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Phase 3a General Practice and Community > New GP Cardiovascular > Flashcards

New GP Cardiovascular Flashcards

1
Q

Define peripheral arterial disease (PAD)

A

Narrowing of the arteries supplying the limbs and periphery → reducing the blood supply to these areas.

It usually refers to the lower limbs → resulting in symptoms of claudication.

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2
Q

What is intermittent claudication?

A

= symptom of ischaemia in the limb
* Occurs during exertion; relieved by rest.
* Typically a crampy,achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity.

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3
Q

What is critical limb ischaemia?

A

The end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest.

There is a significant risk of losing the limb

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4
Q

What are the features of critical limb ischaemia?

A
  • Pain at rest
  • Non-healing ulcers
  • Gangrene
  • Pain = worse at night when the leg is raused and gravity no longer helps pull blood into the foot
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5
Q

What a difference between intermittent claudication and critical limb ischaemia?

A
  • Intermittent claudication → pain relieved at rest
  • Critical limb ischaemia → pain at rest
  • Intermittent claudication = symptom of ischaemia in limb
  • Critical limb ischaemia = end-stage PAD
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6
Q

What is acute limb ischaemia?

A

= Rapid onset of ischaemia in a limb
* Typically due to a thrombus (clot) blocking the arterial supply of the distal limb
* (Similar to a thrombus blocking a coronary artery in myocardial infarction)

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7
Q

Define ischaemia

A

Inadequate oxygen supply to the tissues - due to reduced blood supply

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8
Q

Define gangrene

A

Death of tissue (necrosis) - specifically due to an inaquate blood supply

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9
Q

What is atherosclerosis?

A

Combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls).

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10
Q

What sized vessels does atherosclerosis effect?

A

Medium and large arteries

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11
Q

What causes atherosclerosis?

A

Chronic inflammation + activation of the immune system in the artery wall

Lipids = deposited in the artery wall → followed by the development of fibrous atheromatous plaques

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12
Q

What do atherosclerotic plaques cause?

A
  • Stiffening of the artery walls → leading to hypertension + and strain on the heart (whilst trying to pump blood against increased resistance)
  • Stenosis → leading to reduced blood flow (e.g., in angina)
  • Plaque rupture → resulting in a thrombus that can block a distal vessel and cause ischaemia (e.g., in acute coronary syndrome)
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13
Q

Name 3 non-modifiable risk factors for atherosclerosis

A
  • Older age
  • Family history
  • Male
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14
Q

Name 3 modifiable risk factors for atherosclerosis

A
  • Smoking
  • Alcohol consumption
  • Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s)
  • Low exercise / sedentary lifestyle
  • Obesity
  • Poor sleep
  • Stress
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15
Q

Name a couple of medical co-morbidities that increase the risk of atherosclerosis (which therefore should be carefully managed to minimise the risk)?

A
  • Diabetes
  • Hypertension
  • Chronic kidney disease
  • Inflammatory conditions (e.g. rheumatoid arthritis)
  • Atypical antipsychotic medications
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16
Q

What questions should you take in a history from someone presenting with suspected atherosclerotic disease (e.g. intermittent claudication)?

A
  • Excerise
  • Diet
  • Alocohol intake + smoking
  • PMH
  • FHx
  • Occupation
  • Medications
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17
Q

Name a couple of end results of atherosclerosis

A
  • Angina
  • Myocardial infarction
  • Transient ischaemic attack
  • Stroke
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
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18
Q

How does peripheral arterial disease present in patients?

A

Intermittent claudication

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19
Q

A 62 year old patient attends your clinic and describes a crampy pain in his calf muscles that occurs after walking a certain distance, however after stopping the pain disappears. Possible diagnosis?

A

Intermittent claudication

Crampy pain also occurs in the thighs and buttocks

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20
Q

What are the 6Ps of acute limb ischaemia?

