CVD Flashcards
What is the best measure for obesity as a predictor of CVD outcome?
Waist/hip ratio or hip circumference
State 10 RF for CVD
Non-modifiable:
1) Age
2) Male
3) Personal/family hx
4) IUGR/Low-birth weight
Modifiable:
1) Smoking/Drink (environmental factors)
2) DM
3) HTN
4) Hyperlipidemia
5) Physical Inactivity
6) Obesity (Waist-hip ratio)
7) HF
8) Coronary-prone behaviour
What is Coronary prone behaviour
Aggressiveness, competitiveness.
Behaviour modification is associated with reduced risk
What primary prevention tool used in the clinic is for CVD? Discuss it
Qrisk3 which predicts the individual’s 10-year CVD risk.
This is a program that incorporates RF of CVD to predict this. This includes age, sex, smoking, diabetes, angina, cholesterol, SBP, and treatments
Give 2 conditions that may increase the risk of CVD other than DM, HTN, and obesity?
Psoriasis
IBS
APS
There are national screening programs for those aged 40-75 for people at risk for CVD, DM, and cancer. These do not target the high risk individuals but those in the moderate risk category. Why?
What factors would indicate that a person is of high risk of CVD?
Most CVD events occur in the moderate risk populations as it is the largest group. The high risk group on the other hand has the greatest benefit from treatment (foreshadowing to statins)
High Risk:
1) >85yo
2) Familial Dyslipidemia
3) Qrisk3>10%
4) eGFR <60/albuminuria
5) T1DM and >40yo, or T2DM for >10 years
A patient presents with 3 consecutive high BP readings. They have not been diagnosed with hypertension before. What is your next step?
Ambulatory blood pressure monitoring/24 hour monitoring.
If this is not available I will offer Home BP monitoring
How does ABPM work?
How would you interpret the results?
A monitor is worn on the patient for 24 hours. It takes their BP every 20-30 minutes during the day and every hour at night.
The average day-time measures are taken and if >135/85 then it indicates hypertension. The night time average is also taken (>120/70) but it is used more to demonstrate a night-time dip. No dip is correlated with CVD
How does House BP monitoring work?
How would you interpret the results?
This is useful if ABPM not available or not tolerated. While seated, the patient takes 2 measurements (1 during day and 1 during night), each with 2 readings 1 minute apart for 4-7 days.
Discard first day of results and take average of all remaining measurements. HTN is diagnosed if average >135/85
What method of BP monitoring is best to assess progress of tx/effectivity of tx?
House BP monitoring
How does your blood pressure react to standing up?
How does your blood pressure react to standing up in a patient with postural hypotension?
Drop in systolic pressure while there is a rise in diastolic
In Postural hypotension both drop
How does a patient with postural hypotension present?
What would you do to assess for postural hypotension?
Presents with dizziness and lightheadedness when getting up from bed or standing up => falls and injuries
Measure the patient’s BP when supine+/- seated and then ask them to stand where you would take another BP measurement.
What medication would you prescribe to a patient suffering from postural hypotension?
What type of medication is it?
Midodrine (Vasopressor)
25% of adults and 50% of those over 60 suffer from hypertension. State 5 causes of hypertension
1) Alcohol
2) Obesity
3) Endocrine (DM, Cushing’s, secondary to steroid use, Hyperparathyroidism, phaeochromocytoma)
4) Renal disease
5) Coarctation of the aorta
What is Phaeochromocytoma?
Phaeochromocytoma is a rare neuroendocrine tumor that arises from the adrenal medulla or extra-adrenal chromaffin tissue. It causes excessive production of catecholamines, leading to symptoms such as severe hypertension and palpitations.
Hypertension is typically an incidental funding as most are asymptomatic. What are the signs and symptoms of Hypertension?
Give 3 Sequele of HTN
Headaches
Visual disturbances
Signs: Oedema, Displaced apex beat, !raised JVP. Papilloedema (or lesser form, silver wiring), Retnal haemorrhage on fundoscopy
Sequele: End-organ damage:
1) Left ventricular hypertrophy
2) CVA (accident), previous/current angina
3) Renal impairment
4) PVD
Increasing the BP by 2mmHg is equivalent to a 7% and 10% increase in the risk of mortality from ischemic HD and stroke respectively. How is hypertension classified?
How does the this influence the management of a patient according to the NICE guidelines?
Stage 1 = >140/90 or ABPM >135/90 => Offer tx after ABPM only if evidence of end-organ damage, established CVD, Renal disease, DM, or Qrisk >10%.
Stage 2 => 160/90 or ABPM >150/95 => Offer tx after ABPM
Severe HTN => 180/110 => Start tx directly without waiting for ABPM (Refer for same-day specialist)
A patient comes in for a routine checkup and their BP is 155/94. How would you classify this hypertension. What would you check for on a focused exam?
Once you have completed your exam, what else would you do as part of his workup
Must include:
Fundoscopy for Papilloedema, Retinal haemorrhage, AV nipping, cotton wool spots
CVS: Heart size, sounds, murmurs, JVP
Resp: Basal craps in case of pulmonary oedema
Other: Ankle oedema
Labs: Creatinine, U&E (eGFR), Glucose, HbA1c, Lipid profile, GGT, Urine dipstick, ACR
Imaging: ECG + ECHO
+ Q Risk 3
What is the treatment ladder for managing HTN?
Step 1:
<55 - ACEi/ARBs
>55/afrocarribean - CCB/Thiazide-like diuretic
Step 2: ACEi(or ARBs) + CCB (or Thiazide-like diuretic)
Step 3: Ensure step 2 adherence and concordance. If good, then give ACEi (or ARBs) + CCB + Thiazide-like
Step 4: Consider adding Spironolactone and if not Beta blocker.
