Valvular disease and HTN Flashcards

1
Q

How is hypertension defined?

A

Systolic over 140 and diastolic over 85 on over three occasions

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2
Q

How to diagnose hypertension?/What investigations are done for hypertension?

A

If one clinic reading over 140/85, take second measurement + if this is significantly different, take third measurement

then ABPM

  • Confirm Dx of HTN in people with a:
  • clinic blood pressure of 140/90 mmHg or higher and
  • ABPM daytime average or HBPM average of 135/85 mmHg or higher
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3
Q

What is malignant hypertension?

A

Hypertension where bp=

>200/130 mmHg

Can cause organ failure

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4
Q

Aetiology of hypertension?

A

Primary- idiopathic-> essential hypertension [most cases]

Secondary:

Endocrine- Phaeochromocytoma, Cushing’s, Conn’s, Acromegaly, Congenital adrenal hyperplasia, diabetes, hyperthyroidism, hyperparathyroidism

Renal- renal artery stenosis, chronic glomerulonephritis/pyelonephritis, polycystic kidney disease, renal failure

Cardio- coarctation of aorta

Drugs- adrenaline/sympathomimetics, steroids, OC

Pregnancy- pre eclampsia

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5
Q

Symptoms of hypertension?

A

Mostly asymptomatic

Symptoms of underlying cause in secondary hypertension: endocrine, cardiac, drug side effects, renal symptoms, signs of pregnancy

Malignant hypertension causes symptoms: headaches, blurred vision, scotoma [loss of central visual field], seizures, nausea, vomiting

Symptoms of complications of hypertension: stroke, TIA, IHD, peripheral vasc disease, retinopathy etc.

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6
Q

Management of hypertension?

A

Conservative: lifestyle changes- diet and exercise

If under 55 or not Afro-Carribean:

First line: ACEi/ARB

Second line: + CCB/thiazide diuretics

Third line: ACEi + CCB + Thiazide

Fourth line: Add alpha/beta blocker or spirinolactone

If over 55 or Afro Carribean:

Start with CCB

Then add ACEi/ARB/thiazide

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7
Q

What are the stages of hypertension?

A

Stage 1= 140/90-159/99mmHg

Stage 2=160/100-179/119

Stage 3= sbp >180 or dbp>120

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8
Q

Hypertension

Definition

Aetiology

Diagnosis/Investigations

Symptoms and signs

Management

Monitoring

Red flags

Complications

Prognosis

A

Hypertension

Definition

Blood pressure higher than 140/90 mmHg

Aetiology

Either primary/essential- unknown cause

Or secondary: endocrine, renal [see other slide for more details on these two], cardio[coarctation of aorta], drugs [sympathomimetics, steroids, COCP]

Diagnosis/Investigations

Clinic blood pressure

Ambulatory blood pressure monitoring [automatically at least two measurements an hour] or Home blood pressure monitoring [twice daily for four to seven days] [if former not tolerated]

Investigations into secondary causes esp if young

Investigations for target organ damage- nine of them:

  • Proteinuria + haematuria + albumin creatinine ratio
  • eGFR
  • Creatinine
  • Electrolytes
  • HbA1C
  • Lipid profile- HDL and total cholesterol
  • Fundocopy
  • ECG
  • CV risk score

Symptoms and signs

Asymptomatic mostly

Unless:

Symptoms of underlying cause in secondary HTN/ Symptoms of complications

or

Malignant hypertension: neuro ish symptoms- headaches, blurred vision, scotoma [central visual field loss], nausea, vomiting

Management

  • See pics

Conservative: Lifestyle changes

Medical if: Persistent stage 2 HTN or Stage 1 HTN + less than eighty years + one of: target organ damage/CVD risk of >10%/renal disease/CVD/diabetes

Consider frailty and effects of multimorbidity in > eighty years

Monitoring

Regular check up- clinic BP measurement

Consider ABPM/HBPM - if white coat hypertension or masked hypertension

Monitor sitting and standing BP if: >eighty years / T2DM / postural hypotension symptoms

Target BP

< eighty years old

Target clinic BP: <140/90, home BP: <135/85

> eighty years old

Add 10 to target systolic bp:

Clinic BP: <150/90, home BP: 145/85

Monitor for complications- signs of CVD, stroke, PVD etc

Red flags

  • Stage 3 or Malignant hypertension- >200/130 mmHg = assess for target organ damage ASAP +
  • start drug Tx immediately if target organ damage
  • repeat clinic BP in a week if no target organ damage
  • SAME DAY SPECIALIST REVIEW IF:
  1. Papilloedema or retinal haemorrhage
  2. Life threatening symptoms or signs- suggested HF, AKI, consufsion, chest pain
  3. Phaeochromocytoma suspected

Young age - suggests secondary cause- but not red flag

Complications [if untreated]

8-10 y after onset:

  • Atherosclerotic disease in 30%: eg CVD, PVD, Stroke
  • Target organ damage in 50%- eg, brain, eye, kidney, heart, blood glucose [see pic for examples

Prognosis

If treated, good prognosis

If left untreated/uncontrolled severe consequences

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9
Q

What are the side effects of the hypertension medications?

