Cardiology Flashcards
(172 cards)
1
Q
How do NICE define hypertension? (2)
A
> 140/90 in a clinical setting.
> 135/95 with ambulatory or home readings
2
Q
Give 5 secondary causes of Hypertension
A
ROPED
Renal Disease (most common)
Obesity
Pregnancy/Pre-eclampsia
Endocrine
Drugs
3
Q
If blood pressure is high and does not respond to treatment, what diagnosis should be considered? And what investigation confirms diagnosis?
A
Renal artery stenosis
Duplex ultrasound or MR or CT angiogram
4
Q
Give 6 possible complications of hypertension
A
Ischaemic heart disease (angina and acute coronary syndrome).
Stroke/Intracranial haemorrhage
Vascular disease
Hypertensive retinopathy
Vascular dementia
Heart failure
5
Q
Define stage 1 hypertension
A
Clinic reading >140/90
Ambulatory reading >135/85
6
Q
Define stage 2 hypertension
A
Clinic reading >160/100
Ambulatory reading >150/95
7
Q
Define stage 3 hypertension
A
Clinic reading >180/120
8
Q
What investigations should be performed in new patients with hypertension to test for end organ damage? (4)
A
Urine albumin:creatinine ratio and dipstick (proteinuria/haematirua)
Bloods for HbA1c, renal function and lipids
Fundus examination (hypertensive retinopathy)
ECG (left ventricular hypertrophy)
9
Q
What risk assessment is used to calculate the % risk that a patient will have a stroke or MI in the next 10 years?
A
QRISK
10
Q
What does QRISK assess?
A
The % risk that a patient will have a stroke or MI in the next 10 years
11
Q
When QRISK score is >10% what should be offered?
A
Statin - atorvastatin 20mg at night
12
Q
What is the moa of statins?
A
Reduce cholesterol production in the liver by inhibiting HMG CoA reductase
13
Q
What do NICE recommend with regards to starting patients on statins?
A
To check lipids after 3 months and at 12 months.
Increase the dose to aim for a >40% reduction in non-HDL cholesterol.
14
Q
Other than statins, name 2 other cholesterol lowering drugs.
A
Ezetimibe - Inhibits absorption of cholesterol in the intestine
Evolocumab/Alirocumab (PCSK9 inhibitors - monoclonal antibodies)
15
Q
Name 3 renal diseases that would cause hypertension
A
Glomerulonephritis
Chronic pyelonephritis
Polycystic kidneys
16
Q
Name 3 endocrine diseases that may cause hypertension
A
Cushing’s disease
Conn’s disease (hyperaldosteronism)
Phaochromocytoma
17
Q
Define malignant hypertension and give 3 symptoms
A
Describes acute/rapid rise in blood pressure leading to severe vascular damage.
Symptoms include;
Bilateral retinal haemorrhage and exudates
Headache
Visual disturbance (papilloedema)
18
Q
Give 5 risk factors for hypertension
A
Age >65
Moderate/high alcohol intake + smoking
Physical inactivity, obesity and poor diet
Family history
Diabetes mellitus and hyperuricaemia
19
Q
How is a diagnosis of hypertension confirmed?
A
Ambulatory/Home Blood Pressure Monitoring (ABPM/HBPM)
20
Q
Describe the hypertension treatment ladder for patients <55 and NOT black African/Afro-Caribbean.
A
- ACEi/ARB
- ACE/ARB + CCB or Thiazide-like diuretic (indapamide)
- ACE/ARB + CCB + Thiazide-like diuretic (indapamide)
- Measure potassium levels.
If K+ is LESS than 4.5mmol/L give Spironolactone
If K+ is ABOVE 4.5mmol/L give alpha/beta blocker
21
Q
Describe the treatment ladder for patients >55 and/or are of Black African/Afro-Caribbean origin
A
- CCB
- CCB + ACEi/ARB or Thiazide-like diuretic (indapamide)
- ACE/ARB + CCB + Thiazide-like diuretic (indapamide)
- Measure potassium levels.
If K+ is LESS than 4.5mmol/L give Spironolactone
If K+ is ABOVE 4.5mmol/L give alpha/beta blocker
22
Q
What’s the first drug you would prescribe to a 45 year old white male with hypertension?
A
ACEi/ARB
23
Q
What’s the first drug you would prescribe to a 58 year old white male presenting with hypertension?