Finally, refer for specialist advice
What is the recommended amount of exercise as per NICE guidelines
150 minutes of moderate intensity exercise per week or 75 minutes of high intensity exercise
Book: >30 minutes/day 5/7
What is the recommended alcohol intake/week?
<14 units per week for both genders
What is the recommended salt intake?
<6g/day
What is the recommended fruit and vegetable intake?
> 5 portions/day
A patient presents with long-standing high bp of 145/91. Their Q-risk core is 7%. They have no other significant hx of note. What is your full management plan?
1) Education: Inform the patients of the risks of HTN (end-organ failure).
2) RF reduction:
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Reduce caffeine intake
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Relaxation and stress management
What is your followup protocol with HTN?
Review after 1 month of starting new treatment
If BP is controlled then 3-6 monthly
If BP not controlled then check adherence, repeat ABPM/HBPM and if new medication administered => 1 month again
+ Annual followup where all investigations are repeated
Note: Remember to always offer safety net
A patient presents with long-standing BP of 159/91. You have already given the patient ABPM giving the same result. What is your full management plan and escalation
1) Education: Inform the patients of the risks of HTN (end-organ failure).
2) RF reduction:
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Reduce caffeine intake
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Relaxation and stress management
3) Medications
Step 1:
<55 - ACEi/ARBs
>55/afrocarribean - CCB/Thiazide-like diuretic
Step 2: ACEi(or ARBs) + CCB (or Thiazide-like diuretic)
Step 3: Ensure step 2 adherence and concordance. If good, then give ACEi (or ARBs) + CCB + Thiazide-like
Step 4: Consider adding Spironolactone and if not Beta blocker.
Finally, refer for specialist advice
4) Followup:
Review after 1 month of starting new treatment
If BP is controlled then 3-6 monthly
If BP not controlled then check adherence, repeat ABPM/HBPM and if new medication administered => 1 month again
+ Annual followup where all investigations are repeated
Note: Remember to always offer safety net
Cholesterol can be LDL or HDL (mainly). Which is good and which is bad
LDL bad, HDL good
How is cholesterol assessed?
Checked via a fasting lipid profile
What is included in a lipid profile?
HDL cholesterol (low levels a/w CVD)
LDL cholesterol (high levels a/w CVD)
Triglycerides (independent RF for CVD although not on Qrisk3)
Ratio of TG/HDL
What is considered a raised TG/HDL associated with CVD?
> 6
Give 10 RF for hyperlipidemia
Non-modifiable:
1) HIV and ART
2) Familial dyslipidemia
3) T1DM/T2DM
Modifiable:
1) Smoking
2) Obesity
3) Alcohol
4) Poor glucose control in DM
5) Pregnancy
6) Hypothyroidism
7) Cholestasis
8) Cushing’s
Drugs:
1) Steroids
2) Beta blockers
3) Antipsychotics (olanzapine)
4) Tamoxifen
5) COCP
How is smoking a RF for hyperlipidemia
Reduces HDL cholesterol
Management of hyperlipidemia is primarily based on measuring what?
How do the levels influence your management?
Triglyceride levels
4.5-9.9 - Reduce RF, Dietician referral
10-20 - Repeat fasting TGs within 5-14 days and if >10 refer to specialist
> 20 - Urgent specialist referral
note: if it is due to poor glycemic control of diabetes or alcohol abuse then this is managed in the clinic and advice
What advice would you give someone who has TG levels of 9.8
Lifestyle advice:
!!Reduce intake of fats. avoid saturated fats, low cholesterol diet
+
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Reduce caffeine
Under what conditions would you prescribe statins to a patient?
1) Qrisk3 score >10%
2) >85yo
3) eGFR <60
4) Albuminuria
5) Familial Dyslipidemia
6) T1DM >40 yo or T2DM for >10 yrs
Same criteria as those screened for CVD as primary prevention
What are the different types of familial dyslipidemia
Hypercholesterolemia
Hyperlipidemia
(poly and mono of each)
Statins reduce the risk of CVD by 25%. The higher the risk, the more the benefit. What is the main mechanism of action for Statins?
Give 3 side effects of Statins
What are the contraindications to Statin?
HMG-CoA inhibitor (enzyme in the synthesis of cholesterol)
SE:
1) Myositis
2) Abnormal LFTs (Discontinue if >3x max normal)
3) Nausea, vomiting
4) Diabetes (2x risk)
5) Peripheral neuropathy (rare)
Complications:
Liver disease
Pregnancy
Breastfeeding
Drugs Interactions:
- Warfarin
- Macrolides
- CCB (Care with HTN management)
- Amiodarone
- Grapefruit juice
Before administering a statin, you make sure to assess LFTs, BP, lipid profile, HbA1c, and U&E to rule out contraindications. The patient is complaining of muscle pain. What other test will you perform
CK should be measured.
If it is raised and <5x max => Start low dose
If >5x max => contraindicated
You are administering A statin to a patient. What is the first line drug? What dose will you prescribe?
When should statins be taken?
When will you check back for followup? What is the aim of successful statin therapy?
What alternatives are available to the first-line?
Starting dose for:
Primary prevention: Atorvastatin 20mg
Secondary prevention: Atorvastatin 80mg
Nighttime
followup in 3 months and then yearly. Goal is reduction in non-HDL cholesterol by 40% from baseline
Alternative: Rosuvastatin and Simvastatin (very strong, increased risk of myositis)
Would you offer a preventative dose of statin to an individual with moderate CVD risk (5-10% Qrisk)?
Show Qrisk to patient
There is a slight benefit to having this drug. Advise the side effects of myositis, nausea, vomitting and the need to take the statin lifelong. The benefit is not as clear cut as with a high risk patient
Define:
Stable Angina
Unstable Angina
Stable Angina: Episodic constant crushing/band-like chest pain radiating to the neck, shoulder or arms.
