New GP Cardiovascular Flashcards
(133 cards)
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.
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.
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
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
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
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)
7
Q
Define ischaemia
A
Inadequate oxygen supply to the tissues - due to reduced blood supply
8
Q
Define gangrene
A
Death of tissue (necrosis) - specifically due to an inaquate blood supply
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).
10
Q
What sized vessels does atherosclerosis effect?
A
Medium and large arteries
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
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)
13
Q
Name 3 non-modifiable risk factors for atherosclerosis
A
- Older age
- Family history
- Male
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
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
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
17
Q
Name a couple of end results of atherosclerosis
A
- Angina
- Myocardial infarction
- Transient ischaemic attack
- Stroke
- Peripheral arterial disease
- Chronic mesenteric ischaemia
18
Q
How does peripheral arterial disease present in patients?
A
Intermittent claudication
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
20
Q
What are the 6Ps of acute limb ischaemia?
A
- Pain
- Pallor
- Pulseless
- Paralysis
- Paraesthesia (abnormal sensation or ‘pins and needles’)
- Perishingly cold
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
22
Q
What is the clinical triad for Leriche syndrome?
A
- Thigh/buttock claudication
- Absent femoral pulses
- Male impotence
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)
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
25
What pulses may be weak on palpation in a patient with PAD?
* Radial
* Brachial
* Carotid
* Abdominal aorta
* Femoral
* Popliteal
* Posterior tibial
* Dorsalis pedis
26
If examining a patient with suspected PAD and some pulses are difficult to palpate how do you accurately assess the pulses?
A hand-held Doppler
27
What are the clinical signs of peripheral arterial disease?
* 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)
28
What on examination may you find in a patient with suscpeted PAD?
* Reduced skin temperature
* Reduce sensation
* Prolonged capillary refill time (more than 2 seconds)
* Changes during Buerger’s test
29
What test (examination) is used to assess for peripheral arterial disease in the leg?
Buerger's test
30
Why do you develop ulcers with peripheral arterial disease?
Skin + tissues = strugglung to heal - due to impaired blood flow
31
What is the cause of arterial ulcers?
**Arterial** ulcers = caused by **ischaemia** secondary to **inadequate blood supply**
32
What are the features of arterial ulcers?
* 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
33
Why do venous ulcers occur?
Venous ulcers = occur by **impaired drainage + pooling of blood** in the legs
34
What are the clinical features of a venous ulcers?
* 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)
35
What are the investigations for peripheral arterial disease?
* **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
36
What is the ankle-brachial pressure index (ABPI)?
**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
37
What does a ABPI of 1.3 mean?
Normal (no PAD)
38
What does above and below 1.3 ABPI mean?
* Above 1.3 = calcification of arteries
* Below 1.3 = peripheral arterial disease
39
What are the ABPI ranges?
* **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**
40
What does an ABPI above 1.3 mean?
Claification of the arteries → making them difficult to compress
(More common in diabetic patients)
41
What lifestyle and exercise changes can be done to manage intermittent claudication?
* **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.
42
What are the medical treatments for intermittent claudification?
* **Atorvastatin** **80mg**
* **Clopidogrel 75mg** once daily (aspirin if clopidogrel is unsuitable)
* **Naftidrofuryl oxalate** (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
| **C**laudication → **C**lopidogrel
43
What are the surgical options for intermittent claudification?
* **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
44
What is the management for critical limb ischaemia?
* 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
45
What is the management for acute limb ischaemia?
* **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
46
What readings suggest hypertension?
* Clinical setting: Above 140/90 mmHg
* Ambulatory home readings above 135/85 mmHg
47
What is essential/primary hypertension?
High blood pressure that has developed on its own (does not have a secondary cause).