A
CCB
24
Q
Name 4 calcium channel blockers
A
Verapamil
Diltiazem
Nifedipine
Amlodipine
25
What drug should NOT be given with verapamil (CCB)? And why?
Beta Blockers
Can cause a heart block
26
Give 4 side effects of verapamil (CCB)
Heart failure
Constipation
Hypotension/bradycardia
Flushing
27
Give 3 side effects of diltiazem
Hypotension/bradycardia
Heart failure
Ankle swelling
28
What is the moa of ACEi? (2)
Inhibits conversion of angiotensin I to angiotensin II.
Decreases in angiotensin II levels = vasodilation and reduced blood pressure + decrease in sodium and water retention in the kidney.
29
Describe 1 renoprotective mechanism of ACEi
Angiotensin II constricts the efferent glomerular arterioles.
ACEi therefore dilate the efferent arterioles which reduces glomerylar capillary pressure, reducing mechanical stress on the filtration barriers of the glomeruli.
This is important in preventing diabetic nephropathy
30
Give 4 side effects of ACEi
Cough (due to increased bradykinin levels)
Angioedema
Hyperkalaemia
First-dose hypotension
31
Give 4 contraindications for ACEi use
Pregnancy and breastfeeding
Renovascular disease (may result in renal impairment)
Aortic stenosis (may result in hypotension)
Hereditary of idiopathic angioedema
32
When using thiazide like diuretics, ACE inhibitors and spironolactone, what is it useful to monitor? and why?
U+Es
As Spironolactone and ACEi's increase risk of hyperkalaemia
33
Name 4 drugs used in a hypertensive emergency (malignant hypertension)
Sodium nitroprusside
Labetalol
Glyceryl trinitrate
Nicardipine
34
Give 4 factors contributing to endothelial damage within blood vessels.
Bacterial infection (pneumonia)
Smoking
Inflammation
Low Density Lipoproteins (LDLs)
35
Describe the pathophysiology of atherosclerotic plaque formation (3)
1. Initiation - Fatty streaks and Foam Cells
2. Recruitment - Intermediate lesion formation (formed from smooth muscle cells, platelets and T lymphocytes)
3. Advanced Lesions - Atheromatous plaque formation w/ Dense fibrous cap made from collagen, elastin and smooth muscle cells
36
Define angina
Describes chest pain caused by insufficient blood supply to heart muscle.
Here the myocardial oxygen demand transiently exceeds the supply, resulting in reversible myocardial ischaemia.
37
Name 4 types of angina
Stable angina (induced by effort, relieved by rest)
Unstable angina (occurs on minimal exertion or at rest)
Prinzmetal angina (occurs at rest due to coronary vasospasm)
Syndrome X (angina pain with NO evidence of atherosclerosis)
38
Give 4 causes of angina (which is the main?).
Atherosclerosis (main cause)
Anaemia
Aortic Stenosis
Arteritis/small vessel disease
39
Give 3 modifiable and 3 non-modifiable risk factors of angina
Modifiable; Hypertension, Smoking, Obesity
Non-modifiable; Age, Male, Family History
40
Describe the clinical presentation of Typical Angina (3)
Presents with all 3 of the following;
- Precipitated by physical exertion
- Constricting discomfort in the chest, neck, shoulders or jaw.
- Relieved by GTN spray or rest
41
Desribe the clinical presentation of atypical angina
Presents with 2 of the typical symptoms and atypical symptoms such as;
GI discomfort and/or breathlessness and/or nausea
42
What investigation confirms a diagnosis of angina?
CT coronary angiography
Confirmed when coronary artery disease is found or when irreversible myocardial ischaemia is found.
43
What other investigations may be useful to perform when investigating angina? And why? (5)
ECG (may show signs of previous MI - Pathological Q waves, LBBB, ST elevation, flat/inverted T waves)
Troponin (should be unchanged in angina due to ischemia not infarction)
LFTs - required before starting statins
HbA1c - exclude diabetes
FBC - exclude anaemia
44
What are the 5 principles of angina management?
RAMPS;
Refer to cardiology
Advise about diagnosis, management and when to call an ambulance
Medical treatment
Procedural or surgical investigations
Secondary Prevention
45
What are the 3 aims of medical management of angina?
Immediate symptomatic relief (GTN spray)
Long term symptomatic relief (Beta blocker/CCB)
Secondary prevention (4As Aspirin, Atorvastatin, ACEi, Already on a beta blocker)
46
What is the 1st line treatment for angina?