Unstable Angina: Pain on minimal/no exertion => pain at rest, rapidly worsening in intensity, frequency, and duration => unstable
What are the causes of Angina? Not RF!
1) CHD - Coronary heart disease
2) Valvular disease
3) HOCM - Hypertrophic Obstructive Cardiomyopathy
4) Arteritis
5) Anemia
6) Thyrotoxicosis
Diagnosis of angina is typically clinical. What would you like to elicit in a PC of chest pain for the diagnosis of angina?
Stable Angina: Episodic constant crushing/band-like chest pain radiating to the neck, shoulder or arms.
Unstable Angina: Pain on minimal/no exertion => pain at rest, rapidly worsening in intensity, frequency, and duration => unstable
Precipitated by exertion, cold, emotion, heavy meals
Relieved by rest or GTN spray
Associated sx: Palpitations, sweating, nausea, breathlessness
RF: Personal/family hx of vascular disease, CVA, PVD, increased BMI, Smoking
Episodic constant crushing/band-like chest pain radiating to the neck, shoulder or arms. What are your differentials?
Stable/Unstable angina
MI
Pericarditis
Dissection thoracic aneurysm
PE
Pneumothorax
Musculoskeletal pain/costochondritis
Oesophageal spasm
Episodic constant crushing/band-like chest pain radiating to the neck, shoulder or arms worse on exertion. They have a history of smoking and a family history of stroke and an amputation (PVD). What investigations would you perform as a GP?
Bloods:
FBC, U&E
Fasting Glucose
Lipid profile
ESR (rule out arteritis)
TFTs (rule out thyrotoxicosis)
ECG - Check for A.fib, heartblock, previous MI, myocardial ischemia, ventricular hypertrophy
You conduct an ECG as part of your investigations for angina. A normal ECG does not exclude angina but an abnormal ECG identifies a high risk for a CV event to occur in the next year.
What are you looking for on ECG
Typical rate, rhythm
Check for A.fib, heartblock, previous MI, myocardial ischemia, ventricular hypertrophy
What are the 2 main types of CCB (calcium channel blockers)? Give an example for each
How are they different?
What are the contraindications to CCBs?
Dihydropyridine: Amlodipine
BV>HR
Non-dihydropyridine:
Diltiazem, Verapamil
BV and HR (Called “rate-limiting”) because it affects the heart
CI: Heart-block and heart failure
GTN spray is typically prescribed for symptom relief in angina. How would you advise a patient to take it?
State 2 side-effects
1-2 puffs as needed in response to pain and before expected exertion
SE: Flushing, headache, lightheadedness.
A patient is on GTN spray PRN and on Verapamil. They complain of having to use the GTN spray too much and are looking for an update to their medications. What will you do?
This is first line tx => we move to second line. We should swap verapamil with a dihydropyridine CCB (Amlodipine) + Add beta blocker
What is the full medical management of angina
1) Symptom control:
GTN spray PRN
+
1st line: Beta blockers OR Non-dihydropyridine CCB (Verapamil, diltiazem)
2nd line: Combine beta blocker and !Dihydropiridine (Amlodipine)
3rd line: Long-acting nitrates (Isosorbide Mononitrate)
2) Secondary prevention
a) Antiplatelet (Aspirin/Clopidogrel) 75mg OD
b) Statin (Atorvastatin)
c) ACEi (Ramipril)
How would you refer a patient presenting with angina?
If stable - Rapid Access chest pain clinic
If unstable - Urgent referral to cardiology
Give your full management plan for Angina
1) Referral:
If stable - Rapid Access chest pain clinic
If unstable - Urgent referral to cardiology
2) RF reduction:
Reduce intake of fats. avoid saturated fats, low cholesterol diet
+
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Reduce caffeine
3) Medical:
a) Symptom control:
GTN spray PRN
+
1st line: Beta blockers OR Non-dihydropyridine CCB (Verapamil, diltiazem)
2nd line: Combine beta blocker and !Dihydropiridine (Amlodipine)
3rd line: Long-acting nitrates (Isosorbide Mononitrate)
b) Secondary prevention
a) Antiplatelet (Aspirin/Clopidogrel) 75mg OD
b) Statin (Atorvastatin)
c) ACEi (Ramipril)
Why can we not prescribe both a non-dihydropyridine CCB with beta blockers.
Dihyropyridines affect the HR => additive effect if combined with beta blockers
How do beta blockers work?
What are the main indications for Beta blockers?
Differentiate between selective and non-selective beta blockers giving 2 examples of each.
Explain the main side effects of each type
What are some contraindications?
They inhibit !beta adrenergic receptors! => blocking release of noradrenaline (remember this acts mostly on alpha adrenergic) and adrenaline (acts on alpha and beta where alpha deals with vasoconstriction and beta deals with heart rate and contractility) => inhibit SNS => reduce HR and BP
Indications: Coronary Heart Disease, Compensated Heart Failure, Cardiac Arrhythmias (Sotalol)
Selective Beta blockers (Atenolol, Bisoprolol, Metoprolol)
These drugs are selective for blocking the B1 receptor which is located in the heart.
Side Effects:
Bradycardia and Syncope (hypotension)
Bradyarrhythmia
At higher doses, affects B2 as well
Non-selective: Propanalol, Timolol, Sotalol Acts on B1 and B2
Beta-2 receptors are found in the bronchial tree, blood vessels, and other organs. This broader action leads to bronchoconstriction and vasoconstriction.
