

A

Complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired.

287
Q

What are the different Types of Heart Failure?

A

Left Ventricular Systolic Dysfunction (Most common) - caused by contractility dysfunction

Heart failure with preserved ejection fraction (HFPEF) - caused by dysfunction during diastole (filling)

Acute/Chronic Heart Failure

288
Q

What is the underlying principle of treatment of heart failure?

A

Vasodilator therapy via neurohumoral blockade (RAAS-SNS)

289
Q

What is used in the symptomatic treatment of heart failure?

A

Diuretics - often loop

290
Q

What are the stages involved in disease influencing neurohumoral blockade therapy?

A

A (first Line) - ACEi + BB therapy (low dose titrated up slowly)

B: Aldosterone Antagonist (Spironolactone)

C: ARNI (ARB + Neprilysin inhibitor) - Entresto ( combination of Valsartan + Sacubitril)

D: SGLT2 inhibitor - Dapagliflozin

E: ACEi intolerance - ARB

F: ACEi and ARB intolerance - Hydralazine/nitrate combination

G: consider Digoxin

291
Q

What are Nitrates when used as a treatment?

A

Arterial and Venous dilators
These reduce both preload (venous dilation) and afterload (arterial dilation) to lower the BP

292
Q

What are the main indications for nitrates?

A

IHD (Angina)
Heart Failure

293
Q

Give Examples of nitrates?

A
  • Isosorbide mononitrate (tablet)
  • GTN spray
  • GTN infusion (acute/ severe angina)
294
Q

What are the ADRs associated with Nitrates?

A
  • Headache
  • GTN spray syncope
  • Potential tolerance to the drug
295
Q

What are the cardiac natriuretic peptides (CNPs?)

A

Atrial Naturetic Peptide (ANP) - Atria
Brain Naturetic Peptide (BNP) - Brain and Ventricles

296
Q

What causes the physiological release of cardiac natriuretic peptides?

A

Stretching of atrial and ventricular muscle cells, raised atrial or ventricular pressures and volume overload

297
Q

What effect do CNPs have on renal excretion?

A

Increases renal excretion of sodium (natriuresis) and water (diuresis)

298
Q

What effect do CNPs have on vascular smooth muscle?

A

Relax vascular smooth muscle (except efferent arteriole) of renal glomeruli to preserve filtration pressure in kidney whilst still removing Na+ and thus water thus no renal damage)

299
Q

What effect do CNPs have on vascular permeability?

A

Increased vascular permeability

300
Q

What effect do CNPs on the release of other chemical mediators?

A

Reduces aldosterone, angiotensin II, endothelin (most potent vasoconstrictor) and ADH release

301
Q

What are CNPs a counter-regulatory system to?

A

Counter-regulatory system to the renin-angiotensin system

302
Q

What are NPs metabolised by?

A

NEP or Neprilysin

303
Q

How can the inhibition of NP metabolism be used for in the treatment of HF?

A

NEP inhibition increases levels of natriuretic peptides

304
Q

Name examples of NEP inhibitors.

A

Sacubitril - is a neprilysin inhibitor

Entresto (ARNI) - is a combination of sacubitril and valsartan (ARB) - VERY EFFECTIVE IN HEART FAILURE

305
Q

What are the Class I antiarrhythmic Drugs?

A

Sodium Channel Blockers:

1A: quinidine

1B: lidocaine

1C: flecainide

306
Q

What are the Class II Anti-arrhythmics?

A

Beta-blockers:
- non-selective (e.g.propranolol, nadolol, carvedilol)
- beta-1 selective (e.g. bisoprolol, metoprolol)

307
Q

Why Is Propranolol useful for arrhythmias immediately post MI?

A

It blocks both Beta adrenoceptors and can block sodium channels too

308
Q

What are the Class III Anti-arrhythmics?

A

Prolongs action potential:

Amiodarone blocks potassium channels during repolarisation to increase the AP.

Cause QT prolongation; potential for significant side effects in patient with QT prolongation

309
Q

What are the Class IV Anti-arrhythmics?

A

Calcium channel blockers (only phenylalkylamines and benzothiozepines):
Verapamil and Diltiazem

Verapamil is more effective than amlodipine as it does not affect calcium channel at rest

310
Q

What do Class I and III anti-arrythmics do?

A

Rhythm control (sympathetic drive, e.g. adrenaline worsens arrhythmias)

311
Q

What do Class II and IV anti-arrythmics do?

A

Rate control (sympathetic drive, e.g. adrenaline worsens arrhythmias)

312
Q

What are the ADRs associated with Amiodarone?

A
  • Bradycardia
  • Interstitial Lung Disease
  • Thyroid (hyper and hypo)
  • Corneal (ocular)/cutaneous (skin)
  • Hepatic dysfunction/hypotension when IV (due to solvents)
  • Photosensitivity
  • Drug interactions
313
Q

What type of drug is Digoxin?

A

Cardiac glycoside

314
Q

By what mechanism does Digoxin affect the heart?

A

Inhibits Na/K pump;
Therefore Na/Ca exchanger is not active as Na conc increases in the cell
Therefore Ca is not removed from the cell
causes an increase in Ca2+ inside the cells of the heart
Increases contraction of myocytes

315
Q

What affect does Digoxin have on the heart?

A
  • Bradycardia (increased vagal tone)
  • Slows AV conduction (increased vagal tone)
  • Increased ectopic activity
  • Increased force of contraction (direct +ve inotropic effect) by increasing intracellular calcium
316
Q

What are the indications for Digoxin?

A
  • Atrial Fibrillation; reduces ventricular rate response
  • Severe heart failure; has a positive inotropic effect
317
Q

What are the ADRs of Digoxin?

A
  • Narrow therapeutic range
  • Nausea
  • Vomiting
  • Diarrhoea
  • Confusion
318
Q

What are Structural Heart defects?

A

These are often Congenital defects that occur during pregnancy to the heart that are not necessarily inherited that cause heart problems.
They can range from minor to life incompatible

319
Q

Give examples of some structural heart defects?

A

Artial Septal Defect (ASD)
Ventricular Septal Defect (VSD)
Coarctation of the Aorta
Bicuspid Aortic Valve
Fallot’s Tetralogy
Patent Ductus Arteriosus
Patent Foramen Ovale

320
Q

What is Tetralogy of Fallot?

A

Combination of four congenital abnormalities affecting the structure of the heart. This causes oxygen-deficient blood to flow out of the heart and to the rest of the body.

321
Q

What are the four abnormalities associated with Tetralogy of Fallot?

A

Ventricular Septal Defect (VSD) - hole between 2 ventricles
Over-riding Aorta - Allows blood from both ventricles to entre the aorta
RV Hypertrophy - thickening of RV muscle
Pulmonary Stenosis - Narrowing of the exit from the RV to pulmonary circulation

322
Q

What are the consequences of the abnormalities in Tetralogy of Fallot?

A

There is a greater pressure in the RV than the LV and so blood is shunted into the LV → cyanosis as blood is not oxygenated

323
Q

What are the symptoms associated with Tetralogy of Fallot?

A

Severity dependent on degree of pulmonary stenosis

Cyanosis
Systolic Murmur
Increase Hb concentration

324
Q

What is the cause of Tetralogy of Fallot?

A

Unknown but likely genetic influence

325
Q

What is the Epidemiology of Tetralogy of Fallot?

A

Most common complex cardiac abnormality.
10% of congenital heart conditions

326
Q

What are the investigations for Tetralogy of Fallot?

A

CXR - boot shaped heart

ECHO CG - anatomy and degree of stenosis

327
Q

What is the Treatment for Tetralogy of Fallot?

A

Early surgical intervention within 2 years

328
Q

What is Ventricular Septal Defect (VSD)?

A

An abnormal connection between the LV and RV causing a left to right shunt enabling more blood to enter the pulmonary circulation.

329
Q

Why is there not cyanosis in VSD?

A

There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic.

330
Q

What are the clinical signs of a VSD?