90% of hypertension
48
Nmeumonic for secondary causes of hypertension
ROPED
* **R** - **R**enal disease
* **O** - **O**besity
* **P** - **P**regnancy-induced hypertension or **P**re-eclampsia
* **E** - **E**ndocrine
* **D** - **D**rugs (e.g. alcohol, steroids, NSAIDs, oestrogen and liquorice)
49
What is the most common cause of secondary hypertension?
**Renal disease**
When the blood pressure is very high and **does not respond to treatment** → consider **renal artery stenosis**
50
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?
**Duplex ultrasound** or an **MRI or CT angiogram**
51
What endocrine condition may be present in 5-10% of patients with hypertension?
Hyperaldosteronism (Conn's syndrome)
52
Name a couple of complications for hypertension
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**
53
What complication in the heart may patients with hypertension develop?
**Left ventricular hypertrophy**
(The left ventricle is straining to pump blood against increased resistance in the arterial system, so the muscle becomes thicker)
54
What are the findings of left ventricular hypertrophy on examination?
**Sustained + forceful apex beat **
55
What are the investigations for left ventricular hypertrophy?
* ECG: using voltage criteria
* **Gold standard: Echocardiogram**
56
How often does NICE recommend you screen for hypertension?
Every 5 years
It should be measured more often in borderline cases and every year in patients with type 2 diabetes.
57
What blood pressure difference does a white coat effect involve?
More than a 20/10 mmHg difference in BP between clinic + ambulatory or home readings
58
What stage of hypertension is:
* Clinic reading: Above 140/90 mmHg
* Home/Ambulatroy readings: Above 135/85 mmHg
Stage 1
59
What stage of hypertension is:
* Clinic reading: Above 160/100 mmHg
* Home/Ambulatroy readings: Above 150/95 mmHg
Stage 2
60
What stage of hypertension is:
* Clinic reading: Above 180/120 mmHg
Stage 3
61
What invesigations should be performed on a patient with newly diagnosed hypertension?
(For assessing end organ damage)
* **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
What risk score is recommended to use in a pteint that has just been diagnosed with hypertension?
**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
When a person's QRISK score is above 10% what should be offered?
A **statin**
**Atorvastatin 20mg** at night
64
What is the first line **lifestyle advice** you would recommend for someone with hypertension?
* Healthy diet
* Stop smoking
* Reducing alcohol, caffeine, salt intake
* Regular exercise
65
What medications are used in hypertension A-D and ARB?
* **A** – **A**CE inhibitor (e.g., **ramipril**)
* **B** – **B**eta blocker (e.g., **bisoprolol**)
* **C** – **C**alcium channel blocker (e.g., **amlodipine**)
* **D** – Thiazide-like **d**iuretic (e.g., **indapamide**)
* **A**RB – **A**ngiotensin II receptor blocker (e.g., **candesartan**)
66
What is are the first line medication for Black African or African-Caribbean?
**Angiotensin receptor blockers (ARBs)**
(instead of ACE inhibitors)
67
What medications are used as an alternative to ACE inhibitors (commonly due to a dry cough)?
ARBs
(ACE inhibitors and ARBs = NOT used together)
68
What medications are used instead of calcium channel blockers (if patient does not tolerate them - commonly due to ankle oedema)?
Thiazide-like diuretics
69
Hypertension management: What is stage 1?
* Aged **less than 55** and non-black use **A**.
* Aged **over 55** or **black** of African or African-Caribbean descent use **C**.
70
Hypertension management: What is stage 2?
**Step 2**:
** **A** + **C**
* Alternatively **A** + **D** or **C** + **D**.
If black then use an **ARB** instead of **A**.
71
Hypertension management: What is stage 3?
A + C + D
72
Hypertension management: What is stage 4?
**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
How does spironolactone work?
Spironolactone = potassium-sparing diuretic
* **Blocks** the action of **aldoesterone** in the kidneys → **resulting in sodium excretion + potassoim reabsorption**
74
What can thiazide diuretics cause?
**Hypokalaemia**
(Could use potassium-sparing diuretics instead)
75
What is the main complication of using potassium-sparing diuretics like spironolactone?