ACE inhibitors

CCB

Thiazide diuretics

Beta/alpha blockers

A

ACEi- dry cough, increased potassium, increased creatinine

CCB- ankle swelling, angioedema

Thiazide diuretics- low potassium, dry mouth

Beta/alpha blockers- dizziness [postural hypertension]

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10
Q

What are red flag symptoms and signs of hypertension?

A

SEVERE RED FLAGS [Same day specialist review]:

Papilloedema/retinal haemorrhage

Symptoms of life threatening disease- chest pain, confusion etc.

Phaechromocytoma suspicion

Stage three hypertension- immediately assess for target organ damage and if present, start treatment immediately

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11
Q

What are the complications and prognosis of hypertension?

A

If untreated + mild to moderate:

30%= atherosclerotic disease- eg CVD, PVD

50%= organ damage- brain, eye, heart, kidney, blood vessels+ high blood glucose

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12
Q

SBA 1

a] 48-year-old woman, diagnosed with essential hypertension + commenced on treatment three months ago. She presents with a dry cough which has not been getting better despite taking cough linctus and antibiotics.

Which of the following antihypertensive medications is responsible for the patient’s symptoms?

A. Amlodipine

B. Lisinopril

C. Bendroflumethiazide

D. Furosemide

E. Atenolol

b] Which medication should she be started on as next line management instead?

A. Amlodipine

B. Spironolactone

C. Bendroflumethiazide

D. Furosemide

E. Losartan

A

B Lisinopril [ACE inhibitor]

and

E Losartan [ARB]

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13
Q

SBA 2

57-year-old man, Kevin, is reviewed in a hypertension clinic, where it is found that his blood pressure is 165/105 mmHg despite standard doses of amlodipine, perindopril, doxazosin and bendroflumethiazide. Electrolytes and physical examination have been, and remain, normal.

Which of the following would be your next stage in his management?

A.Arrange for his medication to be given under direct observation

B.Add spironolactone to his medication

C.Arrange urinary catecholamine assays

D.Request an adrenal CT scan

E.Add verapamil to his medication

A

A = poor adherence = most common cause of ineffective hypertension treatment

If good adherence, then B

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14
Q

SBA 3

47-year-old woman presents to clinic after being referred from her GP for consistently elevated blood pressure. Her last reading was 147/93. The female does not report any symptoms but recently lost her job and attributes the elevated reading to stress. Her blood tests are as follows:

Sodium = 146 (135-145 mmol/L)
Potassium = 3.4 (3.5-5 mmol/L)
Random glucose= 7.7 (4.4-7.8mmol/L)
Urea = 4 (2.5-7.8 mmol/L)

The next most appropriate investigation is:

A.CT scan

B. 24-hour ambulatory blood pressure

C. Abdominal ultrasound scan

D. Aldosterone-renin ratio

E. Glucose tolerance test

A

B

The main differential in this patient is hyperaldosteronism arising from an adrenal tumour (Conn’s syndrome). The excess aldosterone causes hypertension, elevated sodium reabsorption and potassium excretion. However, given the patient history, the elevated blood pressure could easily be due to the stress of having blood pressure measured or the patient’s personal situation. A 24-hour ambulatory blood pressure measurement (B) is therefore the most appropriate investigation to eliminate essential hypertension. Since the blood results are only mildly deranged and essential hypertension has not been eliminated, an aldosterone–renin ratio (D), CT scan (A) or abdominal ultrasound (C) would not be the first-line investigations to consider. They would be useful to investigate Conn’s syndrome if essential hypertension was excluded as a differential.

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15
Q

What are the normal heart sounds and the physiological causes of them?

A

S1- mitral/tricuspid valve closing- start of systole

S2- aortic/pulmonary semilunar valves closing- end of systole

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16
Q

When are heart sounds split?