A

Size Matters:
Small - Asymptomatic
Large - Exercise intolerance, failure to thrive, murmur

331
Q

What is the epidemiology of VSD?

A

25% of congenital abnormalities

2/1000

332
Q

What are the treatments for VSD?

A

May close on its own
Surgical repair

333
Q

What is the pathology of Eisenmenger’s Syndrome?

A

High pressure pulmonary blood flow leads to damage in pulmonary vasculature
→ increased resistance to blood flow (pulmonary hypertension)
→ RV pressure increases
→ shunt direction reverses (RV to LV)
→ cyanosis

334
Q

What condition often leads to Eisenmenger’s Syndrome as a complication?

A

VSD

335
Q

What are the risks associated with Eisenmenger’s syndrome?

A
  • Stroke
  • Endocarditis
  • Risk of death
336
Q

What is Atrial Septal Defect (ASD)?

A

A common structural defect where there is a hole in the septum between the 2 atria

337
Q

What are the types of ASD?

A

Ostium Primum - associated with AV valve abnormalities

Ostium Secundum (85% of ASD) - Asymptomatic

338
Q

What is the pathophysiology of ASD?

A

There is a higher pressure in the LA than the RA and so blood is shunted from the left to right; not cyanotic.

This may be reverse if Eisenmenger’s Syndrome develops

339
Q

What are the clinical signs of a large ASD?

A

Pulmonary ejection systolic and mid systolic murmur -Significant increase in blood flow through the right heart and lungs

Enlarged pulmonary arteries.

Right heart dilatation - can lead to RHS failure

SOB on exercise

Increased chest infection.

340
Q

How are ASDs treated?

A

Surgical Repair
Percutaneous repair

341
Q

What are Atrio-Ventricular Septal Defects (AVSD)?

A

A hole between the atria and the ventricles
2 per 10,000
Strong association with Downs

342
Q

What are the symptoms of AVSD?

A

Breathlessness
Poor feeding
Poor weight gain

343
Q

What are the clinical signs of a large AVSD?

A
  • Enlargement of the heart
  • Heart failure - inability to adequately supply body oxygen
  • Eisenmenger’s Syndrome
  • Exercise intolerance
  • Pulmonary hypertension
  • Pneumonia
344
Q

What is Patent Ductus Arteriosus (PDA)?

A

Ductus arteriosus fails to close after birth;
allows abnormal transmission of blood from the aorta to the pulmonary artery.
Pulmonary arterial and left atrial flow increase

345
Q

What are the symptoms of PDA?

A
  • Pulmonary hypertension and RHF (due to Eisenmenger’s reaction)
  • Breathlessness
  • Poor feeding, failure to thrive
  • Risk of endocarditis
346
Q

What are the clinical signs of PDA?

A
  • Tachycardia
  • Machine murmur
  • Enlarged heart - breathlessness
  • Eisenmenger’s Syndrome
347
Q

What is Coarctation of the Aorta?

A

Narrowing of the Aorta
Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing of the aorta distal to the ductus arteriosus

348
Q

What is the result of a Coarctation of the aorta on body perfusion?

A

Blood is diverted massively through the aortic arch branches and therefore you have increased perfusion to the upper body and less to the lower body.

349
Q

How is Coarctation of the Aorta Diagnosed?

A

CXR - notched ribs
CT angiogram

350
Q

What are the Clinical signs of Coarctation of the Aorta?

A

Right arm Hypertension (may have left arm hypotension)
Lowe pressure in vessels distal to Coarctation
Bruits (buzzes) over the scapulae and back
Murmur

351
Q

What is a Patent Foramen Ovale?

A

Failure of the foramen ovale to close after birth

352
Q

What are the effects of a patent foramen Ovale?

A

No symptoms
If no other abnormalities then normal health

353
Q

What percentage of people may have a patent foramen ovale?

A

1/4

354
Q

What is a bicuspid aortic valve?

A

Aortic valve has 2 cusps rather than 3.
Get turbulence generation instead of laminar flow in the aorta

355
Q

What are the issues with a bicuspid aortic valve?

A

Can work well at birth and go unoticed
Exercise exacerbates complications
Abnormal degradation of the aortic valve over time - requires valve replacement

356
Q

What is the epidemiology of a bicuspid aortic valve?

A

1-2% of general Population.

357
Q

What is a common complication of bicuspid aortic valves?

A

Aortic Aneurysm development

358
Q

What is the most common inherited heart defect?

A

Bicuspid Aortic Valve

359
Q

Which structural heart abnormalities are not cyanotic and why?

A

VSD
ASD
PDA

Left to right shunt

360
Q

Which structural heart abnormalities are cyanotic and why?

A

Tetralogy of Fallot

Right to left shunt.

361
Q

What is pulmonary stenosis?

A

Narrowing of the outflow tracts of the right ventricles
This results in increased resistance of the pulmonary circulation leading to RV hypertrophy

362
Q

What are the categories for Hypertension?

A

Normotensive
Stage 1 Hypertension
Stage 2 Hypertension
Severe Hypertension (Stage 3)

363
Q

What is the normal range for blood pressure?

A

90/60 - <120/ <80

364
Q

Define stage 1 hypertension

A
  • ABP 135/85
  • Clinic 140/90
365
Q

Define Stage 2 Hypertension?

A
  • ABP 150/95
  • Clinic 160/100
366
Q

Define severe hypertension

A

Clinic 180/120

367
Q

What is Primary Hypertension?

A

When it is Idiopathic (no known cause)
95% of cases

368
Q

What is Secondary Hypertension?

A

When the underlying cause is known
5% of cases

369
Q

What are some underlying causes of secondary hypertension?

A

CKD - as a result of diabetic nephropathy
Endocrine - Phaeochromocytoma, Cushings, Conns
Iatrogenic
Pregnancy

370
Q

What are the risk factors of hypertension?

A

Increased Age
Blacker ethnicity
Overweight - biggest RF
Decreased exercise/sedentary lifestyle
smoking
diabetes
stress
increased salt intake
Family Hx

371
Q

What is the most common cause of secondary hypertension?

A

CKD as a result of diabetic nephropathy

372
Q

Define malignant hypertension

A

Rapid rise in blood pressure which damages vasculature
Pathological hallmark is fibrinoid necrosis
Usually with severe hypertension + bilateral retinal haemorrhages and exudates

373
Q

When is hypertension an emergency?

A

When there is sign of immediate damage:
Papilloedema
Acute kidney injury
Acute stroke
ACS
Aortic dissection

374
Q

What is the pathogenesis of Hypertension?

A

All mechanisms where there is increased CO from Increased RAAS and SNS activity.
Mechanisms where there is increased TPR will increase BP

375
Q

What is the equation for BP?

A

BP = CO x TPR

376
Q

What are the vascular causes of Secondary Hypertension?

A

CKD
OSA
Glomerulonephritis - increased renin
Renal Artery stenosis - increase renin

377
Q

What are the endocrine causes of Hypertension?

A

Phaeochromocytoma
Cushings
Conns (hyperaldosteronism)
Acromegaly
Thyroid Dysfunction

378
Q

What are some autoimmune causes of Hypertension?

A

Lupus
Scleroderma

379
Q

What are the symptoms of Hypertension?

A

Mostly Asymptomatic
May have a pulsatile headache (but no more than general population)
Found on screening

380
Q

When should you screen to find the cause of a patients hypertension?

A

Early onset (<30yrs) with no risk factors
Hypertension resistant to 3 drugs
Malignant hypertension
If patient has other specific symptoms indicative of secondary causes

381
Q

What drugs can increase blood pressure?

A

NSAIDS
SNRis
Corticosteroids
Oestrogen contraceptives
Stimulants
Anti-anxiety drugs (gabapentin)
Anti-TNFs

382
Q

Which investigations are ordered to quantify overall risk in patients with hypertension?

A

Fasting glucose
Cholesterol

383
Q

How is Hypertension diagnosed?

A

BP reading in hospital of 140/90 +
Then ABPm for 24 hours to confirm diagnosis (BP 135/85 + throughout day)
Assess end organ damage

384
Q

What investigations are used to assess end organ damage in Hypertension?