**Hyperkalaemia**
76
Which hypertension medications cause electrolyte disturbances? And therefore need to monitor U+Es in these patients.
* ACE inhibitors + potassium-sparing diuretics → hyperkalaemia
* Thiazide-like diuretics → hypokalaemia
77
What are the hypertnsion treatment targets?
* Under 80: less than 140/90
* Over 80: less than 150/90
78
What is malignant/accelerated hypertension?
Extremely high blood pressure (**above 180/120**) with **retinal haemorrhages** or **papilloedema**
79
What examination do patients with malignant/accelerated hypertension require?
**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
What is the management for malignant/accelerated hypertension (hypertensive emergency)?
* **Sodium nitroprusside**
* Labetalol
* Glyceryl trinitrate
* Nicardipine
81
What is a complication of hypertensive emergency treatment in elderly frail patients?
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
What are the 4 possible rhythms in a pulseless patient?
**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
What is narrow complex tachycardia?
Narrow complex tachycardia = **fast heart rate** with a **QRS complex duration < 0.12s** (3 small squares)
84
What are the 4 main differentials for narrow complex tachycardia? What are the treatments?
* **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
What does sinus tachycardia look on an ECG?
* Narrow QRS complex (<0.12s)
* Normal P wave, QRS comples, T wave pattern
86
Is sinus tachycardia an arrhythmia?
No!
It is usally a response to an **underying cause** (sepsis or pain)
87
What does supraventricular tachycardia (SVT) look like on an ECG?
**(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
How can you distinguish SVT from atrial fibrillation and atrial flutter?
* SVT →regular rhythm
* Atrial fibrillation → irregularly irregular
* Atrial flutter → saw-tooth pattern
89
How can you distinuish between SVT and sinus tachycardia?
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
What are the features of atrial fibrillation on an ECG?
* Absent P waves
* Irregularly irregular ventricular rhythm
* Narrow QRS complex (<0.12s)
91
What does atrial flutter look like on an ECG?
* **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
Name a couple of life-threatening features of atrial flutter
* Loss of consciousness (syncope)
* Heart muscle ischaemia (w.g. chest pain)
* Shock
* Severe heart failure
93
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?
* **Synchronised DC cardioversion** under sedation or general anaesthesia
* **Intravenous amiodarone** added is initial DC shocks are unsuccessful
94
What is a broad complex tachycardia?
**Broad complex tachycardia** = **fast heart rate** with a **QRS complex duration > 0.12s** (3 small squares)
95
What are the 4 types of broad complex tachycardia? What are their treatments?
* **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
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?
* **Synchronised DC cardioversion** under sedation or general anaesthesia
* **Intravenous amiodarone** added is initial DC shocks are unsuccessful
97
What is the pathophysiology underlying atrial flutter?
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
What is the treatment for atrial flutter?
* **Anticoagulation** (based on CHA2DS2-VASc score)
* **Radiofrequency ablation** of the re-entrant rhythm = can be a permanent solution
99
Where is the QT interval measured from?
**Start** of the **QRS complex** → **End** of **T wave**
100
What is the **corrected QT interval (cQT)**
cQT = estimates the QT interval if the HR were 60 beats per minute
101
What is **threshold** for the **cQT** to be **prolonged** at for men and women?
* More than 440 milliseconds in men
* More than 460 milliseconds in women
102
What does a prolonged QT interval represent in terms of physiology?
**Prolonged QT = prolonged repolarisation** of the myocytes after a contraction
103
What can happen as a result of prolonged repolarisation (in prolong QT)?
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
What is Torsades de pointes?
* 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
What type of arrhythmia is torsades de pointes?
Polymorphic ventricular tachycardia
106
What does torsades de pointes look like on an ECG?
* '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
What can torsades de pointes lead to? (That makes it so dangerous)
* **Torsades de pointes** = will **terminate spontaneously** → **revert to sinus rhythm** OR **progress to ventricular tachycardia**.