A
  • Pain
  • Pallor
  • Pulseless
  • Paralysis
  • Paraesthesia (abnormal sensation or ‘pins and needles’)
  • Perishingly cold
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21
Q

What is Leriche syndrome?

A

Occurs with occlusion in the distal aorta pr proximal common iliac artery

Clinical triad:
* Thigh/buttock claudication
* Absent femoral pulses
* Male impotence

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22
Q

What is the clinical triad for Leriche syndrome?

A
  • Thigh/buttock claudication
  • Absent femoral pulses
  • Male impotence
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23
Q

What are 2 clinical signs when looking for the risk factors of atherosclerosis?

A
  • Tar staining on the fingers
  • Xanthomata (yellow cholesterol deposits on the skin)
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24
Q

What are some clinical signs of previous substance peripheral arterial disease?

A
  • Missing limbs or digits after previous amputations
  • Midline sternotomy scar (previous CABG)
  • A scar on the inner calf for saphenous vein harvesting (previous CABG)
  • Focal weakness suggestive of a previous stroke
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25
Q

What pulses may be weak on palpation in a patient with PAD?

A
  • Radial
  • Brachial
  • Carotid
  • Abdominal aorta
  • Femoral
  • Popliteal
  • Posterior tibial
  • Dorsalis pedis
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26
Q

If examining a patient with suspected PAD and some pulses are difficult to palpate how do you accurately assess the pulses?

A

A hand-held Doppler

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27
Q

What are the clinical signs of peripheral arterial disease?

A
  • Skin pallor
  • Cyanosis
  • Dependent rubor (a deep red colour when the limb is lower than the rest of the body)
    Muscle wasting
  • Hair loss
  • Ulcers
  • Poor wound healing
  • Gangrene (breakdown of skin and a dark red/black change in colouration)
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28
Q

What on examination may you find in a patient with suscpeted PAD?

A
  • Reduced skin temperature
  • Reduce sensation
  • Prolonged capillary refill time (more than 2 seconds)
  • Changes during Buerger’s test
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29
Q

What test (examination) is used to assess for peripheral arterial disease in the leg?

A

Buerger’s test

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30
Q

Why do you develop ulcers with peripheral arterial disease?

A

Skin + tissues = strugglung to heal - due to impaired blood flow

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31
Q

What is the cause of arterial ulcers?

A

Arterial ulcers = caused by ischaemia secondary to inadequate blood supply

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32
Q

What are the features of arterial ulcers?

A
  • Well defined borders
  • Have a “punched-out” appearance
  • Occur peripherally (e.g., on the toes)
  • Have reduced bleeding
  • Are painful
  • Smaller + deeper than venous ulcers
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33
Q

Why do venous ulcers occur?

A

Venous ulcers = occur by impaired drainage + pooling of blood in the legs

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34
Q

What are the clinical features of a venous ulcers?

A
  • Irregular gently sloping borders
  • Affect teh gaiter area of the leg (from the mid-calf down to the ankle)
  • Occur after a minor injury to the leg
  • Are larger and less painful than arterial ulcers
  • Are more superficial than arterial ulcers
  • Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)
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35
Q

What are the investigations for peripheral arterial disease?

A
  • Ankle-brachial pressure index (ABPI)
  • Duplex ultrasound - ultrasound that shows the speed and volume of blood flow
  • CT or MRI angiography - using contrast to highlight the arterial circulation
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36
Q

What is the ankle-brachial pressure index (ABPI)?

A

Ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm

E.g. Ankle SBP (80)/ Arm SBP (100) = 0.8

Taken manually or using a Doppler probe

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37
Q

What does a ABPI of 1.3 mean?

A

Normal (no PAD)

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38
Q

What does above and below 1.3 ABPI mean?

A
  • Above 1.3 = calcification of arteries
  • Below 1.3 = peripheral arterial disease
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39
Q

What are the ABPI ranges?