A

ECG/ECHO - LV Hypertrophy
Fundoscopy - papilloderma
U&Es - hypokalaemia in Conns
Urinalysis, Proteinuria and Haematouria
Serum creatine
GLucose
Renal function

385
Q

What is the lifestyle management of Hypertension?

A

Stop Smoking
Exercise - lose weight
Control diet

386
Q

What are the main drugs used to lower blood pressure?

A

CCBs
ACEi/ARBs
Diuretics
B-blockers

387
Q

What is the medical management of hypertension in a patient who is <55yrs old or has T2DM?

A

1st Line - ACEi/ (ARB if ACEi are Contraindicated)
2nd Line - ACEi/ (ARB if ACEi is CI) + CCB
3rd Line - ACEi/ (ARB if ACEi is CI) + CCB + Thiazide
4th Line (resistant HTN) - ACEi/ (ARB if ACEi is CI) + CCB + Thiazide + 4th drug:
4th drug if K+ > 4.5 = alpha/beta blocker
4th drug if K+ < 4.5 = Spironolactone

388
Q

What is the Medical Management for a Patient with HTN who is >55+yrs old or from Afro-caribeean origins?

A

1st Line - CCB
2nd Line - ACEi/ (ARB if ACEi is CI) + CCB
3rd Line - ACEi/ (ARB if ACEi is CI) + CCB + Thiazide
4th Line (resistant HTN) - ACEi/ (ARB if ACEi is CI) + CCB + Thiazide + 4th drug:
4th drug if K+ > 4.5 = alpha/beta blocker
4th drug if K+ < 4.5 = Spironolactone

389
Q

If a patient is Black, over 55yrs old and has T2DM which medical management line of HTN would you use?

A

T2DM takes precedence and Therefore first line is ACEi

390
Q

What are the possible complications of hypertension?

A

Chronic heart disease
MI
Stroke - Common complication
Heart failure
Peripheral arterial damage
Aortic aneurysm
Chronic kidney disease
Vascular dementia

391
Q

When should hypertension treatment be withheld?

A

When patients are undergoing general anaethesia

392
Q

What is the monitoring for hypertension?

A

Renal function impairement
Otherwise, no monitoring as concordance with treatment an issue
Evidence shows going off medication causes hypertension to return

393
Q

What are the thresholds for treatment of hypertension?

A

Low risk patients - 160/100
High risk patients (diabetes, sign of end organ damage, risk of coronary events) - 140/90

394
Q

What is aortic Stenosis?

A

Narrowing of the aortic valve

395
Q

What is the basic overlying pathogenesis of valvular stenosis?

A

Stiff/thick valve leaflets
Obstructs forward flow
leads to systemic or pulmonary congestion

Stenotic Valve on RHS = Systemic Venous Congestion
Stenotic Valve on LHS = Pulmonary Venous Congestion

396
Q

What valves are often affected by valvular stenosis?

A

Mitral
Aortic
Pulmonary
Tricuspid

397
Q

What would a regurgitant valve cause?

A

Causes insufficiency and proximal chamber dilation.
This is due to loss of structural chamber integrity and strength

398
Q

What is a regurgitant valve?

A

Poorly sealed valve leaflets
Defective and floppy
backflow of the blood through thte valve (incompetance)

Valvular Regurgitation on RHS = Systemic Venous congestion
Valvular Regurgitation on LHS = Pulmonary Venous congestion

399
Q

What occurs as a result of stenosis?

A

Increased upstream pressure resulting in proximal chamber dilation and hypertrophy
This leads to the heart becoming large and rigid and poorly compliant

400
Q

What is the difference between a regurgitant valve and a stenotic valve?

A

Regurgitant - Defective and floppy

Stenotic - Narrowed valve lumen

401
Q

Which valve defects commonly cause murmurs?

A

Aortic Regurgitant and stenosis
Mitral Regurgitant and stenosis

402
Q

Where are Right sided defects commonly heart as murmurs?

A

RILE (Right = inspiration and Left = Expiration)
Pulmonary/Tricuspid on RHS on insipration

403
Q

Where are Left sided defects commonly heard as murmurs?

A

RILE (Right = inspiration and Left = Expiration)
Aortic/Mitral heard on LHS on Expiration

404
Q

What is the nmeonic for when you would hear aortic regurgitance/stenosis and mitral valve reguritance and stenosis?

A

ARMS (Aortic regurgitance / Mitral Stenosis) on Diastolic

ASMR (Aortic Stenosis / Mitral Regurgitance) on Systolic

405
Q

What is the main cause of Mitral Valve Stenosis?

A

Rheumatic Heart disease
(Most common - post strep pyogenes infection)

406
Q

What are some less common causes of Mitral Valve Stenosis?

A

Valve calcification
Infective endocarditis

407
Q

What is the pathology of Mitral Valve Stenosis?

A

RHD causes mitral reactive inflammation
Over years this is exacerbated w/ calcification
results in LA hypertrophy and chamber dilation.
Raised LA pressure - causes pulmonary hypertension
RV hypertrophy and failure

408
Q

What are the symptoms of Mitral Valve Stenosis?

A

Malar Flushed Cheeks - due to low CO2
Pulmonary HTN - Dyspnoea
A wave on JVP
Loud S1 Snap - due to thickend valve cusps
Low pitched MID-DIASTOLIC murmur - loudest at apex and expiration when Px lies on LHS

409
Q

What murmur is heard in Mitral Valve Stenosis?

A

Low pitched - due to decreased pulse and decreased CO
MID DIASTOLIC Murmur
Loudest at APEX
Best heard on EXPIRATION when Px is lying on LHS

410
Q

What is the Diagnosis/investigations for Mitral valve stenosis?

A

CXR - LA enlarged
ECG - Afib, M shaped P waves due to LA enlarged
GS - ECHO - Assess valve area

411
Q

What is the Treatment for Mitral Valve Stenosis?

A

Diuretics - Furosemide
Rate control
Anticoagulants

Surgical:
Percutaneous balloon Valvotomy - Stent opening mitral valve
Mitral valve replacement

412
Q

What is the main cause of Mitral Valve Regurgitation?

A

Myxomatous Mitral Valve
Connective tissue disorders - Marfans, Ehlers Danlos
Infective Endocarditis

413
Q

What are the risk factors for Mitral Valve Regurgiation?

A

Females
Increased Age
Low BMI
Prior MI or Connective Tissue disorder

414
Q

What are the symptoms of Mitral Valve Regurgitation?

A

Exertion Dyspnoea - due to Pulmn HTN from backlogged blood
Murmur - PAN SYSTOLIC BLOWING MURMUR

415
Q

What is the pathogenesis of Mitral Valve regurgitation?

A

Mitral valve fails to prevent reflux of blood into LA
Increased LA pressure
increased pulmonary pressure
Pulmonary Oedema

416
Q

What is the Murmur Like in Mitral Valve Regurgitation?

A

PAN SYSTOLIC BLOWING murmur
RADIATES to AXILLA
Loudest at APEX

Soft S1 and Prominent S3 in heart failure (severe cases)

417
Q

What is the diagnostic investigations for mitral valve regurgitation?

A

Gold standard = ECHO - LA size and LV function analysis
ECG
CXR

418
Q

What is the second most common valvular condition requiring surgery?

A

Mitral Valve Regurgitation

419
Q

How is Mitral Valve Regurgitation Treated?

A

ACEi + beta blockers
Serial ECHO Monitoring

If severe (Sx at rest) then Valve repair/replacement

420
Q

What is the normal area of the aortic valve?

A

3-4cm^2

421
Q

What is the lumen size of the aortic valve when you get symptoms?

A

1/4 of the lumen size

422
Q

What is the most common valve disorder?

A

Aortic Stenosis

423
Q

What are the consequences of Aortic Valve Stenosis?

A

LV dilation and hypertrophy

424
Q

What are the causes of Aortic Stenosis?

A

Congenital Bicuspic valve <70yrs
Calcification due to Age >70yrs

Rheumatic Valvular Disease

425
Q

What are the 3 types of aortic valve stenosis?