Side Effects:
Vasoconstriction and Bronchoconstriction => Contraindicated in PVD/PAD and asthma/COPD
Bradycardia and Syncope (hypotension)
Contraindications: Recent stroke/TIA, Active bleeding, HIT, Uncontrolled hypertension
MOA of ACE inhibitors
Main indications of ACE inhibitors
Give 2 examples of ACE inhibitors
Give the major side effects
Inhibits Angiotensin (produced by kidney along with renin) converting enzyme which is responsible for converting Ag1 (produced by liver) into Ag2 which then acts to vasoconstrict (in which the drug will cause vasodilation => reduced BP)
Indications: !HTN, HF, Acute MI!, Nephropathy, Coronary heart disease
Examples: Enalapril, Lisinopril, Ramipril
Side Effects: Hypotension (esp first dose), Dry cough (bradykinin buildup), Hyperkalemia, Renal Dysfunction
Long-acting nitrates (Isosorbide Mononitrate) is typically only given when 1st and 2nd line management has failed + the patient is unfit for surgery. Why?
Therapeutic tolerance rises very fast -> needs to have nitrate-free period
Reflex tachycardia (just like with beta blockers) due to it wearing off
Side effects of Headache, postural hypotension, lightheadedness
A patient presents to you 1 week post-MI to continue their care. What medications would you expect the patient to have been discharged with?
Beta blockers
ACEi/ARBs
Antiplatelet (Aspirin + Clopidogrel 75mg)
If Afib or failure of antiplatelet => Anticoag => Apixaban, enoxaparin
If HF/LVF/evidence of oedema => Spironolactone
What is the main pathophysiology of Chronic Heart Failure?
What are the 2 ways of classifying HF (go into detail)
When cardiac output<metabolic demand. It is the end-stage of all heart disease
High vs Low-output CF
High output CF = Heart is working normally but there is increased metabolic demand
Low output CF = Reduced heart function, normal demand
Ejection fraction:
Ejection fraction is Stroke volume/End-diastolic volume where is the normal is 55-70%
HFrEF is <40%
HFmrEF is 40-49% => borderline
HFpEF is >50%
What does a reduced ejection fraction (HFrEF) indicate?
What does a preserved ejection fraction (HFpEF) indicate?
HFrEF is <40% => impaired contractility
HFpEF is >50% => normal contracting, ventricles do not relax during diastole => reduced preload => more in system => Fluid overload!!
Give 3 examples of High output cardiac failure
Give 7 examples of Low output cardiac failure
High output CF = Heart is working normally but there is increased metabolic demand e.g. Hyperthyroidism, anemia, congenital AV malformations. (may also cause tricuspid regurg)
Low Output: Reduced heart function, normal demand.
1) Increased preload => Mitral regurgitation, fluid overload
2) Pump Failure:
Cardiac = Ischemic heart disease, cardiomyopathy
Restriction = Restrictive cardiomyopathy, constrictive pericarditis, Cardiac tamponade
Reduced HR => beta blockers, heart block, post-MI
Arrhythmia - A-fib
Reduced contractility - negative inotrope.
3) Increased afterload => Increaed BP and aortic stenosis;
What is paroxysmal nocturnal dyspnoea
Waking up gasping for air
What is Pulsus Alternans?
Alternating strong and weak pulses
You are asked to perform a history and exam on a patient during their general checkup. They have long-standing HTN, for which medication has already been prescribed. They have a past medical and surgical history consistent with stroke/TIA. Family hx includes paternal death from MI. Please take a history and perform an exam
History:
1) SOB - Exertion/angina, Orthopnoea, Proxysmal nocturnal dyspnoea.
2) Reduced exercise tolerance
3) Oedema (esp ankles)
4) Abdominal discomfort
5) Weight changes (either increased or decreased with muscle wasting/cachexia)
6) Nausea/Anorexia
7) Confusion/dizziness
Exam:
Vitals: Increased RR, HR, Pulsus Alternans
Inspection: Cachexia/muscle wasting
Palpation: Raised JVP, Hepatomegaly, RV heave, Displaced Apex! (Cardiomegaly)
Percussion: Shifting Dullness for ascites, lay be dull in lower lung bases.
Auscultation: 3rd HS, Basal Creps, pleural effusion (crackling).
Other: Pedal/ankle oedema
Why would a patient presenting with chronic heart failure be experiencing abdominal discomfort?
Liver distention
What is cachexia
Muscle weakness + Muscle wasting
What is the main investigation to conduct in a patient with chronic heart failure?
How will you then manage the patient?
BNP >400 or NTproBNP >2000
First time -> Send for specialist review. otherwise
1) Regular review assessing for:
a) Clinical state (incl functional capacity, fluid status…)
b) Depression (affects 40%)
c) Manage comorbidities
d) Labs: U&E, Creatinine, eGFR
2) Educate + RF reduction
RF reduction:
Reduce intake of fats. avoid saturated fats, low cholesterol diet
+
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Reduce caffeine
3) Medical:
For Fluid retention (all) => Loop Diuretic (Furosemide) escalated to Thiazide diuretic
For impaired LV contractility => only for HFrEF - ACEi/ARBs + Beta blocker (Bisoprolol)
4) Referral to specialist
When prescribing a thiazide diuretic as a second line diuretic in addition to furosemide for chronic heart failure, what would we need to monitor for?
Gout
Hypokalaemia
When treating patients with a certain disease, it is important to consider co-morbidities. CVS co-morbidities are the most common. Give 4 co-morbidities and the relevant medication you would add.
If AF or Hx of VTE -> Anti-coag (Clopidogrel 75mg)
If HF + Atherosclerotic disease (Aspirin 75mg)
If hyperlipidema, Qrisk >10… Atorvostatin
If Angina or raised BP (Dihydro CCB => Amlodipine) theyre probably on beta blockers so better to be safe with this
What is special about sotalol as compared to other beta blockers?
It is also an anti-arrhythmic
you have been treating a patient with chronic HF but they have begun to deteriorate. You have decided to refer the patient to a specialist for review of medications. What medications can this specialist initiate?
Spironolactone
Hydralazine + Nitrate (2nd line for impaired contractility => HFrEF)
Digoxin
Amiodarone
Implanted device (defibrillator)
What is Digoxin?
