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CCC > Primary Care - Cardiovascular > Flashcards

Primary Care - Cardiovascular Flashcards

1
Q

Define hypertension

What are the risk factors for hypertension?

A
  • BP persistently above 140/90mmHg.
  • has to be confirmed by either HBPM or ABPM (135/85)

Unmodifiable

  • black African or black Caribbean
  • age
  • family history of HTN/CVD/ high cholesterol/diabetes/kidney problems/stroke/heart attack
  • sex (men more at risk <65, women more at risk >65)

modifiable

  • high salt diet
  • lack of exercise
  • drinking
  • obesity
  • smoking
  • anxiety/stress
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2
Q

Describe how the renin-angiotensin system works

A

1) If renal perfusion is low, kidney juxtaglomerular cells convert pro-renin (present in blood) into renin
2) Renin converts angiotensinogen (secreted by liver) into angiotensin I
3) Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE), released from lungs
4) Angiotensin II is potent vasoconstrictor + promotes adrenal glands to produce aldosterone
5) Aldosterone makes kidneys reabsorb sodium and water into blood (and excrete potassium to maintain electrolyte balance)

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3
Q

What are the stages of hypertension? Explain how you would manage the stages?

A

Stage 1: clinic blood pressure at least 140/90 and (confirmed by ABPM 135/85)

Stage 2: clinic BP >160/100; ABPM >150/95.

Stage 3: Severe hypertension: >180/110

Malignant: >200/120

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Management
-For stage 1 and 2 do ABPM/HBPM and while your waiting check for end organ damage. Review both in 1 month. In the mean time advise lifestyle

  • For severe do not bother with the ABPM or HBPM, start medications right away
  • For severe with signs of end organ damage (accelerated) (papilodemia/retinopathy/chest pain/AKI) you should refer them for same day special care

IF LESS THAN 40 refer to CVD specialist

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4
Q

10% of hypertension is caused by secondary causes, what are some examples? (6)

A

Low renal flow (effects of renin and aldosterone)
- glomerulonephritis/atherosclerosis/vasculitis/aortic dissection/fibromuscular dysplasia

  • Conn’s adenoma - tumour of adrenal gland leading to high levels of aldosterone
  • Phaeochromocytoma - tumour in the adrenal medulla that causes sympathetic nervous system activation leading to increased BP, HR, anxiety, palpitations and skin presentations (urgent referral)
    ↑ 24hr Urinary metenepherine
    Give Phenoxybenzamine (a blocker) then Propanolol (BB)
  • Pregnancy
  • Steroids, OCP and HRT
  • White coat hypertension (discrepancy more than 20/10mmHg)
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5
Q

While your waiting for your ABPM/HBPM what investigations would you do?

A

ABPM/HBPM - required to confirm diagnosis, in the meantime investigate for end organ damage and risk factors:

  • Lipids
  • Hba1C
  • Total cholesterol and HDL cholesterol

Kidneys:

  • U+Es, creatinine and egfr
  • Urine dipstick (heamaturia) and Albumin:creatinine (proteinuria) >3 signif

Cardiovascular:

  • Qrisk3 >20%
  • ECG

Eyes:
-Fundoscopy (arteriolar constriction, arteriovenous nicking, vascular wall changes, flame-shaped hemorrhages, cotton-wool spots, yellow hard exudates, and optic disk edema)

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6
Q

What is ABPM?

How do you do home BP monitoring?

A

ABPM (ambulatory)
- For for 12 hours
- It automatically takes 2 readings every hour
- The cuff might tight unexpectedly and it might not be predictable when it is going to do it.
- It needs to take AT LEAST 14 measurements before it can start to calculate averages (24 hours)
If < 80 treat BP ≥ 135/85; if > 80 treat BP ≥ 145/85

HBPM (if they cant do ABPM due to unpredictability)

  • Twice a day for 7 days (morning and eve)
  • Each of BP recording must be done twice at least 1 minutes apart with patient seated
  • Discard readings for day 1 (getting used to it)
  • Take an average of the rest
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7
Q

What score is relevant to HTN?

How do the results effect management?

A

QRISK3

  • Estimates 10-year risk of developing CVD
  • If over 20%, consider high risk and encourage patient to take statin
  • Between 10-20% is moderate risk; NICE recommends discussing with patient about starting a statin
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8
Q

When would you treat HTN with medications?