A
  • 0.9 – 1.3 = normal
  • 0.6 – 0.9 → mild peripheral arterial disease
  • 0.3 – 0.6 → moderate to severe peripheral arterial disease
  • Less than 0.3 → severe disease to critical ischaemic
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40
Q

What does an ABPI above 1.3 mean?

A

Claification of the arteries → making them difficult to compress
(More common in diabetic patients)

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41
Q

What lifestyle and exercise changes can be done to manage intermittent claudication?

A
  • Lifestyle changes: Modifiable risk factors (e.g. stop smoking). Optimise medical treatment of co-morbidities (hypertension + diabetes)
  • Exercise training: structured and supervised program of regularly walking to the point of near-maximal claudication and pain, then resting and repeating.
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42
Q

What are the medical treatments for intermittent claudification?

A
  • Atorvastatin 80mg
  • Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
  • Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)

Claudication → Clopidogrel

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43
Q

What are the surgical options for intermittent claudification?

A
  • Endovascular angioplasty and stenting
  • Endarterectomy – cutting the vessel open and removing the atheromatous plaque
  • Bypass surgery – using a graft to bypass the blockage

Endovascular treatments (under x-ray) = lower risks. Not for extensive

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44
Q

What is the management for critical limb ischaemia?

A
  • Analgesia for pain

Urgent revascularisation:
* Endovascular angioplasty and stenting
* Endarterectomy
* Bypass surgery
* Amputation of the limb if it is not possible to restore the blood supply

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45
Q

What is the management for acute limb ischaemia?

A
  • **Endovascular thrombolysis **– inserting a catheter through the arterial system to apply thrombolysis directly into the clot
  • Endovascular thrombectomy – inserting a catheter through the arterial system and removing the thrombus by aspiration or mechanical devices
  • Surgical thrombectomy – cutting open the vessel and removing the thrombus
  • Endarterectomy
  • Bypass surgery
  • Amputation of the limb if it is not possible to restore the blood supply
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46
Q

What readings suggest hypertension?

A
  • Clinical setting: Above 140/90 mmHg
  • Ambulatory home readings above 135/85 mmHg
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47
Q

What is essential/primary hypertension?

A

High blood pressure that has developed on its own (does not have a secondary cause).
90% of hypertension

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48
Q

Nmeumonic for secondary causes of hypertension

A

ROPED
* R - Renal disease
* O - Obesity
* P - Pregnancy-induced hypertension or Pre-eclampsia
* E - Endocrine
* D - Drugs (e.g. alcohol, steroids, NSAIDs, oestrogen and liquorice)

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49
Q

What is the most common cause of secondary hypertension?

A

Renal disease
When the blood pressure is very high and does not respond to treatment → consider renal artery stenosis

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50
Q

A patient has very high blood pressure and it is not responding to treatment. The most probable diagnosis is renal artery stenosis. How can this be diagnosed?

A

Duplex ultrasound or an MRI or CT angiogram

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51
Q

What endocrine condition may be present in 5-10% of patients with hypertension?

A

Hyperaldosteronism (Conn’s syndrome)

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52
Q

Name a couple of complications for hypertension

A

Head to toe:
* Cerebrovascular accident (stroke or intracranial haemorrhage)
* Vascular dementia
* Hypertensive retinopathy
* Ischaemic heart disease (angina and acute coronary syndrome)
* Left ventricular hypertrophy
* Heart failure
* Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
* Hypertensive nephropathy

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53
Q

What complication in the heart may patients with hypertension develop?

A

Left ventricular hypertrophy
(The left ventricle is straining to pump blood against increased resistance in the arterial system, so the muscle becomes thicker)

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54
Q

What are the findings of left ventricular hypertrophy on examination?

A

**Sustained + forceful apex beat **

55
Q

What are the investigations for left ventricular hypertrophy?

A
  • ECG: using voltage criteria
  • Gold standard: Echocardiogram
56
Q

How often does NICE recommend you screen for hypertension?

A

Every 5 years
It should be measured more often in borderline cases and every year in patients with type 2 diabetes.