GTN Spray + Beta blocker/Calcium Channel Blocker
47
Describe CCB use in the treatment of angina
If using CCB as a monotherapy, use RATE LIMITING CCB - Verapamil/Diltiazem
If using in conjunction with BB use SLOW RELEASE DIHYDROPYRIDINE - Nifedipine
48
What are the 2nd line treatments of angina? (4)
Isosorbide mononitrate (Long acting nitrate)
Ivabradine (inhibits funny channels)
Nicorandil (K channel inhibitor)
Ranolazine (inhibits late Na currents - prolongs ventricular action potential)
49
What is the moa of a beta blocker
Reduce force of contraction (negative inotrope) by acting on B1 receptors
50
What is the moa of CCB
Primary arterodilators - Dilate systemic arteries so reduces afterload (reducing blood pressure)
51
What drugs are used in the secondary prevention of angina?
4As
Aspirin 75mg OD
Atorvastatin 80mg OD
ACEi (If diabetes, hypertension, CKD or Heart failure are also present)
Already on a beta blocker
52
Name 2 surgical options for the treatment of angina.
Percutaneous coronary intervention (PCI)
Coronary artery bypass graft (CABG)
53
Name 3 potential graft vessels used for CABG
Saphenous vein (inner leg)
Internal thoracic artery (internal mammary artery)
Radial artery
54
Define acute coronary syndrome.
An umbrella term used to describe a range of conditions associated with a sudden reduction to blood flow to the heart.
(Acute presentations of ischaemic heart disease).
55
Name 3 types of Acute Coronary Syndrome
Unstable Angina
Non-ST elevation myocardial infarction (NSTEMI)
ST elevation myocardial infarction (STEMI)
56
Name 2 investigations (and their findings) used in diagnosis of STEMI
ECG - ST elevation (V2/V3), Pathological Q waves, LBBB)
Elevated Troponin
57
Give 5 clinical features of STEMI
Acute central chest pain lasting >20 mins
Nausea
Sweatiness
Palpitations
Dyspnoea
58
59
Describe the immediate management of a STEMI
MONA;
Morphine (if in severe pain)
O2 (only if sats <94%)
Nitrates
Aspirin 300mg (with ticagrelor unless there is a bleeding risk, otherwise offer clopidogrel)
60
What are the 2 types of coronary reperfusion therapy offered to STEMI patients? When are they offered?
Percutaneous coronary intervention (PCI) - Offered if presentation is within 12 hours of onset AND PCI can be delivered in 120 of time fibrinolysis could have been given
Fibrinolysis - Offered if presentation is within 12 hours of onset and PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given.
61
What medications are used in fibrinolysis? What is their moa?
Streptokinase/Alteplase
Act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and breaks up thrombi.
62
Describe the secondary prevention of MI.
ADBSA
ACEi (ramipril) (or ARB - candesartan)
Dual Antiplatelet Therapy (Clopidogrel + Aspirin)
Beta Blocker (Propranolol) (Use CCB - verapamil if bb contraindicated)
Statin (Atorvastatin)
Aldosterone antagonists (Spironolactone) (offered to patients who had an acute MI AND who have symptoms of heart failure)
63
How do NSTEMIs differ to STEMIs?
NSTEMI patients present with moderate myocardial necrosis (not as much as STEMI), typically due to partial occlusion of a coronary artery.
64
What may an NSTEMI ECG display? (3)
ST Depression
Deep T wave inversion
No pathological Q waves
65
Describe troponin levels in NSTEMI
Elevated (due to infarction)
66
Describe troponin levels in unstable angina
Unchanged (due to ischemia, not infarction)
67
What score is used in NSTEMI/Unstable angina? What does it predict?
GRACE score.