Anti-arrhythmic + Positive inotrope (Good for HFrEF)
What is Amiodarone?
What would you need to monitor when putting a patient on amiodarone?
Antiarrythmic
Must monitor for TFTs and LFTs
Define Atrial Fibrillation
Paroxysmal or chronic disturbance in cardiac rhythm characterised by
1) Rapid irregularly irregular rhythm
2) Narrow QRS
3) Absent P waves
Give 3 causes of chronic and 4 causes of Acute Afib
Chronic:
1) Idiopathic
2) Atrial dilatation => Valvular disease (Stenosis), fibrosis, or inflammation causing fibrosis
3) Increased muscle mass: LV hypertrophy secondary to HTN or cardiomyopathy.
Acute:
1) Infection
2) Surgery
3) MI
4) PE
5) Hyperthyroidism
6) High alcohol intake
You are assessing a patient’s pulse and notice a pulse deficit.
What is a pulse deficit?
What does it indicate?
A pulse deficit is when there is an increased pulse rate at the apex beat as compared to the radial.
This is indicative of Atrial fibrillation, other arrhythmias, HF, and valvular disease.
Atrial fibrillation is typically found incidentally or post-stroke/TIA as most are asymptomatic. How would a symptomatic patient with Afib present?
Only state what would you want to check on exam?
Palpitations +/- chest discomfort
SOB
Postural hypotension +/- dizziness/lightheadedness
Exam:
1) !!Pulse rate/rhythm Apex>radial
2) Raised BP
3) Displaced apex beat (cardiomegaly)
4) HS/Murmurs
5) Raised JVP
6) Signs of anaemia
7) Signs of thyrotoxicosis
What investigations would you conduct on a patient with a pulse deficit of 9bpm
1) ECG/24hr ECG
2) Bloods (FBC, U&E, eGFR, TFTs)
3) CXR -> evaluate for cardiomegaly, lung fibrosis
4) ECHO -> LV function, atrial size
What are the biggest complications of A.Fib
Embolic events
Stroke/TIA
PE
PVD
Give me the medical management of Atrial fibrillation
1) Rate limitation =>
1st line - B-blocker, Non-dihydropyridine (Diltiazem, verapamil), or Digoxin
2nd line - Any 2 mixed
2) Restoration of Sinus rhythm: Referral for DC cardioversion
3) Thromboembolism prevention: DOAC (Rivaroxaban/apixaban) or Warfarin
DC cardioversion has the highest success rate in young people with a normal heart and those with Afib for <1 year. What are the indications for DC cardioversion with out trial of rate-limiting drugs?
What drug is involved in the management of A.fib with DC cardioversion. How is it incorporated?
1) HF caused by Afib
2) Atrial flutter suitable for ablation
3) Reversible causes (e.g. chest infection causing acute A.fib)
Amiodarone should be started prior to DC cardioversion and then for 1 year after
What is the role of aspirin in the management of A.Fib
It is not effective in the prevention of thromboembolic events due to A.fib. DOACs and Warfarin are the mainstay prevention drugs for stroke.
What is the mechanism of action of Warfarin?
how is it countered?
Vitamin K antagonist
Vitamin K -> Fresh frozen plasma -> Pro-thrombin Complex
Define Atrial flutter (as you would see it on an ECG)
!Regular! Sawtooth appearance with baseline rate of 300bpm
+ superimposed tachycardia with narrow QRS
Atrial flutter is managed the same way as Atrial fibrillation (Rate control + rhythm control). What extra management option is available for Atrial flutter
Ablation
Heat or freezing to eliminate areas of the heart muscle causing irregular contractility
PVD is typically atherosclerotic, affecting arteries supplying the lower limb. Examination involves assessing arterial pulses. What are the 3 most common indications for assessing LL pulses?
1) Sx suggestive of PVD
2) DM, non-healing wounds on legs/feet, unexplained leg pain
3) When being considered for interventions in the foot or leg including compression stockings (ABPI>0.8)
What is the typical presentation of a patient with PVD?
What are your 2 main differentials and how would you rule them out?
Intermittent claudication: Muscular, cramp-like pain in LL on exertion, relieved by resting
Ddx:
Sciatica (Straight leg raise test + MRI)
Spinal stenosis (Typically bilateral + MRI)
Give 7 RF for PVD
1) Male
2) Smoking
3) Obesity
4) Raised BP
5) Hyperlipidemia
6) Physical inactivity
7) DM
8) Post-menopausal
9) Hyper-coagulable states
You are conducting an exam on a patient with PVD. They are stable and not in any pain (why? because at rest). What findings would suggest Aortic/iliac atherosclerosis vs Superficial femoral?
Both may have atrophic skin changes, ulceration, gangrene etc
Aortic/Iliac: Weak/absent femoral pulse +/- femoral bruit
Superficial femoral: Calf claudication. Absent popliteal/post-tibial/dorsalis pedis
Message: It affects what is below site of atherosclerosis
Where is the femoral pulse palpated?
Below inguinal ligament, midway between the ASIS and pubic symphysis
Where is the popliteal pulse palpated?
Flex knee at 90 degrees, palpate deep in the midline
Where is the post-tibial pulse palpated?
1cm behind the medial malleolus
Where is the dorsalis pedis palpated?
Lateral to the extensor tendon of the 1st metatarsal. Find the midpoint of the medial and lateral malleolus then draw an imaginary line into the first webspace. Palpate 1/3 of the way there.
What is the gold standard for diagnosing PVD?
ABPI <0.95 (oxford) <0.9 (everywhere else)
What investigations would you perform on a patient presenting with calf tenderness when walking that is relieved by rest?
What is the most likely problematic artery?