A

Supravalvular
SubValvular
Valvular

426
Q

What is the pathogenesis of Aortic Valve stenosis?

A

Ageing leads to aortic valve thickening and clacifications obstructing the normal LV outflow.
Increased afterload
Leads to increased LV pressure and compensatory LV hypertrophy.

May lead to relative ischaemia causing angina arrhythmia and LV failure

427
Q

What are the symptoms of aortic valve stenosis?

A

SAD:
Syncope (exertional)
Angina
Dyspnoea - related to HF

Murmur - EJECTION SYSTOLIC CRESCENDO DECRESCENDO

428
Q

What is the Murmur like in aortic valve stenosis?

A

Ejection Systolic Crescendo Decrescendo
Radiates to CAROTIDS
At Right sternal Boarder - 2nd IC space

Prominent S4 seen in LVH
Narrow pulse presssure

429
Q

What is the diagnostic investigations for aortic valve stenosis?

A

ECHO - LV size and function, aortic valve area (doppler derived gradient)
ECG - LVH
CXR

430
Q

What is the treatment for Aortic Valve stenosis?

A

Surgical Tx if symptomatic:
Healthy Px - Open repair/replacement
More at risk (>75yrs) TAVI - transcutaneous valve implant

431
Q

What are the main causes of Aortic valve regurgitation?

A

Congenital Bicuspid Valve
RHD
Connective tissue disorders - Marfans, Ehlers Danlos

432
Q

What is the pathophysiology of Aortic Regurgitation?

A

Leakage of blood back into the LV during diastole due to ineffective closure of the cusps
LV dilation and hypertrophy to maintain CO
Reduced diastolic BP
Relative ischaemia
Leads to LV failure

433
Q

What are the signs and symptoms of Aortic Reguritation?

A

Signs:
Quincke - nailbed pulases when pressed
De Musset - Head bobbing signs
Wide pulse pressure
LV failure
Early Diastolic Murmur
Austin Flint Murmur (severe)

Symptoms:
Angina
Dyspnoea - on exertion

434
Q

What is the murmur like in Aortic Regurgitation?

A

EARLY DIASTOLIC BLOWING murmur
At RIGHT Sternal boarder - 2nd IC space

Austin Flint murmur (severe)

435
Q

What is the Diagnostic investigations for Aortic Regurgitation?

A

ECHO - Evaluate Aortic valve root and dimensions
ECG
CXR

436
Q

What are the treatments for Aortic Regurgitation?

A

Consider Infective endocarditis prophylaxis - Also considered as a DDx
Vasodilators (ACEi to improve SV and reduce regurgitance if Px is asymptomatic or HTN)
Surgical Valve replacement if symptomatic

437
Q

What is Infective Endocarditis?

A

Infection of the heart valves or other endocardial lined structure within the heart (e.g. septal defects, pacemaker leads, surgical patches)

438
Q

What are the different types of Infective Endocarditis?

A

Left-sided Native (mitral or aortic)
Left-sided Prosthetic (early - within a year, late - after a year)
Right-sided IE (rarely prosthetic).
Device related (e.g. pacemakers, defibrillators)

439
Q

How does the nature of Infective Endocarditis affect the outcome?

A

Left-sided; are more likely to cause thrombo-emboli systematically.
Right-side more likely to spread to cause a pulmonary embolism

440
Q

What are the Causes of Infective Endocarditis?

A

Bacteria:
S.aureus (most common in IVDU, T2DM, surgery)
S. Viridans
P.aeruginosa
S.bovis
HACEK Organisms

441
Q

What are the risk factors for Infective Endocarditis?

A

Male, Elderly, Prosthetic Valves
Young IV Drug user
Young w/Congenital heart defect
Rheumatic Heart Disease

442
Q

Where does Infective endocarditis usually affect?
When may it affect other regions?

A

Usually Mitral valve (LHS)
In IVDU it will more commonly affect Tricuspid Valve (RHS)

443
Q

What is the Pathogenesis of Infective Endocarditis?

A

Abnormal/damaged endocardium leads to increased platelet deposition.
Bacteria virulence factors can adhere to this
Vegetation Propagation involves activation of clotting cascade
Inhabiting MOs cause cardiac valve distortion and cardiac failure + sepsis
Typically around the valves

444
Q

What is a common consequence of Infective Endocarditis?

A

Valvular Regurgitation
Than can lead to Ventricular insufficiency and subsequent increased risk of HF

445
Q

What are the symptoms of Infective Endocarditis?

A

Fever + Non-specific Symptoms
New valve regurgitation
Sepsis
Emboli of unknown origin

446
Q

What are the specific signs of infective endocarditis?

A

OSLER NODES - Finger nodules
JANEWAY LESIONS - Painful marks on hands
SPLINTER HAEMORRHAGES - on finger nails
ROTH SPOTS - Retinal Haemorrhage

447
Q

What are the diagnostic investigations for infective endocarditis?

A

Made using DUKE CRITERIA - 2 major or 1 major + 2 minor:
Major:
Positive blood culture with typical IE microorganism
Echocardiograph showing endocardial involvement (e.g. vegetation, abcess) or new valvular regurgitation.
Minor:
Fever (>38)
Pre-disposing factor (e.g. predisposing heart condition, IV drug user)
Vascular phenomena (e.g. major arterial emboli, septic pulmonary infarcts, intracranial haemorrage, Janeway lesions, conjunctival haemorrhage)
Immunological problems (e.g. glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor)
Microbiological evidence (e.g. positive blood culture (non-IE typical microorganism) or serological evidence of infection with organism consistent with IE)

448
Q

What are the two main sites vegetation adheres to in IE?

A

Atrial surface of AV valves
Ventricular surface of SL valves.

449
Q

What is the Treatment for Infective Endocarditis?

A

S.aureus - Vancomycin + rifampicin ( +gentamycin if prosthetic valve)

S.viridans - Benzypenicillin + gentamycin for 4-6 weeks

Surgery - remove valve if incompetent and replace with prosthetic

450
Q

What are the complications of infective endocarditis?

A

Heart failure
Aortic root abscess
Septic emboli
Sepsis

451
Q

Define Heart Failure

A

Inability of the heart to deliver blood thus oxygen that is commensurate with the requirement of the metabolising tissues despite normal or increased cardiac filling

452
Q

How is HF categories by the New York Heart Association (NYHA)?

A
  • Class I - no limitation (asymptomatic)
  • Class II - slight limitation (mild HF)
  • Class III - marked limitation (symptomatically moderate HF)
  • Class IV - inability to carry out any physical activity without discomfort (symptomatically severe HF)
453
Q

What is the median age for Heart Failure?

A

80-years-old (men; 78, women; 82)

454
Q

What is Ejection Fraction?

A

Measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction

455
Q

What is the normal range for Ejection Fraction?

A

65-75%

456
Q

What are the 2 main pathologies of heart failure?

A

Systolic Heart failure - blood cant be pumped out of the LV well enough

Diastolic Heart Failure - Not enough blood fills the ventricles during diastole

In both cases blood builds up in the lungs causing congestion and fluid build up.2

457
Q

What are the different types of Heart Failure?

A

HF-Reduced Ejection Factor (Left Ventricular Ejection Factor <40%)

HF-Preserved Ejection Factor (Left Ventricular Ejection Factor >50% with dilated LA(>34ml/m2 AND and LVH)

HF-Pulmonary Hypertension (Pulmonary Artery Pressure >40mmHg)

HF-Valve (stenosis or regurgitation)

458
Q

What is the most common aetiology of Heart Failure?

A

Myocardial dysfunction resulting from IHD

459
Q

Name some other common causes of Heart Failure.

A

Hypertension
Ischaemic Heart Disease
Alcohol excess
Cardiomyopathy
Valvular disease - Aortic Stenosis, Mitral Regurgitation
Arrythmias - Atrial Fibrillation
Endocarditis
Pericarditis

460
Q

What ejection fraction would suggest borderline HF and Systolic HF?