Used to predict 6 month mortality + risk of future cardiac events
68
Describe the immediate management of NSTEMI/Unstable angina (4)
Immediate coronary angiography
Aspirin (ASAP)
Fondaparinux (antithrombin) (unless high bleeding risk)
MONA - Morphine, Oxygen, Nitrates, Aspirin
69
Instead of fondaparinux, what should be given to patients where therapeutic levels of anticoagulation are required? (i.e mechanical prosthetic valves, AF, DVT ect)
Dalteparin or IV dose adjusted heparin
70
Describe the management for patients who are deemed LOW risk via GRACE score (6 month mortality <3%)
Consider conservative management without angiotherapy
Offer ticagrelor with aspirin (unless bleeding risk)
71
Describe the management for patients who are deemed intermediate/high risk risk via GRACE score (6 month mortality >3%)
Offer angiotherapy
Offer prasugrel or ticagrelor with aspirin (unless bleeding risk)
72
Give 5 factors associated with an increased risk of death in NSTEMI/Unstable Angina
History of unstable angina
ST depression or widespread T wave inversion
Raised troponin
Age >70
General comorbidity - previous MI, poor LV function, DM
73
Define afterload
The load the heart must push against during contraction.
Ventricular pressure (P) x ventricular radius (r)/ 2x wall thickness
74
Define cardiac output
The volume of blood being pumped out of the left and right ventricle per unit time
CO = Heart rate x Stroke volume
75
Define pre-load
The amount of ventricular myocyte stretch at the end of diastole (prior to contraction)
76
Describe 3 heart sounds
S1 - tricuspid and mitral valves closing (atrioventricular) (occurs at start of systolic ventricular contraction)
S2 - Aortic and pulmonary valves (semi-lunar) (occurs once systolic contraction is complete)
S3 - Occurs due to rapid ventricular filling. (occurs in older HF patients as chordae tendinae and ventricles are stiff and weak, so reach their limit much quicker)
77
Define stroke volume
The volume of blood ejected from the left ventricle during each systolic contraction
78
Define end diastolic volume
The volume of blood in the ventricles at the end of diastole
79
Describe the Frank-Starling mechanism (3)
Represents the relationship between stroke volume and end diastolic volume
States that, the stroke volume of the left ventricle will increase if there is an increase in end diastolic volume.
Occurs because increased volume of blood present induces stretching of cardiac myocytes. The greater the degree of stretching, the more forceful the contraction.
80
What effect does a positive inotrope have on the frank starling curve?
Shifts curve to the left as there is an increase in stroke volume and end diastolic pressure.
81
What effect does a negative inotrope have on the frank starling curve?
Shifts the curve to the right.
82
Define heart failure
The efficiency of the heart as a pump is impaired.
Cardiac output is inadequate for the body's requirements, due to impaired ventricular function.
The heart is unable to deliver oxygenated blood at a rate commensurate with the requirements of the metabolizing tissues, despite normal or increased filling pressures.
83
Give 5 clinical signs/symptoms of heart failure
Breathlessness (dyspnoea)
Fatigue/tiredness
Fluid overload/peripheral oedema
Basal crepitations
Orthopnoea (breathless when lying flat)
84
Describe paroxysmal nocturnal dyspnoea
Describes a symptom of heart failure characterised by suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.
85
Define ejection fraction
The volume of blood ejected from the left ventricle during systole.
Usually 70% in healthy individuals.
86
Name 2 types of heart failure
HF-REF (heart failure with reduced ejection fraction)
HF-PEF (heart failure with preserved ejection fraction)
87
Define HF-REF
Describes an inability for the ventricles to contract (characterised by dilated LV) resulting in reduced cardiac output.
Defined by Left Ventricular Ejection Fraction of <40%
88
Define HF-PEF
Describes an inability of the ventricles to relax and fill normally (usually due to thickening or stiffening of cardiac muscle), resulting in increased filling pressures.
Defined by a Left Ventricular Ejection Fraction of >50%
89
Give 5 causes of chronic heart failure (state the most common)
Ischemic heart disease (most common)
Hypertension
Excessive smoking/alcohol intake
Valvular disease (aortic stenosis)
Cardiomyopathies
90
Give 5 complications of heart failure
Atrial fibrillation (most common arrhythmia in HF patients)
Ventricular arrythmias
Depression
Cachexia (muscle wasting)
Chronic Kidney Disease
91
Describe the New York Classification of Heart Failure (4)
Class I - No limitation to physical activity (asymptomatic)
Class II - Slight limitation - Comfortable at rest but ordinary physical exercise causes symptoms
Class III - Marked limitation - Comfortable at rest but less than ordinary physical exercise causes symptoms
Class IV - Inability to carry out physical exercise without discomfort.
92
What blood test is used to aid heart failure diagnosis?
Anti NT-proBNP (N-terminal Pro Brain Natriuretic Peptide)
(released from heart in response to increased wall tension. Levels correlate with ventricular wall stress and severity of heart failure).