57
Q

What blood pressure difference does a white coat effect involve?

A

More than a 20/10 mmHg difference in BP between clinic + ambulatory or home readings

58
Q

What stage of hypertension is:
* Clinic reading: Above 140/90 mmHg
* Home/Ambulatroy readings: Above 135/85 mmHg

A

Stage 1

59
Q

What stage of hypertension is:
* Clinic reading: Above 160/100 mmHg
* Home/Ambulatroy readings: Above 150/95 mmHg

A

Stage 2

60
Q

What stage of hypertension is:
* Clinic reading: Above 180/120 mmHg

A

Stage 3

61
Q

What invesigations should be performed on a patient with newly diagnosed hypertension?
(For assessing end organ damage)

A
  • Eyes: Fundus examination → hypertensive retinopathy
  • **Heart: **ECG → cardiac abnormalities (left ventricular hypertrophy)
  • Kidneys: Urine albumin:creatinine ratio → proteinuria; dipstick for microscopic haematuria to assess for kidney damage
  • General: Bloods for HbA1c, renal function and lipids
62
Q

What risk score is recommended to use in a pteint that has just been diagnosed with hypertension?

A

QRISK
Estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

When the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.

63
Q

When a person’s QRISK score is above 10% what should be offered?

A

A statin
Atorvastatin 20mg at night

64
Q

What is the first line lifestyle advice you would recommend for someone with hypertension?

A
  • Healthy diet
  • Stop smoking
  • Reducing alcohol, caffeine, salt intake
  • Regular exercise
65
Q

What medications are used in hypertension A-D and ARB?

A
  • A – ACE inhibitor (e.g., ramipril)
  • B – Beta blocker (e.g., bisoprolol)
  • C – Calcium channel blocker (e.g., amlodipine)
  • D – Thiazide-like diuretic (e.g., indapamide)
  • ARB – Angiotensin II receptor blocker (e.g., candesartan)
66
Q

What is are the first line medication for Black African or African-Caribbean?

A

Angiotensin receptor blockers (ARBs)
(instead of ACE inhibitors)

67
Q

What medications are used as an alternative to ACE inhibitors (commonly due to a dry cough)?

A

ARBs
(ACE inhibitors and ARBs = NOT used together)

68
Q

What medications are used instead of calcium channel blockers (if patient does not tolerate them - commonly due to ankle oedema)?

A

Thiazide-like diuretics

69
Q

Hypertension management: What is stage 1?

A
  • Aged less than 55 and non-blackuse A.
  • Aged over 55 or black of African or African-Caribbean descent useC.
70
Q

Hypertension management: What is stage 2?

A

Step 2:
** A+C
* AlternativelyA+DorC+D.

If black then use anARBinstead ofA.

71
Q

Hypertension management: What is stage 3?

A

A+C+D

72
Q

Hypertension management: What is stage 4?

A

A + C + D + fourth agent (see below)

Fourth agent = depends on potassium:
* ≤4.5 mmol/L → potassium-sparing diuretic (spironolactone)
* >4.5 mmol/L → alpha blocker (doxazosin) or beta blocker (atenolol)

73
Q

How does spironolactone work?

A

Spironolactone = potassium-sparing diuretic
* Blocks the action of aldoesterone in the kidneys → resulting in sodium excretion + potassoim reabsorption

74
Q

What can thiazide diuretics cause?

A

Hypokalaemia
(Could use potassium-sparing diuretics instead)

75
Q

What is the main complication of using potassium-sparing diuretics like spironolactone?

A

Hyperkalaemia

76
Q

Which hypertension medications cause electrolyte disturbances? And therefore need to monitor U+Es in these patients.

A
  • ACE inhibitors + potassium-sparing diuretics → hyperkalaemia
  • Thiazide-like diuretics → hypokalaemia
77
Q

What are the hypertnsion treatment targets?

A
  • Under 80: less than 140/90
  • Over 80: less than 150/90
78
Q

What is malignant/accelerated hypertension?