A

HTN and medications
offer all patients lifestyle advice diet (↓salt, sugar, fats), weight loss, ↑exercise, smoking, ↓alcohol, ↓caffeine

  • treat all stage 3/severe HTN >180/110
  • if stage 1 (140/90) or stage 2 (160/100) they will have an ABPM
  • if ABPM <135/85 don’t treat (unless clear end organ damage)
  • if ABPM 135/85+ then treat if QRISK2 score ≥20% (or if end organ damage)
  • Treat all confirmed stage 2 (ABPM 150/95+)
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9
Q

What is the drug treatment of hypertension?

A

Step 1: A or C

  • <55 years or diabetic of any age - ACE INHIBITOR (ramipril 2.5mg OD)
  • If patient doesn’t tolerate then consider ARB (sartan)

55 years+ or Black of any age- CALCIUM CHANNEL BLOCKER (amlodipine 5mg PO OD)
-if patient doesn’t tolerate give thiazide like diuretic

xxxxxxxxx

Step 2: A and C (or A and D if CCB not tolerated)

  • If patient was on ACEi, then add calcium channel blocker
  • If patient was on calcium channel blocker then consider adding ARB

xxxxxxxxx

Step 3: A and C and D
ACEi/ARB + Ca channel blocker + thiazide diuretic
Ramipril, Amlodipine + (Indapamide or Chlortalidone)

xxxxxxxxx
Step 4: REFER TO SPECIALIST
If potassium <=4.5 add spironolactone
If potassium>4.5 add beta (atenolol) or alpha blocker (tamsulosin/carvedilol)

Ramipril, Amlodipine, Indapamide, spironolactone (check K+)

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10
Q

When are beta-blockers first line for HTN?

A

1) Resistant hypertension when potassium is high so cant use spirolactone
2) Pregnant women - ACEi are teratogenic in 1st trimester (give labetolol)

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11
Q

Give an example of a thiazide

What is the mechanism of action of thiazides?

A

Thiazide diuretics e.g. Indapamide or Chlortalidone

  • INHIBIT sodium REABSORPTION at DISTAL convoluted tubule by binding to Na/Cl co-transporter
  • This causes increased Na + K excretion
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12
Q

When are thiazides contraindicated?

A

(Thiazides increase Na+ and K+ excretion)

  • Hyponatraemia - in the elderly, thiazides are a common cause of hyponatraemia
  • Hypokalaemia
  • Hypercalcaemia
  • Renal impairment
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13
Q

Example of a loop diuretic? What is the mechanism of action of loop diuretics?

How do they compare to thiazides?

A

Loop diuretic e.g. Furesamide

  • They inhibit resorption of sodium in ascending loop of Henlé
  • This causes increased Na+ and K+ excretion

Compared to thiazides:

  • more potent
  • shorter half-life
  • better tolerated in patients with CKD
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14
Q

Example of potassium sparing diuretic? What is the mechanism of action of potassium-sparing diuretics?

A

Potassium sparing diuretic e.g. spironolactone

  • Aldosterone antagonist
  • Competitively inhibit aldosterone-dependant sodium-potassium exchange channels in the distal convoluted tubule
  • This action leads to increased sodium and water excretion, but more potassium retention
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15
Q

When are ACE inhibitors contraindicated?

A
  • Renal artery stenosis
  • Pregnancy
  • Hyperkaleamia (reduced aldosterone>reduced K excretion)
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16
Q

What the side effects of ACE inhibitors?

A
  • Dry cough
  • Impotence/sexual dysfunction
  • Hypotension - take the first one in bed at night
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17
Q

What is decubitus angina?

A

Occurs when lying down

Impaired left ventricular function due to severe coronary artery disease

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18
Q

What differentiates stable angina/CAD from ACS?

A
  • relieved by GTN spray
  • relieved by rest
  • lasts less than 20 minutes
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19
Q

What are the 5 types of MI?

A
  1. Spontaneous MI due to plaque rupture
  2. Low oxygen/hypoperfusion due to increased oxygen demand (fibrillation/tachycardia) or decreased supply (septic shock, anaemia)
  3. Sudden unexpected cardiac death
  4. Associated with PCI or stent thrombosis
  5. Associated with cardiac surgery
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20
Q

What are the risk factors for prinzmetal (spazmodal) angina?