93
What may a chest x-ray of a patient with heart failure show? (5)
ABCDE
A - Alveolar Oedema
B- Kerley B lines
C - Cardiomegaly
D - Dilated prominent upper lobe veins
E - Pleural Effusions
94
List 4 investigations used in the diagnosis of heart failure
Blood Anti-NTproBNP
Chest x-ray (ABCDE)
Transthoracic Echocardiography (exclude valve disease and assess function of left ventricle)
ECG
95
Describe the urgency for heart failure referral and assessment relative to NT-proBNP levels.
Levels from 400-2000ng/L should be seen and have an echocardiogram within 6 weeks.
Levels above 2000ng/L should be seen and have an echocardiogram within 2 weeks.
96
Give 4 lifestyle changes required for those with chronic heart failure
Stop smoking and alcohol
Low salt diet
Avoid exacerbating factors (NSAIDs = fluid retention, Verapamil - negative inotrope)
Annual flu vaccine + one off pneumococcal vaccine
97
What is the management of HF-PEF?
Low Dose Loop Diuretic (Furosemide)
98
What is the management of HF-REF?
1st line - ACEi (ramipril) + Beta Blocker)
(Offer ARB in afro-caribbean)
(Offer hydralazine with nitrate if ACEi/ARB are not tolerated)
2nd line - Add Aldosterone antagonist (spironolactone)
Adjuncts;
- Diuretics (furosemide) to relive symptoms
99
What medications should be avoided in patients with HF-REF?
Calcium channel blockers
100
What blood test should be routinely performed in patients being managed for HF-REF? Why?
U&Es
As diuretics, ACEi's and aldosterone antagonists can cause electrolyte imbalances, such as hyperkalaemia
101
Name 4 specialist treatments for patients with heart failure
SGLT2 inhibitors (dapagliflozin)
Ivabradine
Hydralazine with a nitrate
Digoxin
102
Name 3 drugs used in the secondary prevention of heart failure
Aspirin (anti-platelets)
Statins (lower LDL levels)
Anticoagulants (ticagrelor, prasugrel, clopidogrel)
103
Name 1 procedural/surgical intervention used in the treatment of HF-REF and state when it is offered?
Cardiac resynchronisation therapy (CRT).
Used in severe failure with an ejection fraction of <35%.
Involves biventricular pacemakers with leads in the right atrium and ventricle and left ventricle.
Aim is to synchronise the contractions in these chambers to optimise heart function
104
Describe acute heart failure
Describes a life-threatening emergency characterised by sudden onset or worsening of HF symptoms.
More commonly occurs due to decompensated chronic heart failure (in patients with a Hx of HF)
105
Give 4 potential triggers for decompensated chronic heart failure
Iatrogenic (aggressive IV fluids in a frail elderly patient with impaired left ventricular function)
Myocardial infarction
Sepsis
Hypertensive emergency (acute, severe increase in blood pressure)
106
Give 3 symptoms of acute heart failure
Acute shortness of breath (exacerbated by lying flat and improves on sitting up)
Cough with a frothy white/pink sputum
Orthopnoea
107
Give 5 clinical signs of acute heart failure
Raised respiratory rate
Reduced O2 sats
Tachycardia
Bilateral basal crackles
Raised JVP + peripheral oedema (if HF is right sided)
108
What type of respiratory failure is caused by acute heart failure?
Type 1 respiratory failure (low oxygen with normal Co2)
109
Give 6 assessments for a patient presenting with ? acute heart failure
Clinical assessment (Hx, examination, ABCDE)
ECG
Bloods (FBC, U&E, LFTs, BNP, Troponin)
ABG
CXR (May show cardiomegaly, ABCDE)
Echocardiogram (assessing ventricular function)
110
Describe the MOA of BNP (4)
Relaxes smooth muscle in blood vessels, promoting vasodilation.
Reduces systemic vascular resistance.
Acts on kidneys to promote water excretion in the urine.
Overall reduces circulating volume in someone that is fluid overloaded.
111
Describe the management of acute heart failure
SODIUM;
Sit Up (helps oxygenate the lungs)
Oxygen (if sats are <95%)
Diuretics (furosemide)
IV fluids should be STOPPED
Underlying causes (need to be identified and treated)
Monitor fluid balance
112
Decompensated heart failure can lead to pulmonary oedema. What is the treatment of this?