A

Extremely high blood pressure (above 180/120) with retinal haemorrhages or papilloedema

79
Q

What examination do patients with malignant/accelerated hypertension require?

A

Fundoscopy examination
(For retinal haemorrhages)

Additional complications also warrant same-day assessment, such as confusion, heart failure, suspected acute coronary syndrome or acute kidney injury.

80
Q

What is the management for malignant/accelerated hypertension (hypertensive emergency)?

A
  • Sodium nitroprusside
  • Labetalol
  • Glyceryl trinitrate
  • Nicardipine
81
Q

What is a complication of hypertensive emergency treatment in elderly frail patients?

A

Risk of ischaemia if the blood pressure is reduced too quickly
(As the high pressure may be required to force blood through narrowed vessels)

82
Q

What are the 4 possible rhythms in a pulseless patient?

A

Shockable:
* Ventricular tachycardia
* Ventricular fibrillation

Non-shockable:
* Pulseless electrical activity (all electrical activity except VF/VT - including sinus rhythm without a pulse)
* Asystole (no significant electrical activity)

Baso if the patient is pulseless and not in VT or VF its non-shockable

83
Q

What is narrow complex tachycardia?

A

Narrow complex tachycardia = fast heart rate with a QRS complex duration < 0.12s (3 small squares)

84
Q

What are the 4 main differentials for narrow complex tachycardia? What are the treatments?

A
  • Sinus tachycardia → underlying cause
  • Supraventricular tachycardia → vagal manoeuvres + adenosine
  • Atrial fibrillation → rate control or rhythm control
  • Atrial flutter → rate control or rhythm control (similar to atrial fibrillation)
85
Q

What does sinus tachycardia look on an ECG?

A
  • Narrow QRS complex (<0.12s)
  • Normal P wave, QRS comples, T wave pattern
86
Q

Is sinus tachycardia an arrhythmia?

A

No!
It is usally a response to an underying cause (sepsis or pain)

87
Q

What does supraventricular tachycardia (SVT) look like on an ECG?

A

(Narrow QRS → T wave → Narrow QRS → T wave)

  • Narrow QRS complex (<0.12s)
  • QRS complex followed immediately by a T wave then a QRS complex then T wave etc
  • (There are P waves but they are often buried in the T waves - so can’t see them)
88
Q

How can you distinguish SVT from atrial fibrillation and atrial flutter?

A
  • SVT →regular rhythm
  • Atrial fibrillation → irregularly irregular
  • Atrial flutter → saw-tooth pattern
89
Q

How can you distinuish between SVT and sinus tachycardia?

A

SVT:
* Abrupt onset
* Very regular pattern (without variability)
* Can appear at rest w/ no apparent cause

Sinus tachycardia:
* Gradual onset
* More variability in the rate
* Usually has an explanation (e.g. pain or fever)

90
Q

What are the features of atrial fibrillation on an ECG?

A
  • Absent P waves
  • Irregularly irregular ventricular rhythm
  • Narrow QRS complex (<0.12s)
91
Q

What does atrial flutter look like on an ECG?

A
  • Narrow QRS complex
  • Saw-tooth pattern
  • QRS complex = occurs at regular intervals
  • 2:1 conduction → Atrial rate = approx. 300 beats per min; ventricular rate = approx. 150 beats per min
92
Q

Name a couple of life-threatening features of atrial flutter

A
  • Loss of consciousness (syncope)
  • Heart muscle ischaemia (w.g. chest pain)
  • Shock
  • Severe heart failure
93
Q

If a patient with atrial flutter presents with any lilfe-threatening features (e.g. syncope, chest pain, shock. severe heart failure) - then what is the treatment?

A
  • Synchronised DC cardioversion under sedation or general anaesthesia
  • Intravenous amiodarone added is initial DC shocks are unsuccessful
94
Q

What is a broad complex tachycardia?