A

Physiologically

S2 is split - first sound=aortic valve, second sound= pulmonary valve

-> right ventricular systole is longer because right heart filling augmented during inspiration because intrathoracic pressure decreasing increasing complicance of pulmonary vascular bed

Pathologically

Can be:

  • Paradoxical - prolonged/delayed onset of left ventricle systole- mitral valve closed later
  • Persistent- prolonged/delayed onset or prolongation of right ventricular systole

Normal wide splitting S1 – RBBB, LV pacing, ectopic beats

Paradoxical split S2: prolong LV emptying – aortic stenosis , LBBB – eliminated on inspiration

Widened split S2 – prolong RV emptying – pulmonay stenosis, RBBB

Fixed Split S2 – ASD

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17
Q

What are the abnormal heart sounds?

A

S3

S4

Split S1

Split S2

18
Q

Is the splitting of S2 physiological? Why does it happen?

A

Yes

Aortic valve closes first, then pulmonary

Inspiration causes decrease in intrathoracic pressure + increased complicance of pulmonary vascular bed so prolonged RV filling

19
Q

What is paradoxical splitting?

What things can cause it?

A

Delayed onset/prolonged left ventricular systole

Prolonged LV emptying

Aortic stenosis

LBBB

20
Q

What is persistent splitting?

A

Delayed onset/prolongation of right ventricular systole, or reduced duration of left ventricular systole

21
Q

What causes S3 to be heard?

A
  • Rapid ventricular filling
  • Causes chordae tendinae to stretch to full length and twang
  • Happens in heart failure, because ventricle less able to stretch, reaches capacity quicker
  • Normal in 15-40 y = ventricles allow rapid filling
  • Heart beat sounds like Ken-tucky
22
Q

S4 heart sound

What it is/when does it happen?

Why does it happen?

Is it physiological or pathological?

A

Caused by forced atrial contraction against a stiff hypertrophic ventricle.

Ventricle is hypertrophied in: HTN, hypertrophic cardiomyopathy, aortic stenosis

Always pathological

Additional heart sound just before S1, presystole

Sounds like Tennes-see

23
Q

What is Erb’s point?

A

Point of auscultation at third ICS left sternal border

Best place to listen to heart sounds S1 and S2

24
Q

How do you describe murmurs?

A

SCRIPT

25
Q

Aortic stenosis

Definition

Clinical Signs

Symptoms/Presentation

Causes

A

Aortic stenosis

Definition

Narrowing of left ventricular outflow at level of aortic valve

Clinical Signs

  • Ejection-systolic crescendo decrescendo murmur -> [because blood flow slowest at beginning of systole and fastest at end]
  • Murmur radiates to carotids
  • Heaving apex beat
  • Narrow pulse pressure
  • Slow rising pulse

As it gets more severe: [LV hypertrophies to overcome pressure gradient on both sides of aortic valves]

  • ECG- signs of LVH
  • S4- because LVH + stiff ventricles [due to pressure overload in ventricles]
  • Soft S2

Symptoms/Presentation

  • Exertional syncope
  • Worsening SOB/dyspnoea esp on exertion
  • Angina [due to hypertrophied muscles, compresses coronary arteries]

Can also cause LVF and CHF:

  • Paroxysmal nocturnal dyspneoa
  • Leg swelling

Causes

  • Rheumatic fever
  • Idiopathic age related calcification
  • Congenital bicuspid valve

Sub valvular aortic stenosis

  • HOCM
26
Q

Table classifying types of murmurs

A

Ejection systolic /mid systolic murmur = aortic stenosis

Pan systolic murmur = mitral [or tricupsid] regurgitation OR VSD

Late systolic murmur = valve prolapse

Early diastolic murmur = aortic [or pulmonary] regurgitation

Mid diastolic murmur= mitral [or tricuspid] regurgitation

27
Q

Signs of hypertension?

A

Loud S2 [increased BP= increased pressure on aorta]

S4 = [pressure overload causes LV hypertrophy]

Signs of coarctation of aorta/renal artery stenosis if secondary HTN

28
Q

Mitral regurgitation

Definition

Clinical Signs

Causes

Investigations?

A

Mitral regurgitation

Definition

Mitral valve is incompetent- allows flow of blood back

Clinical Signs

  • Pan systolic murmur
  • High pitched whistling murmur
  • Radiates to left axilla
  • Displaced apex beat [regurgitation causes volume overload in first left atrium and then left ventricle, causing dilated left ventricle [increased end diastolic volume]]
  • S3 [mitral incompetence= backflow of blood + reduced ejection fraction= left and congestive cardiac failure]
  • Soft S1 [mitral valve less powerfully closing]

Signs of right sided heart failure common as well due to left [due to back pressure from increased left atrium pressure into lungs]

  • Raised JVP
  • Signs of congestive cardiac failure- CHF [due to dilated LV and hypertrophy]

Causes

  • Infective endocarditis
  • Rheumatic fever
  • Idiopathic age related weakening
  • Ischaemic heart disease
  • Connective tissue disorders- Ehlers Danlos, Marfans

Trauma- papillary muscle rupture- acute MR

29
Q

Mitral stenosis

Definition

Clinical Signs

Symptoms

Causes

When is it heard louder?