Most likely femoral or popliteal artery
Bloods: FBC, U&E, Cr, eGFR (renal artery stenosis), HbA1c (diabetes), lipids (atherosclerosis, obesity, hyperlipidaemia)
ABPI (<0.95/0.9)
Doppler US to determine site of disease
What is ABPI? How is it performed?
How would you interpret the results?
Ankle brachial systolic pressure index is a non-invasive screening tool for PAD by comparing systolic BP in the ankle and arm.
The patient would be lying down for 5 minutes with BP cuffs placed both on the ankle and arm. The doppler is then used to detect the pulse at both locations. The highest ankle BP is taken and divided by highest brachial to obtain a ratio.
1.4+ -> Non-compressible => Calcifies arteried (e.g. diabetes)
1-1.4 = normal
0.9-0.99 = borderline
<0.9 - Indicates blockage/narrowing => PAD
<0.5 = limb ischemia => claudication at rest
What is the full management plan for a patient presenting with intermittent claudication and an ABPI of 0.89
Conservative:
1) Supervised exercise program (>2h/week for 3 months) with advice to exercise to the point of maximal pain
2) Foot care via regular chiropody/podiatry
3) RF reduction
- Reduce intake of fats. avoid saturated fats, low cholesterol diet
+
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Reduce caffeine
Medical:
1) Anti-platelet therapy (Aspirin/Clopidogrel 75mg OD)
2) Naftidrofuryl (increases walking distance but no clear evidence of improving outcomes)
What is the typical presentation of Critical limb ischemia
Deteriorating claudication /claudication at rest. Pain»> what it looks
+ Nocturnal rest pain (hanging feet out of bed to relieve it)
+ Minor trauma causing ulceration and gangrene
What are atrophic skin changes?
Pallor, cool, hairless, shiny skin (you can add in ulceration and gangrene)
What will you look for on exam and what findings are you expecting in the setting of critical limb ischemia?
Inspection: Atrophic skin changes (Pallor, cool, hairless, shiny skin), Ulceration and gangrene
Palpation: Capillary refill time (>2s), Absent foot pulses, Hard, tender calf, check for blanching, loss of sensation
Special test: Buerger’s test
Explain Buerger’s test
Special test for peripheral vascular disease/critical limb ischemia. Elevate legs (+/-milking) to 45 degress for a few minutes and observe for pallor, venous guttering (indentation)
+
On lowering the legs, Rubor occurs (Dusky, blue-red colour)
What ABPI would indicate critical limb ischemia?
<0.5
How would you manage a patient coming into your clinic with claudication at rest, ulcerations, and excruciating pain when standing? (include secondary care)
Youre still a GP so, Give Opioid analgesia with urgent/emergency admission for specialist care
The specialist will then go for angiography, percutaneous transluminal angioplasty and stenting, aorto-bifemoral bypass and finally amputation
You’ve referred someone with critical limb ischemia to the emergency department. Theyve performed an aorto-bifemoral bypass after confirming occlusion via angiography. What medication would this patient be on to prevent re-occlusion of the artery?
Aspirin
Define Varicose Veins
What are the different types?
Tortuous, twisted, or lengthened veins due to weakness and dilatation of veins => separation of valves leading to their incompetence => Reverse flow of blood and pooling
1) Telangiectasia: Intradermal venules <1mm e.g. spider veins/matted veins, starbursts
2) Reticular: Dilated, tortuous, subcutaneous veins, not main veins
3) Trunk: Varicosities of the long or short saphenous vein or their branches
What are the primary and secondary RF of varicose veins?
Primary:
1) Age
2) Parity
3) Occupation/lifestyle with extended periods of standing
4) Obesity (in women)
Secondary
1) DVT
2) Pelvic tumour
3) Pregnancy
4) AV fistula (=> Dialysis)
What are matted veins
Cluster of spider veins in telangiectasia varicose veins
Telangiectasia and reticular varicose veins are typically asymptomatic. Patients will typically present due to their appearance and prognosis rather than due to symptoms. What is the typical symptomatic presentation of varicose veins?
In terms of past medical/family hx, what would you like to know?
Especially with Trunk Varicose veins
1) Heaviness
2) Tension
3) Aching pain worse on standing and in evening, better with elevation/support stockings
4) Itching
Past personal/family hx:
Pregnancy, past hx of DVT, !Thrombophlebitis, HRT, COCP. Past tx/surgery for varicose veins
Where does the short and long saphenous veins run?
Short: Below knee, posterolateral aspect of gastrocnemius
Long: Thigh and medial aspect of gastrocnemius
You have just taken a history from a patient presenting with large varicose veins running along the posterolateral aspect of the right leg. Their occupation involves them standing for long periods of time. What vein is this?
What examination findings will you look for?
Short saphenous vein
1) Large, tortuous, dilated veins/telangiectasia
2) Lipodermatosclerosis
3) Hemosiderin deposits
4) Oedema or pooling of blood
5) Venous ulcers
6) Capillary refill time (<2s)
7) Atrophic blanche
Special:
1) Bleeding stemmed from elevating foot above level of heart and applying compression
2) Saphena Varix
What is lipodermatosclerosis
Tight, rigid skin due to hardening of fat giving off a champagne bottle appearance
What are hemosiderin deposits
Permanent brown pigment due to breakdown of hemoglobin
What is Atrophie blanche
Venous skin findings of pale, atrophied, porcelaine-like area of skin. White, lacy scar.
Explain What the Saphena Varix is
Explain how you would test for saphena varix and interpret the results
Saphena Varix is the presence of dilatation along the saphenous veins.
Palpate 2-4cm inferolateral to the pubic tubercle and apply pressure to occlude the SFJ (Saphenofemoral junction). Ask the patient to stand while still keeping pressure and then release.
normal = vein fills down -> up which indicates that the valves are competent
Abnormal = vein fills up to down => retrograde flow => venous reflux
+ cough impulse. The saphena varix may be large such that there is a lump due to the dilatation. The saphena varix should disappear when lying down and should be reducible. Ask the patient to cough and if it distends, it is also consistent.
