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PA MATRIX > CARDIOVASCULAR > Flashcards

CARDIOVASCULAR Flashcards

1
Q

What is primary (essential) hypertension? 1A

A

High blood pressure that doesn’t have a known secondary cause.

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2
Q

How is primary (essential) hypertension diagnosed? 1A

A

Blood pressure tested using a BP monitor.

If high, Doc asks p to check their BP at home using the BP monitor at home at regular intervals.

Normal BP = 120/80.

Stage 1 hypertension = BP readings of = 130-139/80-89

Stage 2 hypertension = BP readings of = higher than 140/ higher than 90.

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3
Q

What are the risk factors associated with primary (essential) hypertension? 1A

A

Diet

Stress

Minimal physical activity

Being overweight

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4
Q

What are the clinical features of primary (essential) hypertension? 1A

A

Generally asymptomatic.

Only symptom tends to be raised blood pressure.

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5
Q

How would primary (essential) hypertension be investigated? 1A

A

Serum U+E = can show evidence of renal impairment. If so, conduct more specific renal investigations -> renal ultrasound + renal angiography).

Urine Stix test - for protein and blood - can indicate renal disease (either cause or effect of hypertension).

Blood glucose, serum lipids + ECG which could show LV hypertrophy or ischaemic disease.

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6
Q

Why are investigations carried out for primary (essential) hypertension? 1A

A

To identify end-organ damage.

And identify those patients with secondary causes of hypertension.

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7
Q

How is primary (essential) hypertension managed if severe? 1A

A

Start meds immediately - before home BP checks.

Examine fundi for hypertensive retinopathy.

Refer if it is accelerated hypertension or phaechromocytoma.

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8
Q

What are the non-pharmacological treatments for primary (essential) hypertension? 1A

A

Weight reduction

Low-fat diet

Low-salt diet

Limited alcohol consumption

Exercise

Increase fruit and veg consumption

Stop smoking if a smoker + eat more oily fish

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9
Q

How is primary (essential) hypertension managed if NOT severe? 1A

A

Under 55? -> ACE inhibitor (e.g. lisinopril) but if not tolerated (e.g. due to cough) then ARB (angiotensin-II receptor antagonist e.g. losartan).

Above 55? And/or Afro-Caribbean? -> CCB (e.g. amlodipine) but if not tolerated (e.g due to oedema) then thiazide-type diuretic (e.g. bendroflumethiazide).

If uncontrolled -> add a CCB to ACE/ARB but if CCB isn’t tolerated then thiazide-type diuretic. Afro-Caribbean? -> add ARB to their CCB/thiazide-type diuretic.

Still uncontrolled? -> review meds + ACE/ARB + CCB + thiazide-type diuretic

Still uncontrolled?! -> low dose spironolactone if K+ = <4.5mmol’L (caution if reduced estimated GFR) or higher dose thiazide-type diuretic if K+ = >4.5mmol’L whilst monitoring.

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10
Q

What is assessed during the annual review for someone with primary (essential) hypertension? 1A

A

Lifestyle + meds (inc adverse effects)

Check BP

Renal function (serum creatinine, electrolytes, estimated GFR + dipstick for proteinuria).

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11
Q

What are the risks of having primary (essential) hypertension? 1A

A

Increases risk of CVD (HF, coronary artery disease, stroke, chronic kidney disease, peripheral arterial disease, vascular dementia). But meds reduce the risks.

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12
Q

What is secondary hypertension? 1B

A

High blood pressure that has a known cause e.g. kidneys, arteries, heart or endocrine.

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13
Q

What are the causes of secondary hypertension? 1B

A

Diabetes -> (damage kidney’s filtering system = high bp)

Polycystic kidney disease -> (cysts in kidneys prevent them from working properly = high bp)

Glomerular disease -> ( glomeruli = swollen = can’t work properly = high bp)

Renovascular hypertension -> (stenosis of arteires leading to kidneys = high bp)

Thyroid problems

Hyperparathyroidism -> (too much parathyroid hormone increases amount of calcium in blood = high bp)

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14
Q

What are the malignant/accelerated causes of secondary hypertension? 1B

A

Cushing syndrome -> (corticosteroid meds or pituitary tumour causes adrenal glands to produce too much cortisol)