A

Borderline - 40-50%

Systolic HF - <40%

461
Q

What is the difference between left and right heart failure?

A

Left heart failure would cause congestion in the pulmonary circulation.

Right heart failure would cause congestion in the systemic circulation

Both can affect each other - eg. RHS HF can cause LHS HF

462
Q

What are the main causes of Systolic heart failure?

A

Ischaemic heart disease - myocardial damage/infarction can lead to scarring which doesnt contract and so the EF is reduced

Chronic hypertension - increased afterload causes LV hypertrophy. This increases the O2 demand, and squeezes coronary arteries decreasing O2 supply to the myocardium. Overtime the heart muscle fatigues and becomes inefficient at pumping blood.

Dilated cardiomyopathy - chamber grows and there is increases preload leading to increased contraction strength temporarily. over time the muscle walls get thinner and will end up becoming inefficient

463
Q

What are the main causes of Diastolic heart Failure?

A

Chronic Hypertension can also cause diastolic failure by increasing hypertrophy of LV wall. This then decreases volume of the ventricle leading to a reduced filling room and reduced preload.

Aortic stenosis and hypertrophic cardiomyopathy follows the same pattern as chronic hypertension as there is increased afterload and increased LV hypertrophy

Restrictive cardiomyopathy - less compliant LV walls due to increased stiffness. therefore the walls cannot stretch when filling leading to reduced preload

464
Q

What are the symptoms of Heart failure?

A

Breathlessness (dyspnoea)
Cough
Orthopnoea - SOB on lying flat - relieved by standing (causes crackles on auscultation)
Paroxysmal Nocturnal Dyspnoea
Peripheral Oedema

465
Q

What is Paroxysmal Nocturnal Dyspnoea?

A

Paroxysmal nocturnal dyspnoea is a term used to describe the experience that patients have of suddenly waking at night with a severe attack of shortness of breath and cough.

466
Q

How is Heart Failure diagnosed?

A

Clinical presentation
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)

ECG - ascertain underlying cause - ischaemia, LVH, HTN, Arrhythmia

Echocardiogram - Ascertain underlying cause

CXR - (ABCDE) Alveolar oedema, Kerley Blue lines, Cardiomegaly, Dilated Upper lobe vessels, Plural Effusions

467
Q

What are the key signs of Heart Failure?

A
  • Tachycardia and hypotension
  • Shortness of Breath
  • Fatigue
  • Displaced apex beat
  • Raised JVP - common in RHF
  • Additional heart sounds/ murmurs,
  • Hepatomegaly (e.g. pulsatile/ tender) - RHF
  • Peripheral/ sacral oedema
  • Ascites
468
Q

What are some Risk Factors of Heart Failure?

A

Anything that increases myocardial work:

  • Age over 65 years
  • Men (due to lack of oestrogen protection)
  • Obesity
  • African descent
  • Individuals who have had an MI
  • Alcohol excess
  • Hyperthyroidism
  • Anaemia
  • Pregnancy
469
Q

What lifestyle changes are recommended as a treatment for Heart Failure?

A
  • Avoid large meals
  • Weight loss
  • Smoking cessation
  • Exercise
  • Vaccination
470
Q

What is the first line medical management for Heart Failure?

A

ABAL:
ACEi - Ramipril (ARBs if ACEi contraindicated)
Beta blockers - Bisoprolol
Aldosterone Antagonists - Spironolactone, Eplerenone
Loop Diuretics - Furosemide

471
Q

What is Cor Pulmonale?

A

Right sided Heart failure caused by respiratory disease.

472
Q

What is the pathogenesis of Cor Pulmonale?

A

The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries.

Causes RV Hypertrophy and overtime this will become inefficient leading to HF.

This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.

473
Q

What are some common respiratory causes of Cor Pulmonale?

A

COPD is the most common cause
Pulmonary Embolism
Interstitial Lung Disease
Cystic Fibrosis
Primary Pulmonary Hypertension

474
Q

How do patients with Cor Pulmonale Present?

A

Early Cor pulmonale - Asymptomatic
Later:
SOB
Peripheral Oedema
Dyspnoea - on exertion
Syncope
Chest Pain

475
Q

What are the signs of Cor Pulmonale?

A

Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Third heart sound
Murmurs (e.g. pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

476
Q

What is the Management of Cor Pulmonale?

A

Treat symptoms and underlying cause.

Long term oxygen therapy may be used.

477
Q

What are some end results of Atherosclerosis?

A

Angina
Myocardial Infarction
Transient Ischaemic Attacks
Stroke
Peripheral Vascular Disease
Mesenteric Ischaemia

478
Q

What is Peripheral Vascular Disease?

A

Narrowing of arteries distal to the aortic arch

479
Q

What is the Pathogenesis of Peripheral Vascular Disease?

A

Intermittent Claudication:
Atherosclerosis causing stenosis of arteries and partial lumen occlusion - pain on exertion.

Critical Limb Ischaemia:
Severe occlusion of arteries and blood supply is barely adequate to meet metabolic demand leading to pain at rest and increased risk of gangrene and infection.

480
Q

What are the symptoms of Peripheral Vascular Disease?

A

Varying symptoms:
Asymptomatic
ABPI (ankle brachial Pressure index) <0.9
Bruits (pulsatile regions due to turbulent blood flow)
Intermittent claudication (pain on exercise)
Rest pain (critical limb ischaemia)
Skin ulceration and gangrene.

481
Q

What are some Signs of Peripheral Vascular Disease?

A

Signs: Absent femoral, popliteal or foot pulses. Cold white legs.

482
Q

What can be a complication of acute limb ischaemia?

A

Complete occlusion of the vessel - due to embolic/thrombotic event.
Causes 6 Ps

483
Q

What are the 6Ps of acute complete limb Ischaemia?

A

Pulselessness
Pallor
Pain
Perishingly Cold
Paralysis
Paraesthesia

484
Q

What is the Fontane classification of PVD?

A
  1. Asymptomatic
  2. Intermittent Claudication (pain on exertion)
  3. Chronic Limb Ischaemia (pain at rest)
  4. Ischaemic ulcers - Gangrene
485
Q

What is the diagnosis of PVD?

A

ABPI:
0.5 - 0.9 = Intermitted Claudication
<0.5 = Chronic Limb Ischaemia

Colour Doppler ultrasound - confirm site and degree of stenosis.

CT angiography if surgery considered.

486
Q

What is ABPI and what is the normal range?

A

Compares Blood in post/ant. tibial artery to brachial artery.

0.9-1.3 = normal

487
Q

What is ABPI and what is the normal range?

A

Compares Blood in post/ant. tibial artery to brachial artery.

0.9-1.3 = normal

488
Q

What is the treatment for PVD?

A

Intermittent Claudication - RF management

Chronic Limb Ischaemia - Revascularisation surgery (PCI/Bypass graft)
In Ischaemic limb emergency - PCI within 4-6 hours otherwise amputation.

489
Q

What are the Risk Factors for Peripheral Vascular Disease?

A

Smoking
Hypertension
Ageing
Obesity
CKD
T2DM

490
Q

What are the main complications of PVD?

A

Amputation
Permanent limb weakness
Rhabdomyolysis
Increased risk of CVD.

491
Q

What are the types of aneurysms?

A

True - weakening of arterial wall leading to dilation

False

Mycotic

492
Q

What is an Abdominal Aortic Aneurysm?

A

Permanent dilation of the aorta exceeding 50% where >3cm diameter.
Often Infra-renal (below renal arteries)

493
Q

What are the Risk factors of AAA?

A

Idiopathic,
Smoking, obesity, HTN, Family Hx
Connective tissue disorders - Marfans, Ehlers Danlos

494
Q

What is the Pathogenesis of AAA?

A

Smooth muscle, elastic and structural degradation of the vascular wall in ALL 3 LAYERS of the vascular tunic.
Increased Leukocyte infiltration leads to increased vessel diameter to > 3cm +

495
Q

What diameter of an AAA is at increased risk of rupture?