How would you differentiate between saphena varix and an inguinal hernia?
Both will distend with cough. The saphena varix is reducible whereas the inguinal hernia is irreducible. Also you can talk about the different symptoms and the test itself which should not occlude anything in an inguinal hernia + bowel sounds
A patient presents with a very painful limb. On examination you note pyrexia and a large varicose vein running down the medial aspect of the left leg. There is a patch of redness around the area. What vein is this?
What is the most likely diagnosis?
Long saphenous vein
Thrombophlebitis
ddx: DVT not wrong
A patient presented to the clinic complaining of a large vessel (vein). She does not have any symptoms. She asks you what this means and what can happen as a result of this in the future. What are the complications of varicose veins
1) Haemorrhage (bleeding)
2) Varicose eczema (itching)
3) Skin pigmentation (atrophie blanche, haemosiderin)
4) Lipodermatosclerosis
5) Thrombophlebitis
6) Oedema
7) Venous ulceration
What is the typical presentation of Thrombophlebitis
State 4 causes
How would you manage this thrombophlebitis?
Presentation: Severe pain, erythema, pigmentation over area, hardening of veins
Results from stasis in varicose veins. Otherwise also occurs as a result of trauma, IV insertion, prolonged inactivity, pancreatic carcinoma and infection (septic thrombophlebitis)
Management:
No antibiotics (unless septic thrombophlebitis)
1) Support stockings if ABPI >0.8
2) Ice + elevation
3) Analgesia (NSAIDs)
4) Aspiring 75mg OD
A patient is having recurrent thrombophlebitis. What must be ruled out?
Pancreatic carcinoma
Glasgow scoring and amylase
A DVT may occur anywhere, including the cerebral sinus. Is this considered a stroke?
No it is not an artery
DVT can also occur in the veins of the arms, retina and mesentery
A DVT, although mostly occurring in the lower limbs may also occur in the upper limb. What is the most common cause of that?
Central venous catheter
Give 8 RF for DVT
1) Age >40
2) smoking
3) Obesity
4) Immobility
5) Long-distance travel
6) Pregnancy
7) Surgery/post-op
8) Recent trauma
9) Malignancy
10) IBD
11) Clotting disorders including APS, thrombophilia
12) Oral estrogen (COCP)
What is the traditional presentation of DVT
!Unilateral! leg pain, swelling, warmth +/- pitting oedema
A patient presents with unilateral leg pain, swelling, warmth +/- pitting oedema. Give 6 ddx
1) DVT
2) Cellulitis
3) Ruptured Baker’s cyst
4) Theombophlebitis
5) Acute arterial/limb ischemia
6) Fracture/trauma
7) chronic venous insufficiency
8) Hypoproteinemia
How would you diagnose DVT?
Clinical diagnosis suggestive of DVT + Well’s Diagnostic score (1 point each)
1) Active cancer (malignancy is a RF)
2) Paresis/paralysis
3) Bedridden/immobile for >3 days/major surgery in past 12 weeks
4) Localised tenderness along saphenous vein (long or short)
5) Calf diameter difference >3cm
6) Entire leg swelling
7) Unilateral pitting oedema
8) Collateral superficial veins (not varicose)
9) Previous DVT
Add up points and -2 if another differential is more likely
0-1 = Low risk
2+ = High risk
When doing hx and exam look for these.
What is the role of a D-dimer in the diagnosis of DVT
D-dimer is not diagnostic for DVT. It has a strong -ve predictive value => can be useful to rule out but weak positive predictive value.
How would the Well’s score influence the workup and management of the patient
0-1 = Low risk => D-dimer to exclude. If +ve go with high risk
2+ = High risk => Compression US assessment + D-dimer. If positive refer to DVT assessment clinic or hospital
What is the management of confirmed DVT (including secondary care)
If you are confirming it, refer to DVT assessment clinic or hospital.
Patient will have compression stockings (if ABPI>0.8) for 2 years and will be put on either
a) DOAC -> Rivaroxaban/Apixaban for 3-6 months for 3-6 months
b) LMWH for 4 days or until target INR of 2.5 is reached followed by oral warfarin
What are the complications of DVT
1) Pulmonary embolism
2) Post-thrombotic syndrome
3) Recurrent DVT: increased risk of recurrence especially after surgery, pregnancy…
What is post-thrombotic syndrome?
Chronic venous hypertension causing limb pain, swelling, hyperpigmentation, dermatitis, ulcers, venous gangrene, lipodermatosclerosis… (all the venous sx)
How would you differentiate between a venous and arterial ulcer on exam?
What are the components of the CHADS VASC Score
A patient with HF also has A.fib what will you add to the management
Anti-coagulation (LMWH, edoxaban, warfarin)
A patient with HF also has a history of VTE, what will you add to the management
Anti-coagulation (LMWH, edoxaban, warfarin)
A patient with HF also has a history of atherosclerotic disease, what will you add to the management
Aspirin 75mg + check QRisk for statin indication
A patient with HF also has a history of angina and raised BP, what will you add to the management
CCB - Amplodipine
What investigation is most important in the diagnosis of heart failure?
When referring for specialist treatment of heart failure, what is the main investigation performed?
What is the full management plan for Heart failure including specialist management.