A

Things that cause coronary artery vasospasm e.g.:

  • Cocaine
  • Smoking
  • Low magnesium
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21
Q

What does an ECG of a STEMI show at different time points post-MI?

A 
5-30 mins: tall tented T waves
Hours: ST elevation
Days: inverted T waves + development of Q waves
Months: Q waves remain
might get LBBB
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22
Q

When do troponin levels risk, peak and return to baseline?

A

Levels increase 3-12 hours from pain onset
They peak at 24-48 hours
Return to baseline 5-14 days

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23
Q

What is the acute management of a STEMI?

A 
ABCDEG assessment and ROMANCE 
-Reassure patient 
-Oxygen (low flow) if sats <90% or breathless  
-Morphine (5-10mg IV) and metoclopramide 
-Aspirin (300mg PO, then 75mg OD) 
-Nitrates (GTN spray) 
Ticagrelor (180mg PO, then 90mg OD) 
-ECG monitoring throughout

If <12 hours since onset and PCI available within 120 mins
-PCI and anticoagulant (unfractionated as shorter half-life)

If <12 hrs since onset + PCI NOT available within 120 mins

  • Thrombolysis and anticoagulation (heparin)
  • THEN transferred to PCI centre (either rescue PCI or angiography)

if they cant have either repercussion treatments, give heparin

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24
Q

What should be checked in all post-ACS patients?

A

Echocardiogram - check LV function
Lipid profile
HbA1c

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25
Q

What is the delta change in troponin levels?

A
  • Delta troponin is the percent difference between two troponin results taken in the same patient within a 3 - 8 hour time period
  • If it is greater than 20%, this is consistent with an MI
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26
Q

What are the DVLA regulations regarding ACS?

A

Stop driving for 4 weeks if no PCI/unsuccessful PCI
OR
Stop driving for 1 week if successful PCI
In both cases, the DVLA does not need to be informed

HGV drivers must inform the DVLA and stop driving for 6 weeks then meet with doctor to see if fit

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27
Q

What is the management of angina?

A

MANAGE RISK FACTORS
MANAGE SYMPTOMS
- 1st line - BETA-BLOCKER/CCB + GTN as rescue
-If both beta-blockers and CCBs are contraindicated or not tolerated, consider monotherapy with one of the following drugs:
-A long-acting nitrate (such as isosorbide mononitrate).
-Nicorandil (K+ channel blocker)
-Ivabradine
-Ranolazine

2nd line
Beta blocker and long acting dihydropyridine CCB combined (nifedipine, amlodipine)

SECONDARY PREVENTION

  • Anti-platelet (low dose aspirin 75 mg daily or clopidogrel (If PVD/stroke should continue to use clopidogrel)
  • ACE-I if stable angina and risk factors (diabetes, CKD, HTN)
  • Statin

-Patients with stable angina should be considered for re-vascularisation (with CABG or PCI) CABG better is 65+ or diabetic

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28
Q

What advise do you give to patients about using GTN spray?

A
  • GTN spray - when you have chest pain, stop what you’re doing, sit down and spray GTN under lounge
  • If the symptoms are still there after 5 minutes take another dose… if the symptoms persist after 5 minutes again then ring an ambulance
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29
Q

How can you describe heart failure?

What classification is used to determines someones functionality in heart failure?

A

When the cardiac output is inadequate for the body’s requirements leading to peripheral hypoperfusion

THE NEW YORK CLASSIFICATION (1-4)
(my adaption)
1. Feels fine. No limitation (heart disease but no undue dyspnoea from normal activity)
2. Climbing stairs. Slight limitation (comfortable at rest, dyspnoea on normal activity)
3. Getting dressed. Marked limitation (less than ordinary activities cause dyspnoea)
4. Sitting down. Dyspnoea at rest, all activity causes discomfort (specialist referral)

  1. No limitation (heart disease but no undue dyspnoea from normal activity)
  2. Slight limitation (comfortable at rest, dyspnoea on normal activity)
  3. Marked limitation (ess than ordinary activities cause dyspnoea)
  4. Dyspnoea at rest, all activity causes discomfort
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30
Q

What are some causes of high output heart failure?