Aldosteronism -> (tumour in adrenal glands -> increases growth of normal cells -> excessive release of hormone aldosterone -> kidneys retain salt + water + they lose too much K+ = raised bp)

Pheochromocytoma -> (rare tumour, found in adrenal glands -> increases production of adrenaline + noradrenaline = high bp)

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15
Q

What are the clinical features of secondary hypertension? 1B

A

High bp that does not respond to meds

180/120mmHg bp

Sudden onset of bp before 30yrs

No fam hx of bp

No obesity

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16
Q

How would secondary hypertension be investigated? 1B

A

Same as 1A hypertension

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17
Q

How would secondary hypertension be treated? 1B

A

You treat the underlying medical condition + as 1A hypertension

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18
Q

What are the risks of having secondary hypertension? 1B

A

Damage to heart (HA or stroke)

Aneurysm, HF, weakened + narrowed blood vessels to kidneys

Thickened, narrowed or torn vessels in eyes -> vision loss

Metabolic syndrome

Trouble with memory and understanding

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19
Q

What does phlebitis mean?

A

Inflammation of a vein

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20
Q

What is superficial thrombophlebitis?

A

An inflamed vein near the surface of the skin (usually a varicose vein) caused by a blood clot

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21
Q

How does superficial thrombophlebitis clinically present?

A

Vein looks painful, tender and hard with overlying redness

Usually occurs in the leg

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22
Q

How is superficial thrombophlebitis treated?

A

Simple analgesis -> (e.g. NSAIDs)

Anticoagulation isn’t necessary as embolism does not occur

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23
Q

What are the risk factors for superficial thrombophlebitis?

A

Have varicose veins

Smoker

Overweight

On the pill or hormone replacement therapy

Pregnant

Have previously had a blood clot/ issues with veins

Have a condition that causes blood to clot more easily (thrombophilia), inflammation of the smaller arteries (polyarteritis) or high conc of red blood cells in blood (polycythaemia)

Had drip/injection recently into vein

Have cancer

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24
Q

What is DVT?

A

A blood clot that forms in the deep veins of the body, usually in the leg

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25
Q

How does DVT clinically present?

A

Often asymptomatic

Leg may be warm + swollen with calf tenderness + superficial vein distention

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26
Q

How would DVT be investigated?

A

If Wells score is less than 3 then measurement of serum D-dimer = initial investigation.

If D-dimers = normal then no further investigation needed.

All other patients -> venous compression ultrasonography = indicated.

Above = reliable test for iliofemoral thrombosis but not for calf vein thrombosis.

Repeat scanning 1 week later + interim heparin treatment = indicated if initial scan = negative + high index of clinical suspicion.

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27
Q

How is DVT treated?

A

Injection of heparin if waiting to undergo an ultrasound scan to confirm DVT

Coagulation screen + platelet count before starting treatment to rule out pre-existing thrombotic tendency

LMWH - Enoxaparin - 1.5mg/kg subcut injec every 24 hrs, for at least 5 days till oral anticoagulation is confirmed

Warfarin + heparin at same time

Warfarin dose adjusted to maintain INR @ 2/3x control value

Hep+War overlapped for min 5 days + continued till INR = in therapeutic range

Anticoagulation for 6 weeks should be sufficient after their first thrombosis with precipitating cause - if there are no risk factors

But long-term anticoagulation is needed for those with repeated episodes or continuing risk factors

EXTRA -> Inferior vena cava filter (IVC filter) may be inserted in order to prevent a PE (pulmonary embolism) if anticoagulants are deemed unsuitable

Elastic support stockings to prevent post-thrombotic syndrome

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28
Q

How is a DVT treated in pregnancy?

A

Heparin injections from diagnosis till 6 weeks after baby is born

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29
Q

What are the risks of having a DVT?

A

Could lead to a PE

Post-thrombotic syndrome (permanent pain, swelling, oedema and potentially venous eczema) + recurrence of thrombosis.

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30
Q

What are the risk factors of developing DVT?

