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
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
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 a venous and arterial ulcer on exam?
What are the components of the CHADS VASC Score