A

This is when the heart is working at normal/increased rate but needs of the body are beyond that which heart can supply

  • Hyperthyroidism
  • Anaemia
  • Paget’s disease
  • AV malformation
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31
Q

What is the difference between systolic and diastolic heart failure? (comment on most common cause and ejection fraction)

A

Systolic

  • Ventricles enlarged and can’t contract normally
  • Resulting in reduced cardiac output
  • Most common cause=IHD/MI
  • Ejection fraction <40%

Diastolic

  • Stiff ventricles (increased filling pressures-can’t fill properly)
  • Most common cause=HTN (hypertrophy)
  • Ejection fraction >50% (just do furosemide and ACEinhib if HTN)
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32
Q

What are some causes of systolic/diastolic heart failure?

A

Causes of systolic heart failure

  • Ischaemic heart disease
  • MI
  • Cardiomyopathy

Causes of diastolic heart failure

  • Constrictive pericarditis
  • HTN
  • Cardiomyopathy
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33
Q

How does left ventricular heart failure present? (symptoms and examination findings)

A

Failure of the left side of the heart causes blood to back up into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood

  • Dyspnoea → Orthopnoea → PND (night cough) due to pulmonary oedema
  • Pink frothy sputum
  • Wheeze (cardiac asthma)
  • Fatigue, weight loss, muscle wasting

Examination signs:

  • Cyanosis, increased RR
  • Basal fine crepitations
  • Displaced Apex + RV Heave + S3 (compliant LV)
  • Pulsus alternans (alternate strong and weak beats)
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34
Q

How does right ventricular heart failure present?

A 
Failure of the right ventricle leads to congestion of systemic capillaries, which generates excess fluid accumulation in the body
-Peripheral oedema
-Calf swelling
-Ascites 
•can cause N+V>pressure on stomach 
•can cause dyspnoea>pressure on IVC and diaphragm
•weight gain 
•↑JVP – distended
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35
Q

What is the blood pressure like in heart failure?

A

Low BP with narrow pulse pressure (decreased pumpinig)

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36
Q

What is the pulse like in heart failure?

A

Heart failure

  • Pulse alternans - alternate strong and weak beats
  • Increased HR
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37
Q

What would you feel on palpation of heart failure?

A

Heart failure

  • Displaced apex beat - LV dilated
  • parasternal heave (RVH-closest side to chest wall)
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38
Q

What would you hear on auscultation of LEFT ventricular failure?

A

Left ventricular failure

  • Gallop rhythm due to presence of S3 (blood hitting a non compliant Left ventricle)
  • wheeze (cardiac asthma)
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39
Q

What investigations should be done in suspected heart failure? (bedside, bloods, imaging)

A

BEDSIDE

  • ecg and BNP
  • peak flow or spirometry (may look quite restrictive)

URINE DIPSTICK (elude CKD)

  • for blood/protein
  • increased specific gravity seen in heart failure (and other dehydrating conditions)

BLOODS

  • FBC
  • U+E
  • thyroid profile (increased demand for pumping)
  • HbA1c-risk factor
  • Lipids-risk factor
  • LFTs (back flow)
IMAGING 
Chest X-ray 
Alveolar oedema “bat wings”
Kerley B lines (IS oedema) 
Cardiomegaly
Dilation of upper lobe vessels
Pleural Effusion (bilateral, can be seen in horizontal fissure)
40
Q

What is BNP?

Explain the results of BNP

A

1st line investigation if NT-ProBNP
>400 suggest HF and echo within 6 weeks
>2000 URGENT echo within 2 weeks

IF either ECG or BNP are abnormal- do an ECHO
IF both normal- heart failure is very unlikely

41
Q

What is the criteria used to diagnose congestive cardiac failure?

A

Framingham criteria

diagnosis of congestive heart failure is 2 major criteria OR 1 major + 2 minor criteria

Major criteria:

  • PND Paroxysmal nocturnal dyspnea
  • Crepitations
  • Neck vein distention
  • S3 gallop
  • Hepatojugular reflex
  • Cardiomegaly
  • Increased CVP
  • Weight loss >4.5kg over 5 days

Minor criteria:

  • Bilateral ankle oedema
  • Dyspnoea on normal exertion
  • Tachycardia > 120bpm
  • Nocturnal cough
  • Hepatomegaly
  • Pleural effusion
  • Decreased vital capacity by 1/3
42
Q

What is the management of acute heart failure?