A

Aged over 60

1 or more significant co-morbidities e.g. HD

Obesity

Major abdominal/pelvic surgery

Active cancer

Pregnancy

Oestrogen containing contraception/HRT

Significant immobility

Varicose veins with phlebitis

Diabetic coma

Personal hx/ first-degree relative with hx of venous thromboembolism

Thrombophilia, IBD, Nephrotic syndrome

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31
Q

What are the side effects of having DVT treatment - specifically heparin therapy?

A

Bleeding + thrombocytopenia.

Platelet count should be measured if patient is receiving heparin for more than 5 days.

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32
Q

What is a pulmonary embolism (PE)?

A

A condition where one or more emboli (typically from a thrombus formed in veins) are lodged in + obstruct the pulmonary arterial system = severe respiratory dysfunction

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33
Q

Whar is the pathophysiology of a PE?

A

The embolism means that lung tissue is still ventilated but not perfused -> leading to impaired gas exchange.

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34
Q

How would a PE clinically present?

A

Small/medium PE’s -> breathlessness, pleuritic chest pain + haemoptysis (coughing up blood or blood-stained mucous) if there’s pulmonary infarction

On examination - patient may be tachypnoeic (abnormal rapid breathing) + have a pleural rub + an exudative pleural effusion can develop

Massive PE’s -> medical emergency - patient has severe central chest pain - suddenly becomes shocked, pale + sweaty, marked tachypnoeia + tachycardia -> syncope + death may follow rapidly

On examination - patient is shocked with central cyanosis - elevation of jugular venous pressure + right ventricular heave + accentuation of second heart sound + gallop rhythm (acute right heart failure)

Multiple recurrent PE’s -> symptoms + signs of pulmonary hypertension developing over weeks to months

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35
Q

How would a PE be investigated?

A

Clinical pre-test probability score is used prior to investigation

  • Chest X-ray, ECG + blood gases = may all be normal with small/medium emboli + any abnormalities with massive emboli = non-specific.
  • Chest X-ray may show decreased vascular markings + raised hemidiaphragm (due to loss of lung volume).

With pulmonary infarction - a late feature = wedge shaped opacity adjacent to pleural edge - sometimes with pleural effusion.

ECG findings - sinus tachycardia or may be new onset of atrial fibrillation + non-specific ST segment + T-wave abnormalities, right axis deviation, incomplete/complete right bundle branch block.

Arterial blood gases may show hypoxaemia + hypocapnia with massive PE’s.

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36
Q

How would suspected PE be treated?

A

Wells score of more than 4 points = PE likely so hospital admission for CTPA + other testing e.g. D-dimer testing, ABG, chest X-ray, ECG, lower limb compression venous ultrasound, ventilation perfusion + echocardiography.

If delay in patient getting CTPA -> give immediate low molecular weight heparin (LMWH) + arrange hospital admission.

Pre-test clinical probability = low

-> D-dimer testing -> negative? Look for differential diagnosis. Positive? CTPA -> PE present? Warfarin!

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37
Q

How is confirmed PE treated?

A

Pre-test clinical probability = intermediate/high

  • > Start LMWH
  • > Do CTPA
  • > PE present -> start warfarin
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38
Q

What other treatmenrs could be given alongside warfarin for treatment of PE?

A

High flow oxygen if hypoxaemic

Thrombolysis for massive PE with persistent hypotension

Analgesia - morphine - relieves pain/anxiety

IV fluids (to raise filling pressure) for patients with moderate/severe embolism.

Preventing further thrombi? - LMWH + oral warfarin

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39
Q

What is the initial investigation for suspected PE in pregnancy?

A

Compression ultrasonography of the legs.

CTPA = needed if ultrasound = normal + delivers a lower dose of radiation to foetus than lung VQ scan.

Warfarin = teratogenic so PE in pregnancy is treated by LMWH.

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40
Q

What are the risk factors for PE?

A

DVT

Previous VTE

Active cancer

Recent surgery

Significant immobility

Lower limb trauma/fracture

Pregnancy - 6 weeks postpartum

Other risk factors as listed for DVT

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41
Q

What are the risks of having PE?

A

Death

Cardiac arrest

Pleural effusion

Pulmonary infarction

Arrythmia

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42
Q

What is angina?

A

Central chest tightness/pain caused by myocardial ischaemia.

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43
Q

What are the two types (we’ve learnt) of angina?

A

Stable

Unstable

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44
Q

How does angina (both types) clinically present?