BNP >400 or NTproBNP >2000
First time -> Send for specialist review for Doppler ECHOcardiography. otherwise:
1) Regular review assessing for:
a) Clinical state (incl functional capacity, fluid status…)
b) Depression (affects 40%)
c) Manage comorbidities
d) Labs: U&E, Creatinine, eGFR
2) Educate + RF reduction
RF reduction:
Reduce intake of fats. avoid saturated fats, low cholesterol diet
+
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Reduce caffeine
3) Medical:
For Fluid retention (all) => Loop Diuretic (Furosemide) escalated to Thiazide diuretic escalated to spironolactone
For impaired LV contractility HFrEF => only for HFrEF - ACEi/ARBs + Beta blocker (Bisoprolol) escalated to Hydralazine + Nitrate
4) Referral to specialist:
Apironolactone
Hydralazine + Nitrate
Digoxin
Amiodarone
Implanted device/defibrillator
How does pulmonary arterial pressure compare to systemic
1/5
What is considered pulmonary hypertension?
Pulmonary arterial pressure >25mmHg
Pulmonary hypertension is classified into 5 groups. What are they and which group corresponds to Cor Pulmonale
Pulmonary HTN due to
Group 1 - Idiopathic or Connective tissue disease (scleroderma) (CTD)
Group 2 - Left heart disease/Severe HF OR valvular disease OR Congenital heart disease (CHD)
Group 3 - Lung disease => Cor pulmonale, COPD, Interstitial lung disease
Group 4 - Chronic thromboembolism (PE, sickle cell disease)
Group 5 - Multifactorial or unclear mechanisms
Define Cor pulmonale
What are the 3 most common causes?
Pulmonary heart disease. Right HF (enlargement of the right ventricle) as a response to pulmonary hypertension (group 3)
Most common causes:
COPD (group 3)
Interstitial lung disease (group 3)
PE (group 4)
What is the typical presentation of Cor pulmonale?
What are the examination findings as you go through a focused exam?
Presentation:
1) SOB on exertion
2) Angina on exertion
3) Palpitations
4) Light-headedness, pre-syncope, syncope
5) Fatigue, lethargy
6) Peripheral oedema/Ascites
Inspection: Cyanosis, Peripheral oedema
Palpation: Raised JVP, Hepatomegaly
Percussion: Ascites, pleural effusion
Ausculation: 4th HS, Diastolic Murmur, Crepitations at lung bases (pleural effusion)
The diastolic murmur heard on ausculation would be due to?
Pulmonary regurgitation
What findings on CXR would indicate Cor pulmonale?
Enlargement of the proximal pulmonary arteries
+ Prominent right heart border
What ECG findings would indicate RHF?
Right axis deviation
Peaked P wave I and II
Peaked R wave in V1 and V2
What investigations are performed to assess pulmonary artery pressure? (3)
Where are these tests performed?
1) Doppler ECHOcardiogram (Assesses ventricular function and valve function + estimates pulm artery pressure)
2) Right heart catheterisation: Direct measurement of mean pulmonary pressure
3) Pulmonary capillary wedge pressure
What investigations would be performed in the GP and in the hospital with regards to Cor pulmomale?
GP:
CXR - Enlarged proximal pulmonary arteries + Prominent right heart border
ECG - Right axis deviation, Peaked P wave in I&II, Peaked R wave in V1&V2
Hospital:
1) Doppler ECHOcardiogram (Assesses ventricular function and valve function + estimates pulm artery pressure)
2) Right heart catheterisation: Direct measurement of mean pulmonary pressure
3) Pulmonary capillary wedge pressure
4) 6-minute walk test to assess functional capacity
What result on the 6-minute walk test would indicate poor prognosis?
<300 meters in 6 minutes
What is the surgical management for Chronic cardio-thromboembolic pulmonary hypertension
Group 4 => PE causing cor pulmonale => Pulmonary Endarterectomy
What is Pulmonary Endarterectomy?
Treatment of choice for those with PE causing cor pulmonale or chronic thromboembolic pulmonary hypertension (>90% 5yr survival)
Involves dissection of the pulmonary artery to remove chronic blood clots => improving flow and reducing pulmonary pressure
What is the management of Cor pulmoale?
1) Referral to specialist cardiologist
2) O2 therapy for symptom relief
3) Diuretic tx (Furosemide, thiazide, spironolactone)
4) Vasodilation via CCB (amlodipine)
5) Anticoagulation (remember the etiology with PE)
Surgical: For all: Bilateral lung/heart transplant
Group 4 only (including PE!!) -> Pulmonary endarterectomy
What is the Thrombolytic management of PE and DVT compared to that of stroke?
So.. in stroke there is a narrow window of opportunity <4.5 hours to administer the alteplase (tPA). This is administered as 0.9mg/kg up to 90mg. 10% bolus and 90% over the hour. They are then put on Anticoag therapy after. Large clots via thrombectomy <12 hrs.
With regards to PE and DVT. Management begins with anticoag therapy (not warfarin because that takes a few days to work) while awaiting CT angio. For unstable patients or large clots, however, they are given alteplase. in PE 100mg over 2 hours. In DVT it is injected directly where the clot is and varies based on size of the clot.
Give 3 diagnostic imaging tools used for ischaemic limb
Duplex USS
CT angiography
MR angiography
What is the medical and surgical management of acute limb ischaemia
Medical:
1) Immediate anticoagulation with IV heparin
2) Analgesia
Surgical:
1) Catheter-directed thrombolysis (tPA) directly into clot
2) Bypass surgery (autologous venous graft from great saphenous otherwise synthetic)
3) Embolectomy/Thrombectomy
When performing a cardiovascular exam, youve auscultated the 4 valves of the heart. What is left to ausculate?
How should you report your findings
Carotids for carotid bruit and radiation in aortic stenosis (Ejection systolic)
Listen in left axilla for mitral regurgitation (Pan systolic)
Lean patient forward in full expiration and listen at left lower sternal border for aortic regurg
Turn patient in left lateral position and listen over mitral valve (apex beat for Mitral stenosis.
Report as:
A pan/ejection systolic murmur loudest at X, radiating to the Y, louder on Inspiration/expiration, with a grade of Z/6