A

LMNOPE

  • Loop diuretics - furosemide 40-80mg IV (if already on, either increase dose or add thiazide (Bendroflumethiazide)
  • Morphine and metoclopramide (1.25-2.5mg diamorphine)-reduces preload/afterloud
  • Nitrates - 2 puffs GTN or IV (ensure not hypotensive)
  • Oxygen (15L NRBM), cPAP machine if really bad
  • Prop them up
  • ECG

If systolic BP<100, send to ICU

43
Q

What is the management of chronic heart failure?

A

HEART FAILURE TREATMENT (ABAL)
FIRST LINE
-ACEi AND beta-blocker (E.g. ramipril and bisoprolol)
-only add one at a time (diabetes-ACE 1st. Angina-BB first)
-avoid ACEi in severe valve disease (specialist review first)

SECOND LINE:
-if symptoms not controlled on A+B give an aldosterone antag (spironolactone/eplerenone)

THIRD LINE

  • loop diuretic (Fursemide/Bumetanide)
  • small dose as poss to control SYMPTOMS (not mortality)

**check Us and Es before starting and 2 weeks after starting ACEi and sprionlactone (hyperK)

44
Q

What are some specialist treatments for HF?

A

Heart failure (specialist treatments)

  • Ivabradine (EF <35%)
  • Sacubitril valsartan (EF <35%)
  • Hydralazine+ nitrate (esp Afro-carribean with moderate-severe HF)
  • Digoxin if AF (watch for hypokalaemia in combo with furosemide)
  • Surgery*
  • Offer AV replacement if HF due to severe aortic stenosis.
45
Q

What are some complications of heart failure?

How often should they HF patients be reviewed?

A 
Complications of heart failure 
-Cardiogenic shock 
-AKI/CKD
-Pleural effusion
Every six months should be reviewed (unless change in meds-2 weeks review
46
Q

What is Atrial fibrillation?

How do you describe the rhythm of atrial fibrillation?

A

AF

  • Disorganised electric activity in the atria
  • Signals are not systematically triggered via the SA node,
  • Instead, are generated from all over the atria, resulting in a quivering or fibrillating (don’t contract properly) and uncoordinated atrial activity.
47
Q

What are the most common causes of AF?

A

Coronary artery disease
Hypertension
Valvular heart disease
Hyperthyroidism

(also caused by wolf parkinson white, caffeine/alcohol/pulmonary HTN)

48
Q

What is paroxysmal AF?

A

When the symptoms of AF last less than 48 hours. More at risk of clots (pools, forms clot, then throws it out).

If nothing found on ECG-get them to wear a 24 or even a 72 hour ECG

49
Q

How do you investigate suspected paroxysmal AF?

A

ambulatory ECG

50
Q

What are some symptoms of AF?

A 
Often asymptomatic 
Palpitations
Chest pain
Dyspnoea
Fatigue
Light-headedness or syncope
51
Q

What does an ECG of AF show?

A

Absent p waves
Irregular QRS complexes
Irregular RR intervals

52
Q

What score is relevant to AF?

A

CHA2DS2VASc score - calculates the risk of stroke in AF

o Congestive HF/LVSD 1
o Hypertension 1
o Age 65+ 1point.....75+ 2points
o Diabetes mellitus 1
o Stroke/ TIA/ thromboembolism Hx 2
o Vascular disease 1
o Sex category (female) 1

anti-coagulation medication if 2+ women, or 1+ men

53
Q

What investigations should you do for atrial fibulation

A

Risk factors/causes

  • lipids, cholesterol
  • HbA1C
  • TFT (hyperthyroidism)
  • echo (valvular)
  • Us and Es and LFTs for baseline before drugs
  • ECG
54
Q

What is the first line therapy for AF?

A

ALWAYS ASSESS FOR ANTICOAGULATION

  • DOACS (dabigatran, rivaroxaban, apixaban, edoxaban )
  • vitamine K antagonist (warfarin)
  • thrombin inhibitors (dabigatran)

RATE CONTROL IS 1ST LINE (unless unstable) (aim for <110)

  • 1st line: BB or rate limiting CCB (non:hydro dil/vera)
  • Digoxin (only consider in sedentary patients and heart failure)-beware of vomiting ↓K+
  • 2nd line: combine any combo of 2 above

** don’t use sotalol as BB

RHYTHM CONTROL IS SECOND LINE

55
Q

When would you do RHYTHM control in someone with AF?