A

AAA more than 5.5cm diameter

496
Q

What happens if the AAA ruptures?

A

Medical Emergency requires immediate surgical repair
80% mortality prior to reaching hospital.

497
Q

What are the symptoms of an Unruptured AAA?

A

Usually asymptomatic

498
Q

What are the symptoms of a ruptured AAA?

A

Sudden epigastric pain,
Radiating to flank
Pulsatile mass in abdomen
Hypotensive and Tachycardic

499
Q

What is a differential Diagnosis of a ruptured AAA?

A

Acute pancreatitis.
Does not tend to have a pulsatile feel.

500
Q

What is the diagnostic investigation of AAA?

A

Abdominal Duplex Ultrasound
If ruptured then none - medical Emergency

501
Q

What is the Treatment of an AAA?

A

Unruptured - manage RF

ASx and <5.5cm - monitor

Sx and>5.5 - surgery (endovascular repair or open surgery)

502
Q

What is the Treatment of a Ruptured AAA?

A

Stabilise ABCDE + fluids
AAA Graft surgery repair.

503
Q

What is the incidence of an AAA?

A

25/100,000 incidence at 50yrs.
Rises with age.
Males

504
Q

What is an Aortic Dissection?

A

Tear in the intima resulting in blood dissecting through the tunica media causing separation of the layers of the aortic wall.

505
Q

What are causes of Aortic Dissection?

A

Genetic link, Atherosclerosis, Inflammatory, Trauma:

Mechanical stress causes a tear in the intima of the aortic lining.
This causes blood to enter the aortic wall under pressure causing a haematoma and separates the layers.

506
Q

What are the risk factors for Aortic Dissection

A

Connective tissue disorders - Marfans, Ehlers Danlos
Hypertension
Cocaine Use
Aortic Aneurysm
Smoking
Hypercholesterolaemia

507
Q

What are the most common locations of an Aortic Dissection?

A

Sinotubular junction - Aortic root near aortic valve
Just distal to Left Subclavian Artery (descending thoracic aorta)

508
Q

What are the symptoms of Aortic Dissection?

A

Phase 1: Initial event; severe ‘ripping’ pain and pulse loss. The bleeding then stops. Diastolic murmur

Phase 2: Pressure builds, and causes a rupture, either into pericardium (tamponade), mediastinum or pleural space.

Pain often migrates as dissection progresses.

509
Q

What is the Diagnosis of Aortic Dissection?

A

Transoesophageal ECHO OR CT angiogram (if Px is haemodynamically stable)
Shows intimal Flap and False lumen

CXR - Shows widened mediastinum

510
Q

What are the treatments for Aortic Dissection?

A

Surgical:
Open repair/Endovascular aortic repair

Medication (to reduced HR and BP):
Special Beta Blockers - Esmolol
Vasodilator - Sodium Nitroprusside

511
Q

What are some complications of Aortic Dissection?

A

Cardiac Tamponade
Aortic Insufficiency
Pre renal AKI
Stroke - Ischaemic

512
Q

What is an Arrhythmia?

A

An abnormal electrical conduction in the heart causing a beat disturbance.

513
Q

Define tachycardia.

A

> 100 bpm.

514
Q

Define bradycardia.

A

< 60 bpm.

515
Q

Give 3 potential consequences of arrhythmia.

A
  1. Sudden death.
  2. Syncope.
  3. Dizziness.
  4. Palpitations.
  5. Can also be asymptomatic.
516
Q

Give the two broad categories of tachycardia.

A
  1. Supra-ventricular tachycardia’s.
  2. Ventricular tachycardia’s.
517
Q

Where do supra-ventricular tachycardia’s arise from?

A

They arise from the atria or atrio-ventricular junction.

518
Q

Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?

A

Supraventricular tachycardias are often associated with narrow complexes.

519
Q

Name 5 supra-ventricular tachycardia’s.

A
  1. Atrial fibrillation.
  2. Atrial flutter.
  3. AV node re-entry tachycardia (AVNRT) - Most common SVT
  4. Accessory pathway - Wolfson Parkinson White
  5. Focal atrial tachycardia. (sinus Tachycardia)
520
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles.

521
Q

Do ventricular tachycardia’s have narrow or broad QRS complexes?

A

Ventricular tachycardias are often associated with broad complexes.

522
Q

Name 2 Ventricular Tachycardias?

A

Ventricular Tachycardia
Ventricular Fibrillation

523
Q

Name 3 arrhythmias that come under Bradycardia rhythms?

A

RBBB / LBBB
1, 2, 3 Heart Block
Sinus Bradycardia

524
Q

What is atrial Fibrillation?

A

Irregularly irregular atrial firing Rhythm

525
Q

What are the causes of AF?

A

Heart Failure
HTN
secondary to mitral valve stenosis
Idopathic

526
Q

What are the risk factors for AF?

A

60+
T2DM
HTN
Valve defects
Hx of MI

527
Q

What is the pathogenesis of AF?

A

Rapid re-entrant ectopic foci (300-600 Bpm)
Causes atrial spasm
Causes atrial blood to pool and therefore reduces CO and increases risk of thromboembolic events.

528
Q

What are the symptoms of AF?

A
  1. Palpitations.
  2. Shortness of breath.
  3. Fatigue.
  4. Chest pain.
  5. Increased risk of thromboembolism and therefore stroke.
529
Q

What are the different types of AF?

A

Paroxysmal (episodic)
Persistent (longer than 7 days)
Permanent (sinus Rhythm unrestorable)

530
Q

What is the diagnosis of AF?

A

ECG is diagnostic
Irregularly Irregular pulse w/ narrow QRSs <120ms
No P waves (fibrillatory squiggles)

531
Q

What is the Treatment of AF?

A
  1. Rate control - beta blockers, CCB and digoxin.
  2. Rhythm control - electrical cardioversion or pharmacological cardioversion using flecainide.
  3. Flecainide can be taken on a PRN basis in people with infrequent symptomatic paroxysms of AF.
  4. Long term - catheter ablation and a pacemaker.
532
Q

What score can be used to calculate the risk of stroke in someone with atrial fibrillation?

A

CHADS2 VASc.

533
Q

What does the CHADS2 VASc score take into account?

A
  1. Age.
  2. Hypertension.
  3. Previous stroke/TIA.
  4. Diabetes.
  5. Female.

A score >2 indicates the need for anticoagulation.

534
Q

Atrial fibrillation treatment: what might you give someone to help with rate control?

A

Beta blockers, CCB and digoxin.

535
Q

Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?

A

Electrical cardioversion or pharmacological cardioversion using flecainide.

536
Q

What is the long term treatment of atrial fibrillation?

A

Catheter ablation - it targets the triggers of AF.

537
Q

What are some complications of AF?

A

Heart failure
Ischaemic stroke
Mesenteric Ischaemia

538
Q

What is Atrial Flutter?

A

Irregular organised atrial firing
250-350 bpm

539
Q

What are the risk factors of atrial flutter?

A

Similar to aetiology of AF

540
Q

What is the pathogenesis of Atrial flutter?

A

Atrial flutter is caused by a “re-entrant rhythm” in either atrium.
This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway.
The signal goes round and round the atrium without interruption.
This stimulates atrial contraction at 300 bpm.
The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction.
It gives a “sawtooth appearance” on ECG with P wave after P wave.

541
Q

What are the symptoms of atrial flutter?

A

Dyspnoea
Palpitations

542
Q

What is the diagnosis of Atrial flutter?

A

F wave - saw tooth pattern
Often has a 2:1 block - 2 p waves for every 1 QRS

543
Q

What is the treatment of Atrial flutter?

A

Acutely unstable - DC Synchronised Cardioversion
Stable - Rhythm/Rate control w/ oral coagulation (prevent thromboemboli)
Radiofrequency ablation - long term

544
Q

What is Wolf parkinson White?

A

An AVRT which means there is an accessory pathway that exists for impulse conduction called the bundle of Kent.
This is a Pre excitation syndrome (excites ventricles early causing a delta wave)
This is not re-entry through the AVN.
Often hereditary

545
Q

What are the symptoms of Wolf parkinson white?