* **Ventricular tachycardia** = can lead to **cardiac arrest**
108
What are the causes of prolonged QT?
* **Long QT syndrome** (an inherited condition)
* **Medications**: antipsychotics, **citalopram**, flecainide, sotalol, amiodarone and macrolide antibiotics
* **Electrolyte imbalances**: hypokalaemia, hypomagnesaemia and hypocalcaemia
109
What is the management of a prolonged QT interval?
* Stopping and avoiding medications that prolong the QT interval
* Correcting electrolyte disturbances
* Beta blockers (not sotalol)
* Pacemakers or implantable cardioverter defibrillators
110
What is the acute management of torsades de pointes?
* **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
What are ventricular ectopics?
**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
How do ventricular ectopics appear on an ECG?
Isolated, random, abormal, broad complexes on an otherwise normal ECG
113
What is **bigeminy**?
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
What is the management for ventricular ectopics?
* **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
Where is the delayed conduction in
first-degree heart block?
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
How does first-degree heart block look on an ECG?
PR interval > 0.2s
(5 small or 1 big square)
(If your R is far from your P, then you have first degree)
117
What happens to the atrial impulses in second-degree heart block?
**Atrial impulses** = **do not** make it through the **atrioventricular node** to the ventricles
Sometimes **P waves are not followed by QRS complexes**
118
What are the 2 types of second-degree heart block?
* Mobitz type 1 (Wenckebach phenomenon)
* Mobitz type 2
119
How does Mobitz type 1 (Wenckebach phenomenon) appear on an ECG?
**Increasing PR interval** → until a P wave is not followed by a QRS complex → PR interval returns to normal → cycle repeats
(Longer, longer, longer, drop, then you have Wenkebach)
(Impulses become slower and slower until the heart skips a beat)
120
What happens in Mobitz type 2 physiologically and on the ECG?
* **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**))
(If some P’s don’t get through, then you have Mobitz II)
121
What is the major risk with Mobitz risk 2?
**ASYSTOLE**
122
What is a 2:1 block?
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
What is third-degree heart block?
* Third-degree heart block = **complete heart block**
* **No observable relationship** between the **P waves and QRS complexes **
* **Significant risk of asystole**
124
Name 3 causes of bradycardia
* Medications (e.g. beta-blockers)
* Heart block
* Sick sinus syndrome
125
What HR is typically the threshold for bradycardia (but is normal for healthy fit patients)?
60 beats per min
126
What is sick sinus syndrome?
Sick sinus syndrome = encompasses many conditions that cause **dysfunction** in the **sinoatrial node**
127
What is sick sinus syndrome often caused by?
**Idiopathic degenerative fibrosis** of the **sinoatrial node**
128
What can sick sinus syndrome result in?
* Sinus bradycardia
* Sinus arrhythmias
* Prolonged pauses
129
Define asystole
Absence of electrical activity in the heart → reaulting in **cardiac arrest**
130
Name some cardiac conditions and situations that can result in asystole
* Mobitz type 2
* Third-degree (complete) heart block
* Previous asystole
* Ventricular pauses longer than 3 seconds
131
What is the management of **unstable patients** + those at **risk of asystole**?
* **IV atropine (first line)**
* **Inotropes** (e.g., isoprenaline or adrenaline)
* **Temporary cardiac pacing**
* **Permanent implantable pacemaker**, when available
132
Name 2 options fpr **temporary cardiac pacing**
* **Transcutaneous pacing** using pads on the patients chest
* **Transvenous pacing** using a catheter, fed through the venous system to stimulate the heart directly
133
What is **atropine** and why is it effective?
* Atropine = an **antimuscarinic** medication
* Atropine = works by **inhibiting** the **parasympathetic nervous system**
* Leads to S/E: pupil dilation, dry mouth, urinary retention constipation