A

RHYTHM control in AF

  • 2nd line if rate control not worked (chronic and acute)
  • if heamodynamically unstable (syncope/shock/acute HF/MI)
  • New onset AF <48 hours
  • AF with reversible cause (e.g. infection)
  • Clinical judgment e.g. active young patients (want to avoid rate control)
56
Q

What are the options for RHYTHM control in AF?

A

Electrical conversion

  • DC current shock
  • Preferred if heamodynamically unstable (syncope/shock/acute HF/MI)
  • If not anti coagulated give LMWH first but dont delay shock

Medical conversion (bolus then infusion)
-If symptoms are milder or if electrical conversion not available
1st line = IV Flecainide (if no structural abn)
AMIODARONE (central line) IF STRUCTURAL ABNORMALITY or IHD (300mg 10-20min, 900mg 24hr)

***risk of stroke when cardioverted because coordinated contraction with throw off clots formed in static blood> thrombophylaxis 3 weeks prior if elective

57
Q

What drugs reduce the concentration of warfarin in the body?

A

It is metabolised by the CYP450 system - concentration is reduced by CYP450 INDUCERS

Carbamazepine
Rifampicin
Alcohol (chronic)
Phenytoin

Griseofulvin
Phenobarbitone
Sulfonureas

58
Q

What drugs increase the concentration of warfarin in the body?

A

It is metabolised by the CYP450 system - concentration is increased by CYP450 inhibitors SICKFACES.COM Group (make spirit go down)

Sodium valproate
Isoniazid
Ciprofloxacin
Ketoconazole
Fluconazole 
Alcohol (binge..sick)
Cimetidine
Erythromycin/clarithromycin
Sulphonamide

Chloramphenicol
Omeprazole
Metronidazol
Grapefruit juice

59
Q

What do NOACs do?

A

Inhibit factor Xa

60
Q

What score is relevant to anticoagulation?

A

HAS-BLED score

Hypertension - 1
Abnormal renal and liver function - 1 point each
Stroke - 1
Bleeding - 1
Labile INRs - 1
Elderly >65 - 1
Drugs or alcohol - 1 point each

Max 9 points. Anything higher than 3 should make you consider alternatives to anticoagulation

61
Q

What conditions are NOACs contraindicated in?

A

Mitral stenosis/mechanican heart valves (warfarin better)

Chronic kidney disease

62
Q

When should you anticoagulate if performing cardioversion?

A

if AF>48hours, consider amiodarone 3 weeks before + 4 weeks after to eliminate clots that may have formed in heart

if AF<48hrs, can perform without anticoagulation

63
Q

What is the drug management of coronary artery disease?

A

20mg artovastatin to those with >10% risk of CV disease (calculated with QRisk3)

80mg artovastatin if previous MI, Hx of type 2 diabetes, current ACS symptoms (e.g. angina, total cholesterol >4, LDL>2)

64
Q

What is the mechanism of action of statins?

A

Inhibit HMG Co-A reductase which limits the rate of cholesterol synthesis

65
Q

Explain coronary artery disease to a patent.

A

Coronary artery disease

  • The blood vessels supply the heart with oxygen
  • As we get older plaques form in the vessels, which lead to decreased blood supply to the heart which leads to the heart getting less oxygen which can damage the cells (think of a pipe with limescale)
  • As well as increasing age, lifestyle has a big impact on the formation of the plaques (smoking, exercise, diet, weight)
  • It’s our job to try and minimise those risk factors and keep your heart in the best shape it can be in.
  • Important to treat because increases risk of MI
66
Q

Risk factors of coronary artery disease

A 
Coronary heart disease risk factors 
Modifiable
-Excessive cholesterol/fats
-Diabetes
-smoking
-alcohol intake
-high BP

Unmodifiable

  • Male
  • Age
  • Indian/Pakistani origin
67
Q

How should you manage a patient with coronary artery disease?