A

Tightness or heaviness in chest on exertion/rest /emotion/cold/heavy meals.

May radiate to one or both arms, neck, jaws or teeth.

Other Symptoms: Dyspnoea, nausea, sweatiness, faintness

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45
Q

Note on stable angina

A

Induced by effort, relieved by rest

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46
Q

Note on unstable angina

A

Increasing severity/frequency

Minimal exertion, ^^risk of MI

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47
Q

Pathophysiology of both types of angina

A

Atheroma obstructing or narrowing coronary vessels (rarely; others such as anaemia)

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48
Q

Cause of both types of angina

A

Atheroma

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49
Q

Diagnostic test for both types of angina

A

ECG: usually normal, some ST depression, flat or inverted T waves.

50
Q

Treatment of both types of angina

A

Modify risk factors, aspirin, B Blockers, Nitrates (isosorbide mononitrate or GTN spray),

Long-acting calcium channel blocker, K+ channel activator

51
Q

Sequelae of both types of angina

A

Might indicate higher risk of MI

52
Q

What is a myocardial infarction?

A

Death of heart tissue due to an ischaemic event

53
Q

What are the two types of myocardial infarction?

A

STEMI

NSTEMI

54
Q

How does myocardial infarction clinically present?

A

Crushing chest pain, radiating to left arm.

Sweating, nausea, vomiting, dyspnoea, fatigue, and/or palpitations.

Signs: Fever, hypo/hypertension, 3rd/4th heart sound, signs of congestive heart failure

55
Q

Note on STEMI MI

A

ST elevated. Medical emergency

56
Q

Note on NSTEMI MI

A

Non-ST elevated. Medical emergency.

57
Q

Pathophysiology of myocardial infarction

A

Blockage of a coronary artery by a thrombus.

This leads to ischaemia in cardiac tissue.

The location of necrosis is determing by the coronary artery and where within it the blockage occurs.”

58
Q

Cause of myocardial infarction

A

Atheroma

59
Q

Epidemiology of myocardial infarction

A

600/100,000 for men.

200/100,000 for women

60
Q

Diagnostic test for myocardial infarction

A

Don’t delay treatment.

ECG: ST elevation (if STEMI), Initially peaked T waves and then T wave inversion, New Q waves, New conduction defects.

FBC: Rules out anaemia.

Cardiac enzymes: Troponins T and I are markers for cardiac damage

61
Q

Treatment of myocardial infarction

A

Thrombolytic (aspirin).

Percutaneous transluminal coronary angioplasty.

Possibly CABG, if PCI fails.

Follow up clopidogrel (antiplatelet) for 30 days.

62
Q

Complications of myocardial infarction

A

Ischaemic: Recurrent infarct. Post-infarction angina.

Mechanical: Left ventricular dysfunction -> Heart failure.

Ventricular septal rupture (life threatening).

Free wall rupture -> Pericardial bleed -> Cardiac tamponade.

False aneurysm in ventricular wall.

Acute mitral regurgitation (caused by ischaemic damage to papillary muscle).

Arrhythmias: Ventricular tachycardia, ventricular fibrillation and total AV block. Bradycardia.

Thrombotic/Embolus: Thrombus can form in ventricular wall. DVT and PE possible, but low risk.

Pericarditis: Common after anterior infarct.

Dressler’s syndrome (presents as pericarditis).

Depression: 20% of patients following MI.

63
Q

Sequelae of myocardial infarction

A

Shock, heart failure, pericardiitis

64
Q

What is cardiac failure?

A

Cardiac output inadequate for the body requirements

65
Q

Types of cardiac failure

A

Left

Right

66
Q

How does cardiac failure (eft) clinically present?

A

Dyspnoea, tachypnea, crackles in the lungs (base -> the rest), wheezing, cyanosis (late occuring).

Frothy pink sputum

Signs: Laterally displaced apex beat, ‘gallop’ rhythm. Heart murmurs possible.

67
Q

How does cardiac failure (right) clinically present?