A

Broad complex tachycardia = fast heart rate with a QRS complex duration > 0.12s (3 small squares)

95
Q

What are the 4 types of broad complex tachycardia? What are their treatments?

A
  • Ventricular tachycardia or unclear cause → IV amiodarone
  • Polymorphic ventricular tachycardia e.g torsades de pointes → IV magnesium
  • Atrial fibrillation + bundle branch block → treated as AF
  • **Supraventricular tachycardia + bundle branch block → treated as SVT
96
Q

If a patient with broad complex tachycardia with any lilfe-threatening features (e.g. syncope, chest pain, shock. severe heart failure) - then what is the treatment?

A
  • Synchronised DC cardioversion under sedation or general anaesthesia
  • Intravenous amiodarone added is initial DC shocks are unsuccessful
97
Q

What is the pathophysiology underlying atrial flutter?

A

Atrial flutter = caused by a re-entrant rhythm in either atrium → the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria → the signal goes round and round the atrium without interruption (atrial rate usually 300 beats per minute) → The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node → This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute.

There may be 3:1, 4:1 or variable conduction ratios

98
Q

What is the treatment for atrial flutter?

A
  • Anticoagulation (based on CHA2DS2-VASc score)
  • Radiofrequency ablation of the re-entrant rhythm = can be a permanent solution
99
Q

Where is the QT interval measured from?

A

Start of the QRS complex → End of T wave

100
Q

What is the corrected QT interval (cQT)

A

cQT = estimates the QT interval if the HR were 60 beats per minute

101
Q

What is threshold for the cQT to be prolonged at for men and women?

A
  • More than 440 milliseconds in men
  • More than 460 milliseconds in women
102
Q

What does a prolonged QT interval represent in terms of physiology?

A

Prolonged QT = prolonged repolarisation of the myocytes after a contraction

103
Q

What can happen as a result of prolonged repolarisation (in prolong QT)?

A

Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations.

104
Q

What is Torsades de pointes?

A
  • Prolonged QT → the depolarisations = spread throughout the ventricles → causing a contraction before proper repolarisation
  • When this leads to current contraction without normal repolaridation = torsades de pointes
105
Q

What type of arrhythmia is torsades de pointes?

A

Polymorphic ventricular tachycardia

106
Q

What does torsades de pointes look like on an ECG?

A
  • ‘Twisting of spikes’
  • Looks like standard ventricular tachycardia → but the QRS complex is twisting around the baseline
  • QRS complex height = gets progressively smallerl then larger, then smaller etc
107
Q

What can torsades de pointes lead to? (That makes it so dangerous)

A
  • Torsades de pointes = will terminate spontaneously → revert to sinus rhythm OR progress to ventricular tachycardia.
  • Ventricular tachycardia = can lead to cardiac arrest
108
Q

What are the causes of prolonged QT?

A
  • Long QT syndrome (an inherited condition)
  • Medications: antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
  • Electrolyte imbalances: hypokalaemia, hypomagnesaemia and hypocalcaemia
109
Q

What is the management of a prolonged QT interval?

A
  • Stopping and avoiding medications that prolong the QT interval
  • Correcting electrolyte disturbances
  • Beta blockers (not sotalol)
  • Pacemakers or implantable cardioverter defibrillators
110
Q

What is the acute management of torsades de pointes?

A
  • Correcting the underlying cause (e.g., electrolyte disturbances or medications)
  • Magnesium infusion (even if they have normal serum magnesium)
  • Defibrillation if ventricular tachycardia occurs
111
Q

What are ventricular ectopics?

A

Premature ventricular beats caused by random electrical discharges outside of the atria

  • Patients often present complaining of random extra or missed beats.
  • They are relatively common at all ages and in healthy patients. However, they are more common in patients with pre-existing heart conditions (e.g., ischaemic heart disease or heart failure).
112
Q

How do ventricular ectopics appear on an ECG?

A

Isolated, random, abormal, broad complexes on an otherwise normal ECG

113
Q

What is bigeminy?