A

NICE GUIDELINES ON DIAGNOSIS AND MANAGEMENT OF CHD

IDENTIFY AND TREAT CAUSES 
○ FBC 
○ Hb1ac (diabetes) 
○ BP (hypertension) >ACE inhibitors
○ Lipid profile (hyperlipidemia) 
○ TFT (hypothyroidism) >treat
○ LFT (liver disease)
○ Us and Es (CKD,nephrotic syndrome)

IDENTIFY AND MANAGE RISK FACTORS
○QRisk2 score-repeat every 5 years if over 40 or every 1 year at annual review if on statin (gives % risk of CVD event over the next 10 years)
○ ANYONE WHO HAS 10% RISK OR HIGHER SHOULD BE OFFERED ATORVASTATIN 20mg
▪ Measure LFTF before, 3 and 12 months

MANAGE PROGRESSION OF DISEASE
○ Annual review-assessing management of causes management of risk factors (statin compliance and side effects)

MANAGE COMORBIDITIES AND MENTAL HEALTH
EDUCATE PATIENT-leaflet/support group
SAFTEY NET and FOLLOW UP

68
Q

What long term prevention medication should post MI patents be started on?

A

CARDIOPREOTECTIVE MEDICATION (ABAS)

  • antiplatelet therapy (dual) aspirin 75mg plus ticagrelor 90mg for 12 months. Then lifelong aspirin
  • BETA BLOCKER reduces myocardial demand (verapamil/diltiazam if contraindicated)
  • ACE INHIBITOR if LV dysfunction, diabetes or HTN >140/90
  • high dose statin 80mg
MANAGMENT OF RISK FACTORS
-Diet (low salt, high fibre, reduced fats) 
-Alcohol 
-Exercise
-Weight
-Diabetes control 
-Hypertension control
-Smoking stoping
MANAGE COMPLICATOINS 
MANAGE COMORBIDITIES 
MANAGE MENTAL HEALTH 
SAFTEY NET and FOLLOW UP
69
Q

What drugs should someone with CAD/IHD be put on?

A
  1. Short acting nitrate (GTN) (call ambulance if still have angina after 5 mins after 2nd dose)
  2. Anti anginas
    -1st line: beta blockers or calcium channel blockers (ver/dil)
    -2nd line (in combo with or mono therapy):
    isosorbide mononitrate/nicorandil/Ivabradine/ranolizine
    -3rd line CABG/PCI if not controlled by 2 drugs
  3. Prevention
    - aspirin for all
    - statin for all
    - consider ACE inhibitor (pts. w/ stable angina + DM/previous MI/HTN/HF/LVD/CKD)
70
Q

side effects of thiazide diuretic

A
  • hypercalceamia
  • low sodium
  • low potassium
  • dehydration
71
Q

What is an extra precaution that should be taken for HF?

A

Patients with heart failure should be giving flu vaccine (at 6 monthly review)

72
Q

What medication should patients with preserved ejection fraction be given?

A

low dose of loop diuretics (furosemide)

73
Q

side effects of beta blockers?

A
  • GI upset
  • fatigue
  • cold extremities
  • impotence
  • headache
  • sleep disturbances
74
Q

What investigations should you do for ECG

A

Risk factors

  • lipids, cholesterol
  • HbA1C

causes

  • TFT (hyperthyroidism)
  • echo (valvular)
  • Us and Es and LFTs for baseline before drugs
  • ECG
75
Q

When should we follow up patients with AF?

A
  • Beta-blocker review after one week to see if the patient is tolerating it and their symptoms are being eased
  • DOAC review - every 3 months to see if it is being tolerated. FBCs and U&Es usually taken at follow up reviews
  • WARFARIN REVIEW - regular INRs are really important and should aim for INR between 2 and 3. At first these should be taken every day, then weekly and then up to every 12 weeks
  • Regular CVD checkups-Hba1c/BP/HR> statin
76
Q

iron deficiency anemia vs anaemia chronic disease?

A
  • IDA serum iron <8 whereas ACD is <15
  • IDA the TIBC (total binding capacity) is high whereas ACD is low
  • transferrin is low in both
  • ferritin is high in anaemia chronic disease (low in IDA)
77
Q

What is complication of having uncontrolled AF for a long time?

A

-tachycardiomyopathy can occur with long term uncontrolled AF (heart failure can cause AF but AF can also cause heart failure)

78
Q

What should you do if patient is on aspirin and then gets AF?

A

stop aspirin and start on DOAC/warfarin

79
Q

What can be done to control rhythm?