A

Peripheral oedema, ascites, liver enlargement, raised JVP

68
Q

Pathophysiology of cardiac failure (eft)

A

Blood backs up into the pulmonary circulation

69
Q

Pathophysiology of cardiac failure (right)

A

Blood backs up into the systemic circulation

70
Q

Cause of cardiac failure

A

Systolic: Ischaemic heart disease, MI, cardiomyopathy

Diastolic: Tamponade, constrictive pericarditis, systemic hypertension

71
Q

Epidemiology of cardiac failure

A

1-3/100 general pop, 10% of elderly.

Poor prognosis (25-50% die in first 5yrs of diagnosis)

72
Q

Diagnostic test for cardiac failure

A

ECG, CXR (Bat wing alveolar oedema, Kerley B lines, cardiomegaly, dilated prominent upper lobe vessels, pleural effusion) and BNP.

If abnormal -> Echocardiography

73
Q

Treatment of cardiac failure

A

Stop smoking, eat healthily and exercise.

Chronic: Loop and potassium sparing diuretics for fluid overload, ACEI, Beta-blockers

Acute: Oxygen, monitor ECG, diamorphine, furosemide, GTN spray

LOON: Loop, Oxygen, Opioid Nitrates

74
Q

What is valvular heart disease?

A

Disease process affecting the valves of the heart.

75
Q

What are the four types of valvular heart disease?

A

Mitral stenosis

Mitral regurgitation

Aortic stenosis

Aortic regurgitation

76
Q

How does mitral stenosis clinically present?

A

Pulmonary hypertension -> dyspnoea, pink frothy sputum, left atrial dilatation, right ventricular hypertrophy, palpitations.

Malar flush due to low CO.

Opening snap and diastolic murmur.

77
Q

How does mitral regurgitation clincally present?

A

Variable haemodynamic effects.

Pansystolic murmur.

Mid-systolic click and late systolic murmur in mitral prolapse.

Deviated apex beat.

78
Q

How does aortic stenosis clinically present?

A

Ejection systolic murmur.

Left ventricular hypertrophy.

Syncope, angina, dyspnoea (SAD)

79
Q

How does aortic regurgitation clinically present?

A

Early diastolic murmur.

Wide pulse pressure, collapsing pulse, angina, left ventricular failure.

Austin flint murmur: Fluttering of anterior mitral valve cusp due to regurgitant stream

80
Q

Note on mitral stenosis

A

Mid-diastolic murmur

81
Q

Note on mitral regurgitation

A

Pansystolic murmur

82
Q

Note on aortic stenosis

A

Early systolic murmur

83
Q

Note on aortic regurgitation

A

Early diastolic mumur

84
Q

Pathophysiology of mitral stenosis

A

Inflammation -> Mitral valve thickened/calcified obstructing normal flow.

Raised LA pressure -> LA hypertrophy and dilatation -> palpitations.

Raised LA pressure -> pulmonary hypertension -> RV hypertrophy and failure

85
Q

Pathophysiology of mitral regurgitation

A

Mitral valve fails to prevent reflux of blood.

Regurgitation into the LA -> increased LA pressure -> increased pulmonary pressure -> pulmonary oedema

86
Q

Pathophysiology of aortic stenosis

A

Aortic valve thickened/calcified obstructing normal flow.

Obstructed LV outflow -> Increased LV pressure -> Compensatory LV hypertrophy -> Relative ischaemia -> Angina, arrythmia and LV failure -> Reduced cardiac output.

87
Q

Pathophysiology of aortic regurgitation

A

Aortic valve fails to prevent reflux of blood.

LV hypertrophy to maintain cardiac output -> Reduced diastolic blood pressure -> relative ischaemia.

Eventually leads to left ventricular failure.

88
Q

Cause of mitral stenosis

A

Rheumatic valvular disease (usually Strep pyogenes)

89
Q

Cause of mitral regurgitation

A

Dilatation of mitral valve annulus.

Mitral valve prolapse.

Infective endocarditis.

Rheumatic valvular disease.

Marfan’s and Ehler-Danlos

90
Q

Cause of aortic stenosis

A

Calcific degeneration.

Rheumatic valvular disease.

Congenital bicuspid valve.

91
Q

Cause of aortic regurgitation

A

Aortic root dilatation.

Infective endocarditis, rheumatic fever.

Some rheumatological disorders.

Ascending aortic dissection possible.