A

Palpitations
Dizziness
Dyspnoea

546
Q

What is the ECG of Wolf parkinson white?

A

Slurred DELTA WAVES
Short PR interval (<0.12s)
Wide QRS (>0.12s)

547
Q

What is the treatment of Wolf Parkinson White?

A
  1. Valsalva Manoeuvre
  2. IV adenosine (6mg, then 12mg then 12mg) to cease conduction.
  3. Consider surgical radiofrequency ablation
548
Q

What conditions can radiofrequency ablation be curative for?

A

Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolf parkinson White syndrome

549
Q

What is Long QT syndrome?

A

A ventricular Tachyarrhythmia typically caused by a congenital channelopathy where mutations affect ion channels.
This causes the QT interval to be 480ms +

550
Q

What are some causes of Long QT syndrome?

A

Romano ward syndrome
Hypokalaemia and Hypocalcaemia
Drugs - Amiodarone/magnesium

551
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 into ventricular fibrillation.

552
Q

What is ventricular fibrillation?

A

Shapeless rapid osscillations on ECG
patients becomes pulseless and goes into cardiac arrest - no effective cardiac output

553
Q

What is the first line treatment for Ventricular fibrillation?

A

Electrical defibrillation

554
Q

What are the narrow complex tachycardias?

A

Rapid cardiac rhythm > 100bpm, QRS complex <120ms:

Supraventricular tachycardia

Atrial fibrillation/flutter

555
Q

What are the broad complex tachycardias?

A

Rapid cardiac rhythm >100bpm, QRS complex >120ms

Ventricular tachycardia

Supraventicular tachycardia with bundle branch block/pre-excitation

556
Q

Give 4 causes of sinus bradycardia.

A
  1. Ischaemia.
  2. Fibrosis of the atrium.
  3. Inflammation.
  4. Drugs.
557
Q

Give 3 causes of heart block.

A
  1. CAD.
  2. Cardiomyopathy.
  3. Fibrosis.
558
Q

What are the 3 types of AV block?

A

First degree

Second degree - Mobitz type I and Type II

Third degree

559
Q

What does first degree AV block look like on an ECG?

A

1:1 conduction - Every P wave has QRS followed
Prolonged PR interval >200ms

560
Q

What are the symptoms of First Degree AV Block?

A

No symptoms
No treatment

561
Q

What can cause first degree AV block

A

Drugs - block AVN conduction.
bB
CCB
Digoxin

562
Q

What does second degree AV block look like on an ECG?

A

When some P waves are conducted and others aren’t
2:1 conduction - Every other P wave is followed by a QRS complex

563
Q

What are the types of Second degree AV block?

A

Mobitz I
Mobitz II

564
Q

What is Mobitz type I heart block?

A

PR interval gradually increases until AV node fails and no QRS is seen.
This then Repeats

565
Q

What is Mobitz type 2 Heart Block.

A

PR interval is constant but every nth QRS complex is missing.
There is a sudden unpredictable loss of AV conduction and so loss of QRS.

566
Q

What is the treatment for second degree heart block?

A

Pacemaker

567
Q

What are some causes of Mobitz Type I and type II?

A

Type I - Beta blockers, CCB, Dixogin, inferior MI

Type II - Inferior MI, Rheumatic Fever

568
Q

What is 3rd degree AV block?

A

Atrial activity fails to conduct to the ventricles.
P waves and QRS complexes therefore occur independently.

569
Q

What can cause 3rd degree heart block?

A

Acute MI
HTN
Structural heart disease

570
Q

What is the treatment for 3rd degree heart block?

A

IV Atropine
Permanent Pace maker

571
Q

What is the Pathogenesis of Bundle Branch Block?

A

Where electrical conduction down the left/right bundle branch in the bundle of HIS/septum is blocked/delayed often by fibrosis.
This causes the impulse conduction to the ventricles to occur at different times creating a second R wave in the leads associated with the right/left ventricles on an ECG.

In LBBB - LV contraction later than RV
In RBBB - RV contraction later than LV

572
Q

Give the causes of Left/Right Bundle Branch Block?

A

Left - IHD, valvular disease

Right - PE, IHD, valvular disease

573
Q

LBBB: what would you see in lead V1 and V6?

A

A ‘W’ shape would be seen in the QRS complex of lead V1 and a ‘M’ shape in V6.

WiLLiaM.

574
Q

RBBB: what would you see in lead V1 and V6?

A

A ‘M’ shape would be seen in the QRS complex of lead V1 and a ‘W’ shape in V6.

MaRRoW.

575
Q

What ECG changes are you likely to see in ischaemia and infarction?

A

T wave flattening and inversion

ST segment depression first → progresses to ST elevation

Q waves (old infarction)

576
Q

Infarction involving the left anterior descending coronary artery will give rise to changes in which ECG leads?

A

Anterior leads: V2, V3, V4

577
Q

Infarction involving the L circumflex coronary artery will give rise to changes in which ECG leads?

A

Lateral: V5, V6

578
Q

Infarction involving the R coronary artery will give rise to changes in which ECG leads?

A

Inferior: II, III, aVF

579
Q

Give 3 effects of hyperkalaemia on an ECG.

A
  1. Tall ‘tented’ T waves.
  2. Flat P waves.
  3. Broad QRS.
580
Q

Give 2 effects of hypokalaemia on an ECG.

A
  1. Flat T waves.
  2. QT prolongation.
  3. ST depression.
  4. Prominent U waves.
581
Q

Give an effect of hypocalcaemia on an ECG.

A
  1. QT prolongation.
  2. T wave flattening.
  3. Narrowed QRS.
  4. Prominent U waves.
582
Q

Give an effect of hypercalcaemia on an ECG.

A
  1. QT shortening.
  2. Tall T waves.
  3. No P waves.
583
Q

What is Deep Vein Thrombosis?

A

When a thrombus forms in deep leg vein
Below calf - less concerning and most common
Above calf/thigh - life threatening

584
Q

What are the Risk factors for DVT?

A

Virchows triad:
Venous Stasis
Hypercoagulability
Endothelial Injury

OC pill
HRT
Pregnancy

585
Q

What are the symptoms of DVT?

A

Unilateral swollen calf/engorged leg veins
Typically warm
Oedematous
In severe oedema - leg turns blue

586
Q

What is the diagnosis of DVT?

A

Clinical history + WELLs Score >1

D-dimer raised and Duplex ultrasound (gold standard)
(D dimer normal excludes DVT, but positive does not confirm)

CT or MR venogram

587
Q

What is the treatment of DVT?

A

DOAC anticoagulant therapy
Apixaban
LMWH (if above CI in renal impairment)

588
Q

What are some important differential diagnoses of DVT?

A

Cellulitis - S.aureus / S.pyogenes
Leukocytosis

589
Q

Why does DVT lead to ischaemia and loss of leg?

A

DVT leads to increased compartment pressure resulting in venous hypertension.
This can compress the arterioles reducing their blood suplly and resulting in ischaemia to the local tissues.

590
Q

What is the prevalence of DVT/PE?

A

25,000 people die per year due to DVT/PE in the UK

591
Q

How can DVT be prevented?

A

Mechanical:
Hydration
Early mobilisation
Compression stockings

Chemical:
LMWH

592
Q

What pathophysiological features will cause a murmur

A

Increased Turbulent blood flow:

Increased Velocity of blood:
- Through a stenosed valve/ narrow VSD/ASD
- Increased contractile strength of myocardium
- Decreased Diameters - through HOCM narrowing the exit of the ventricle to the Aorta

Decreased Viscosity of blood - through anaemia

Blood flow back across incompetent valves

593
Q

Where do you listen to different Murmurs/ Heart sounds?
What is the Mnemonic to remember them?

A

All Physicians Earn Too Much:

Aortic Valve - R. 2nd ICS - CoA, AS, AR
Pulmonic Valve - L. 2nd ICS - PS, PR, ASD
ERBS Point - L 3rd ICS - S1 +S2, HOCM
Tricuspid Valve - L 4th ICS - TS, TR, VSD
Mitral Valve - L 5th ICS, (MCL) - MR, MS

594
Q

Where would a murmur caused by Aortic Stenosis best be heard and where would it radiate to?