A

When every other beat is a ventricular ectopic

Normal → ectopic → normal → ectopic

  • ECG shows a normal beat (P wave → QRS complex → T wave) followed immediately by an ectopic beat → normal beat → ectopic beat
114
Q

What is the management for ventricular ectopics?

A
  • Reassurance and no treatment in otherwise healthy people with infrequent ectopics
  • Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
  • Beta blockers are sometimes used to manage symptoms
115
Q

Where is the delayed conduction in
first-degree heart block?

A

1st degree heart block → delayed conduction through atrioventricular node

Despite this → every atrial impulse = leads to a ventricular contraction, meaning every P wave followed by a QRS complex

116
Q

How does first-degree heart block look on an ECG?

A

PR interval > 0.2s
(5 small or 1 big square)

117
Q

What happens to the atrial impulses in second-degree heart block?

A

Atrial impulses = do not make it through the atrioventricular node to the ventricles

Sometimes P waves are not followed by QRS complexes

118
Q

What are the 2 types of second-degree heart block?

A
  • Mobitz type 1 (Wenckebach phenomenon)
  • Mobitz type 2
119
Q

How does Mobitz type 1 (Wenckebach phenomenon) appear on an ECG?

A

Increasing PR interval → until a P wave is not followed by a QRS complex → PR interval returns to normal → cycle repeats

120
Q

What happens in Mobitz type 2 physiologically and on the ECG?

A
  • Intermittent failure of conduction through the atrioventricular node
  • Absence of QRS complexes following P waves
  • PR interval = remains normal
  • Usually a set ratio of P waves to QRS complexes (e.g. 3 P waves for each QRS complex (3:1))
121
Q

What is the major risk with Mobitz risk 2?

A

ASYSTOLE

122
Q

What is a 2:1 block?

A

2 P waves for each QRS complex
(Every other P wave does not stimulate a QRS complex)

It can be difficult to tell whether this is caused by Mobitz type 1 or Mobitz type 2.

123
Q

What is third-degree heart block?

A
  • Third-degree heart block = complete heart block
  • No observable relationship between the **P waves and QRS complexes **
  • Significant risk of asystole
124
Q

Name 3 causes of bradycardia

A
  • Medications (e.g. beta-blockers)
  • Heart block
  • Sick sinus syndrome
125
Q

What HR is typically the threshold for bradycardia (but is normal for healthy fit patients)?

A

60 beats per min

126
Q

What is sick sinus syndrome?

A

Sick sinus syndrome = encompasses many conditions that cause dysfunction in the sinoatrial node

127
Q

What is sick sinus syndrome often caused by?

A

Idiopathic degenerative fibrosis of the sinoatrial node

128
Q

What can sick sinus syndrome result in?

A
  • Sinus bradycardia
  • Sinus arrhythmias
  • Prolonged pauses
129
Q

Define asystole

A

Absence of electrical activity in the heart → reaulting in cardiac arrest

130
Q

Name some cardiac conditions and situations that can result in asystole

A
  • Mobitz type 2
  • Third-degree (complete) heart block
  • Previous asystole
  • Ventricular pauses longer than 3 seconds
131
Q

What is the management of unstable patients + those at risk of asystole?

A
  • IV atropine (first line)
  • Inotropes (e.g., isoprenaline or adrenaline)
  • Temporary cardiac pacing
  • Permanent implantable pacemaker, when available
132
Q

Name 2 options fpr temporary cardiac pacing

A
  • Transcutaneous pacing using pads on the patients chest
  • Transvenous pacing using a catheter, fed through the venous system to stimulate the heart directly
133
Q

What is atropine and why is it effective?

A
  • Atropine = an antimuscarinic medication
  • Atropine = works by inhibiting the parasympathetic nervous system
  • Leads to S/E: pupil dilation, dry mouth, urinary retention constipation

Phase 3a General Practice and Community (14 decks)

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