92
Q

Epidemiology of mitral regurgitation

A

Second most common valvular condition requiring surgery

93
Q

Epidemiology of aortic stenosis

A

Most common valvular condition requiring surgery.

Mostly in the elderly.

94
Q

Epidemiology of aortic regurgitation

A

Moderate or severe common after transcatheter aortic valve replacement.

95
Q

Diagnostic test for mitral stenosis

A

Echocardiography. ECG: AF, LA enlargement, RV hypertrophy

Echocardiography: Definitive diagnosis; measure mitral orifice.

96
Q

Diagnostic test for mitral regurgitation

A

Echocardiography

97
Q

Diagnostic test for aortic stenosis

A

Echocardiography. ECG: LV hypertrophy

98
Q

Diagnostic test for aortic regurgitation

A

Echocardiography. ECG: LV hypertrophy

99
Q

Treatment of mitral stenosis

A

Diuretics (furosemide), rate control + anticoagulation.

Valvotomy. Excise segments of valve, or valve replacement.

Infective endocarditis prophylaxis (amoxicillin?)

100
Q

Treatment of mitral regurgitation

A

Repair preferred over replacement

101
Q

Treatment of aortic stenosis

A

Valve replacement,

Balloon valvuloplasty,

Transcatheter aortic valve replacement,

Surgical valvuloplasty

102
Q

Treatment of aortic regurgitation

A

Treat underlying cause.

Possibly vasodilators or inotropes.

Diuretics.

Valve replacement.

103
Q

Complications of valvular disease

A

Valve replacements can cause clotting.

Anticoagulants prescribed with them.

Endocardititis

104
Q

Sequelae of aortic stenosis

A

Left sided heart failure. Sudden death.

105
Q

Sequelae of aortic regurgitation

A

Left sided heart failure.

106
Q

What is atrial fibrillation?

A

Irrergularly irregular ventricular pulse and loss of association between cardiac apex beat and radial pulsation.

107
Q

How does atrial fibrillation clinically present?

A

Breathlessness, palpitations, syncope, chest discomfort, stroke/TIA.

Irregularly irregular pulse.

108
Q

Pathophysiology of atrial fibrillation

A

Artial activity is chaotic and mechanically ineffective.

Stagnation of blood in the atria -> thrombus formation and a risk of embolism -> stroke.

Reduction in cardiac output -> Heart failure

109
Q

Cause of atrial fibrillation

A

Hypertension, coronary artery disease, valvular heart disease (particularly mitral valve stenosis), cardiac surgery

110
Q

Epidemiology of atrial fibrillation

A

Most common sustained arrhythmia.

111
Q

Diagnostic test for atrial fibrillation

A

ECG: variability in the R-R intervals, absent p waves.

112
Q

Treatment of atrial fibrillation

A

Control arrhythmia; rate: Beta blockers, Calcium antagonists rhythm: cardioversion.

Thromboprophylaxis to prevent strokes.

Treat underlying cause.

113
Q

What is peripheral vascular disease?

A

Narrowing of arteries distal to the aortic arch.

114
Q

How does peripheral vascular disease clinically present?

A

Varying symptoms: Asymptomatic -> Intermittent claudication (on exercise) -> rest pain (critical limb ischaemia) -> skin ulceration and gangrene.

Signs: Absent femoral, popliteal or foot pulses. Cold white legs.

115
Q

Note on peripheral vascular disease

A

50% mortality at 5 years 70% at 10 years.

Gradual progression -> Sudden deterioration.

116
Q

Pathophysiology of peripheral vascular disease

A

Atherosclerosis causing stenosis of arteries.

117
Q

Cause of peripheral vascular disease

A

Atherosclerotic damage.

Risk Factors: Classical atheroma risk factors.

118
Q

Epidemiology of peripheral vascular disease

A

Affects 4-12% of people between 55-70, and 15-20% of 70+

119
Q

Diagnostic test for peripheral vascular disease

A

ECG: 60% of claudication patients have evidence of coronary artery disease.

Doppler ultrasonography: Confirm diagnosis. Site, degree and length.

120
Q

Treatment of peripheral vascular disease

A

Modify risk factors.

121
Q

Complications of peripheral vascular disease

A

Acute limb ischaemia -> Amputation, gangrene, infection, poor healing, ulceration.

PA MATRIX (15 decks)

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