IV loop diuretic (furosemide)
113
Rate control should be offered to all patients with AF, except those with what? What is offered instead (4)
Offer rhythm control instead.
A reversible cause of AF
New onset AF (within the last 48 hours)
Heart failure caused by AF
Symptoms despite being effectively rate controlled
114
Give 3 medications used for rate control of AF
Bisoprolol (Beta blocker)
Verapamil/Diltiazem (Calcium channel blocker)
Digoxin
115
What is used for rhythm control in AF? (2)
Cardioversion
Long term rhythm control
116
Name 2 types of cardioversion used in rhythm control of AF
Immediate cardioversion
Delayed cardioversion
117
When is immediate cardioversion offered in AF?
If AF is;
Present for <48 hours
Causing life threatening haemodynamic instability
118
Name 2 types of immediate cardioversion
Pharmacological - Flecainide/Amiodarone
Electrical - Using a cardiac defib to shock heart into sinus rhythm
119
When is delayed cardioversion offered? What form is offered?
If AF present for >48 hours and are stable
Transoesophageal echocardiography- guided cardioversion.
Amiodarone considered before/after electrical to prevent AF from recurring
120
What is the anticoagulation process for treating AF with delayed cardioversion?
Anticoagulate with DOAC for 3 weeks before delayed cardioversion
121
How is paroxysmal atrial fibrillation managed? (3)
Pill in the pocket approach - Take a pill to terminate AF when symptoms begin.
Flecainide
Anticoagulate according to CHADSVASc score
122
What is the MOA of Dabigatran?
Direct thrombin inhibitor
123
What is the MOA of Apixaban, Edoxaban and rivaroxaban?
Direct factor Xa inhibitor
124
How often are apixaban and dabigatran taken?
Twice daily
125
How often are edoxaban and rivaroxaban taken?
once daily
126
What medication reverses the effects of apixaban and rivaroxaban?
Andexanet alfa
127
What medication is used to reverse the effects of dabigatran?
Idarucizumab
128
What score is used to assess whether a patient with AF requires anticoagulation? What factors does it use?
CHADSVCAc
C - Congestive heart failure
H - Hypertension
A2 - Age above 75 (scores 2)
D - Diabetes
S2 - Stroke or TIA previously (Scores 2)
V - Vascular disease
A - Age 65-74
S - Sex (female)
129
How does the score of CHADSVASc determine treatment?
0 = No anticoagulation
1 = Consider anticoagulation in men
2 or more = Offer anticoagulation
130
What score is used to assess the risk of major bleeding in patients with AF taking anticoagulation? What factors does it use?
ORBIT
O - Older age (Age >75)
R - Renal impairment (GFR <60)
B - Bleeding previously (Hx GI or Intracranial bleed)
I - Iron (low Hb or haematocit)
T - Taking antiplatelet medication
131
What treatment is offered to patients with contraindications to anticoagulation and who have a high stroke risk?
Left Atrial Appendage Occlusion
132
What causes an ejection systolic murmur that is louder on expiration? (2)
Aortic stenosis or Hypertrophic obstructive cardiomyopathy
133
What causes an ejection systolic murmur loudest on inspiration? (2)
Pulmonary stenosis or atrial septal defect
134
What causes a pansystolic murmur?(2)
Mitral/tricuspid regurgitation or ventricular septal defect
(Tricuspid regurgitation is heard loudest during inspiration)
135
What causes a late systolic murmur?
Mitral valve prolapse or coarctation of the aorta (2)
136
What causes an early diastolic murmur?
Aortic regurgitation
137
What causes a mid-late diastolic murmur?
Mitral stenosis
138
What causes a continuous machine-like murmur?
Patent ductus arteriosus
139
Name 3 patterns of presentation in patients with peripheral artery disease
Intermittent claudication
Critical Limb Ischaemia
Acute limb-threatening ischaemia
140
Name 2 ways of assessing for peripheral artery disease by the bedside
Check the femoral, popliteal, posterior tibialis and dorsalis pedis pulses
Check ankle brachial pressure index (ABPI)
141
What is the 1st line is used to diagnose peripheral artery disease?
Duplex ultrasound
142
When investigating PAD, what should be performed prior to any intervention?
Magnetic resonance angiography (MRA)
143
What ABPI result would indicate claudication?