A

Rhythm control

  • Pulmonary vein triggers/ectopic muscles- can be treated with radiofrequency ablation
  • Amioderone
  • Flecainide (sodium channel blocker-cant use for Hx IHD)
  • Sotalol (can increase QT)
  • Electric cardioversion
80
Q

When would you prefer warfarin over DOAC for AF patient?

A

metallic valve-put in warfarin

81
Q

When is rhythm control first line in AF?

A

Reasons to confider more rhythm control

  • AF is reversible cause (drunk young person)
  • HF due to AF
  • New onset AF
  • Symptoms
82
Q

side effects of amioderone?

A 
Amioderone side effects
• Thyrotoxicosis 
• Corneal deposits 
• Liver and lung fibrosis 
•Photosensitivity
83
Q

What HR are we aiming for in AF?

A
  • <110 is adequate rate control for AF

* If they have symptoms- more strict rate control <80 at rest. <120 for exercise

84
Q

Do we need to give anticoagulants when we do electroconversion?

A
  • <48 hours with clear onset can be started without AC (no time for clot to form)
  • if the AF started >48 hours ago they require period of anticoags 3 week min before and 4 weeks after any cardioversion (electric or chemical)
85
Q

What are normal results for ABPI?

A

ABPI (more important to actually look at the patient)
>1.2 abnormally hard (calcified)
1 - 1.2 normal
0.8 - 0.9 mild arterial disease
0.5 - 0.79 moderate arterial disease
< 0.5 severe arterial disease (rest pain, ulceration and gangrene (critical ischaemia))

86
Q

Treatment for raynauds?

A

Raynauds

CCB (nifidepine)

87
Q

What is critical ischemia?

A

pain at REST (naming pain at night, hang over side of bed very different to claudication which is at rest)

88
Q

treatment of peripheral vascular disease?

A
  1. Conservative (monitor RF, smoking exercise, diet)
  2. Medical (statin and anti platelet) + control comorbidities
  3. Surgical (angioplasty and stents)
89
Q

Why is it important to control HTN?

A

If uncontrolled can cause:
-Heart attacks (Heart failure and Coronary artery disease)
-Strokes
-Eye problems
-Kidney problems (CKD)
-Sexual dysfunction (Peripheral arterial disease)
-Vascular dementia
Important we find out early and prevent/lower risk of getting these (the biggest RF for strokes and heart attacks)

90
Q

What are the BP targets for <80 year olds and >80 year olds on treatment?

A

Blood pressure targets
Age < 80 with treatment
< 140/90 clinic
< 135/85 ABPM

Age > 80 with treatment (older so allowed slightly higher)
< 150/90
< 145/85

91
Q

What drugs interact with ACE inhibitors?

A

ACE inhibitors + Sprionlactone +ARB will cause hyPERkalemia (prevent aldosterone from removing K+)

ALSO NEVER PRESCRIBE NSAIDS/ACE INHIBITOR/DIURETICS

Triad - diuretics reduce volume, reducing renal blood flow. ACEi inhibits efferent vasoconstriction, reducing gfr. NSAID vasoconstrict the afferent arteriole, reducing the ability of the kidney to increase glomerular blood flow. When all combined, the kidney is unable to maintain glomerular flow and thus filtration is reduced and creatinine rises

92
Q

What drug interacts with thiazide diuretics?

A

-Digoxin and thiazide diuretics can cause HYPOkaleamia worsens digoxin toxicity

93
Q

What is malignant hypertension?

How do you treat?

A

Malignant HTN >200/120

  • Headache, retinal haemorrhages, epistaxis, nocturia, dyspnoea (LVF), papilloedema
  • Treat urgently with IV Labetalol or GTN
94
Q

When should people be offered a statin?

How often should they be monitered on a statin?

A

ANYONE WHO HAS 10% RISK OR HIGHER SHOULD BE OFFERED ATORVASTATIN 20mg
▪ Measure LFTF before, 3 and 12 months

95
Q

Side effects of CCB?

A
  • headaches
  • flushing
  • nausea
  • dizzyness
  • palpatations
  • swollen ankles
96
Q

what is warfarin

A

vitamine K antagonist

97
Q

What does ST elevation across all leads signify?

A

Pericarditis

CCC (15 decks)

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