A

Best Heard - Right parasternal boarder, 2nd intercostal space

Radiates to - Carotids as it flows up through the aortic arch vessels

595
Q

Where would a murmur caused by Aortic Regurgitation best be heard and where would it radiate to?

A

Best Heard - Right Parasternal Boarder, 2nd intercostal space

Radiates to - Left upper sternal boarder (2nd/3rd ICS) due to blood flowing back across the left side of the heart

596
Q

Where would a murmur caused by mitral regurgitation best be heard and where would it radiate to?

A

Best Heard - Left 5th ICS, mid clavicular line

Radiates to - Axilla as blood is flowing up into the left atria which is towards the axilla

597
Q

What would a blowing (musical Murmur) suggest?

A

Blowing Murmurs are usually regurgitation murmurs:
Aortic Regurgitation
Mitral Regurgitation

598
Q

What would a Rumbling (Harsh) murmur suggest?

A

Valvular Stenosis:
Aortic Stenosis
Mitral Stenosis

599
Q

What would a Machine Like Murmur suggest?

A

Patent ductus Arteriosus

600
Q

what kind of pitch would a VSD murmur have?

A

High pitch
due to high pressure gradients as the blood flows from the LV to the RV through the VSD

601
Q

What kind of pitch would a Mitral stenosis murmur have?

A

Low pitch
Due to low pressure gradient from the atria to the ventricles
But high blood flow across the valve creates a low pitch

602
Q

What kind of pitch would a Aortic Stenosis/ Aortic Regurgitation /Mitral regurgitation murmur have?

A

Harsh High pitch
High pressure gradients
High blood flow across the valve

603
Q

What conditions would cause an Early Systolic Murmur?
What is the motion of the murmur?

A

Aortic/Pulmonic Stenosis:

Valves are rigid and so upon LV contraction the valves bow (not open properly) causing an EJECTION CLICK sound as blood hits the underside of the valve.
CRESCENDO DECRESCENDO murmur as the blood velocity increases during systole and then falls of as the blood is ejected

HOCM:
CRESCENDO DECRESCENDO murmur with NO ejection click

Coarctation of the Aorta

604
Q

What conditions would cause an Holo-Systolic Murmur?
What is the motion of the murmur?

A

Mitral/Tricuspid Regurgitation:
Murmur occurs through entire systolic time period as blood is flowing back across the valve into the atria the entire time the ventricles contract

VSD:
As the LV contracts blood is flowing across the VSD into the RV causing turbulent flow in the RV.

605
Q

What conditions would cause an Diastolic Murmur?
What is the motion of the murmur?

A

Aortic/Pulmonic Regurgitation:
During Early diastole (right at the start) the LV pressure decreases so blood can back flow across the Aortic valve hitting the LV wall causing turbulent flow Lots of blood flows in early diastole which falls off in late diastole. This causes a DECRESCENDO Murmur

Mitral/Tricuspid Stenosis:
OPENING SNAP (immediately at the start of diastole) followed by lots of blood entering the ventricles in early diastole which then reduces as diastole progresses causing a DECRESCENDO murmur

606
Q

What kind of murmur would be heard in a Patent Ductus Arteriosus?

A

A Continuous “Machine” Murmur
due to a constant shunt from the aorta to the pulmonary artery

607
Q

Where does thrombosis occur?

A

Arterial circulation - High pressure (platelet rich)

Venous Circulation - Low pressure (fibrin rich)

608
Q

What are the main sites for Arterial thrombosis?

A

Coronary
Cerebral
Peripheral
Other sites

609
Q

What can lead to arterial thrombosis development?

A

Atherosclerosis
Inflammatory
Infection
Trauma
Tumours
Unknown

610
Q

What conditions can arterial thrombosis lead to?

A

Myocardial Infarction
Cerebral Vascular Disease
Peripheral Vascular Disease

611
Q

What is the Treatment for Arterial thrombosis?

A

Anti-platelets:
Aspirin
LMWH or Fondraparinux

Thrombolytic therapy:
Streptokinase OR TpA

Reperfusion - PCI

612
Q

Why is heparin avoided to treat cerebral vascular disease/ cerebral thrombosis

A

Heparin has a high risk of bleeding

613
Q

What are the main sites of venous thrombosis?

A

Peripheral - Ileofemoral, Femoro-popliteal
Other sites - Cerebral, Visceral

614
Q

What diagnostic tests are required for Venous thrombosis diagnosis?

A

Signs and Sx are very non-specific
Blood tests - D-dimer - sensitive but not specific

Imaging usually required

615
Q

What is the main group of factors that leads to venous thrombosis?

A

Virchows Triad

616
Q

What is important for Venous thrombosis prevention?

A

Mechanical/chemical thromboprophylaxis

Early mobilisation and good hydration

617
Q

What are the treatments for Venous thrombosis?

A

Anti-Coagulants:
Heparin/LMWH
Warfarin
DOAC

618
Q

What is Heparin and how does it work?

A

Glycosaminoglycan

Given by Infusion
Binds to anti-thrombin and increases its activity.
Indirect thrombin inhibitor

619
Q

What is the half life of Heparin and how is it monitored?

A

4 hours
Monitor with APTT (anti-prothrombin time)

620
Q

What is LMWH?

A

Smaller molecule of heparin that is excreted renally.
Weight adjusted dose given via SC injection

Used for Tx and Prophylaxis

621
Q

What is the Half lifeof LMWH?

A

12 hours and therefore can be given once daily and not necessarily needed to be monitored

622
Q

What is Warfarin?

A

Anticoagulant that prolongs the Prothrombin time
Prevents synthesis of Active factors II, VII, IX, X

Antagonist of Vitamin K

623
Q

How can warfarin be reversed?

A

Give Vitamin K

624
Q

What is the half life of Warfarin?

A

36 hours

625
Q

What are NOACs/DOACs?

A

New oral anticoagulant drugs/ Direct oral anticoagulant drugs

Directly act on Factor II or X

626
Q

What is NOAC/DOAC used for?
When would NOAC/DOAC not be used

A

Extended thromboprophylaxis and treatment of AF, DVT and PE

Not used in pregnancy

627
Q

What is the mechanism of action of Aspirin?

A

Inhibits Cyclo-oxygenase irreversibly.

Prevents thromboxane formation and therefore inhibits platelet aggregation

628
Q

What is a pulmonary embolism?

A

When an embolus (often from a thrombus/DVT) travels through the venous circulation and into the pulmonary circulation to get lodged in the pulmonary vasculature.

629
Q

What are the symptoms of PE?

A

Signs:
Tachycardia
Tachypnoea
Pleural rub

SX:
Breathlessness
Pleuritic chest pain
High RFs

630
Q

What are some differential diagnoses to think of for PE?

A

DDx of chest pain and SOB

631
Q

What are the initial investigations for PE?

A

CXR - usually normal
ECG - Sinus Tachy - S1Q3T3

D-Dimer and CTPA (GS - CT scan and Pulmonary angiogram)
Blood gases - Type I resp failure (Decreased O2/CO2)

632
Q

What is the treatment of PE?

A

Supportive Tx and Tx underlying cause

Apixaban
DOAC
LWMH (if CI for renal impairment)

633
Q

What can be done to prevent PE?

A

Early mobilisation and hydration.
Anticoagulation

634
Q

How would a Massive PE be Tx?

A

Thrombolytics - Alteplase (clot buster)

635
Q

When would you hear S3 in pathology?

A

Left ventricular failure (DCM)
Constrictive pericarditis
Mitral Regurgitation

636
Q

When would you hear S3 in pathology?

A

Left ventricular failure (DCM)
Constrictive pericarditis
Mitral Regurgitation

637
Q

When would you hear S4 in pathology?

A

Aortic stenosis
HOCM
Hypertension

Phase 2a (24 decks)

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