1 = Normal
0.6-0.9 = Claudication
0.3-0.6 = Rest pain
<0.3 = Impending
144
How is PAD managed? (4)
Quit smoking
Treat comorbidities (Hypertension, diabetes, obesity)
Start statin (80mg Atorvastatin)
Exercise training
145
Name 2 treatments for severe PAD/critical limb ischaemia
Endovascular revascularisation (Used for short segment stenosis <10cm)
Surgical revascularisation (Used for long segment lesions >10cm)
146
An ABPI of what would indicate critical limb ischaemia?
<0.5
147
What features are seen in critical limb ischaemia? (3)
1 or more of;
Rest pain in foot for more than 2 weeks
Ulceration
Gangrene
148
What features are seen in acute limb threatening ischaemia?
1 or more of the 6 P's;
Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishing with cold
149
How is acute limb threatening ischaemia initially investigated by the bedside? (2)
Handheld arterial Doppler
Ankle-brachial pressure index (ABPI)
150
Name 3 factors that would suggest acute limb threatening ischemia has been caused by a thrombus (as opposed to an embolus)
Pre-existing claudication with sudden deterioration
Reduced or absent pulses in contralateral limb
Evidence of widespread vascular disease (MI, stroke,TIA)
151
Name 4 factors that would suggest acute limb threatening ischemia has been caused by an embolus (as opposed to a thrombus)
Sudden onset of painful leg (<24 hours)
No history of claudication
Clinically obvious source of embolus (AF, recent MI)
No evidence of PAD (normal pulses in contralateral limb)
152
How is acute life threatening limb ischaemia initially managed? (4)
ABC approach
IV opioids
IV Unfractioned Heparin
Vascular review
153
Name 5 definitive managements of acute life threatening limb ischaemia
Intra-arterial thrombolysis
Surgical embolectomy
Angioplasty
Bypass surgery
Amputation (for patients with irreversible ischaemia)
154
Define Wolff-Parkinson White Syndrome
Describes presence of a congenital accessory conducting pathway between the atria and ventricles.
Leads to atrioventricular re-entrant tachycardia (AVRT).
155
What is one harmful complication of WPW?
Accessory pathway does not slow conduction so AF can rapidly degenerate to VF
156
What will an ECG likely show for WPW? (5)
Short PR interval (<120ms)
Delta Waves - Wide QRS complexes with slurred upstroke
QRS prolongation (>110ms)
Left axis deviation (if right sided accessory pathway)
Right axis deviation (if left sided accessory pathway)
157
Name 3 associations with WPW
Hypertrophic Obstructive Cardiomyopathy
Ebsteins anomaly
Mitral valve prolapse
Thyrotoxicosis
158
What ECG findings are seen in Hypertrophic Obstructive Cardiomyopathy? (3)
Left ventricular hypertrophy (Left axis deviation)
T wave inversion
Deep Q waves
159
What ECG leads monitor the Right Coronary Artery?
Inferior Leads (II, III, aVF)
160
What ECG leads monitor the left anterior descending artery?
Anteroseptal leads - V1-V4
161
What ECG leads monitor the Left circumflex artery?
Lateral Leads (V5-6, I and aVL)
162
What is the correct width for a PR interval?
120-200ms (3-5 little squares)
163
What is the correct width for the QRS complex?
Should not exceed 110ms (<3 little squaes)
164
Describe 1st degree heart block
Describes patients experiencing slow conduction velocity, resulting in prolonged PR interval (>200ms)
165
What will an ECG show in a patient with a 1st degree heart block?
Prolonged PR interval (>200ms = >5 small squares)
166
Describe Mobitz I heart block (Second degree)
Progressive prolongation of PR interval followed by blocked/non-conductive P wave
167
Give 2 causes of Mobitz I heart block
Hyperkalaemia
AV nodal blocking dugs (BB, CCB, Digoxin)
168
Describe Mobitz II heart block. What is seen on ECG?
Occurs due to failure of conduction through His-Purkinje system.
ECG shows;
Constant PR interval
Dropped QRS complexes (all that remains is P wave)
169
Do mobitz I heart blocks require a pacemaker?
No
170
Do mobitz 2 heart blocks require a pacemaker?
Yes. Due to high risk of sudden complete AV block
171
Describe third degree heart block
Complete absence of AV node conduction, resulting in no association between P waves and QRS complexes.
172
What may be seen on ECG for 3rd degree heart block?
Bradycardia (due to ventricular escape rhythm)
Independent P waves and QRS complexes