A

Mitral stenosis

Definition

Stiffened/calcified mitral valve, difficult for blood to flow from left atrium to left ventricle

Pathophysiology

Reduced CO, increased volume overload in left atrium

Clinical Signs

  1. Mid diastolic murmur [low pitched rumbling]
  2. Loud S1
  3. Tapping apex beat
  4. Opening snap [due to calcification of the valve]
  5. Accentuated by patient lying on left
  6. Raised JVP, hepatomegaly, ankle swelling, ascites[signs of right heart failure] - [due to raised LA pressure backing up into lungs and right heart]
  7. Atrial fibrillation [strained LA causes this]
  8. Malar flush [CO2 retention causing vasodilation, due to back pressure in pulmonary vessels]

Symptoms

Dyspnoea, fatigue, weakness

Causes

Most common= rheumatic fever

Infective endocarditis

When is it heard louder?

  • Valsalva maneouvre
30
Q

Aortic regurgitation

Definition

Pathophysiology

Clinical Signs

Symptoms

Causes/Aetiology

A

Aortic regurgitation

Definition

Incompetent aortic valve, blood flows back from aorta into left ventricle

Pathophysiology

Left ventricle volume increases- volume overload - left ventricle dilates

Back pressure- decreased flow from left atrium into ventricle, increased pressure back into pulmonary vessels?

Clinical Signs

Early diastolic murmur [soft]

=Accentuated - left sternal edge, sitting forwards, expiration

Collapsing/Waterhammer/Corrigan’s pulse [pulse bounds too due to increased volume]

Wide pulse pressure

Other signs:

Quincke’s sign= blood pulsating in fingernails

de Musset’s= Head bobbing in time with pulse

Traube’s sign= pistol shot, loud systolic + diastolic sounds over femoral artery

Duroziez’s sig= systolic and diastolic murmurs over femoral artery [on partial compression with stethoscope]

Becker’s sign- visible pulsation of pupil and retinal arteries

Muller’s sign - visible pulsation of uvula

Corrigan’s sign- visible pulsation of neck

Rosenbach’s sign - systolic pulsation of liver

Gerhard’s sign- systolic pulsation of spleen

Hill’s- popliteal artery systolic pressure > brachial pressure by >60mmHg

Austin Flint murmur- Can also cause mitral valve vibration due to blood flowing back over mitral, mid diastolic rumbling murmur at apex]

Symptoms

Similar to [left sided] heart failure: dyspnoea, PND, collapse

Causes/Aetiology

Infective endocarditis

Idiopathic age related weakness

Connective tissue disorders- Marfan’s, Ehlers Danlos

31
Q

Tricuspid regurgitation

Signs

Symptoms

Causes/Aetiology/Associations

A

Tricuspid regurgitation

Signs

Pansystolic murmur

Heard best at lower left stenal, on inspiration [Carvallo’s sign, unlike left heart murmurs which are louder on expiration]

Raised JVP= giant V waves

Other signs of RHF- hepatomegaly, ankle oedema [moderate to severe]

Symptoms

Asymptomatic

Causes/Aetiology/Associations

Infective endocarditis

Congenital abnormalities- Ebstein anomaly- downward diaplacement of malfromed tricuspid valve, cleft tricuspid valve

32
Q

Table-

List all systolic murmurs

+ all diastolic

A
33
Q

Summary picture of murmurs in relation to heart sounds

A
34
Q

Rheumatic fever

Definition

Aetiology/Pathophysiology

Epidemiology

Symptoms

Diagnostic criteria

Investigation

A

Rheumatic fever

Definition

Inflammatory multisystem disease caused after an infection with Group A beta haemolytic streptococcus bacteria [Streptococcus pyogenes]

Aetiology/Pathophysiology

Group A beta streptococcus infection occurs- usually pharyngitis

Antibodies are formed against GAS antigens

These antibodies cross react with host antigens- molecular mimicry of GAS antigens

Epidemiology

5-15 years old- peak incidence

Symptoms

Occur 2-5 weeks after GAS infection

General: Fever, malaise, anorexia

Cardiac: SOB, chest pain, palpitations

Joints: Painful, swollen

Diagnostic criteria

JONES criteria

Major and minor [need two major + one minor, or one major + two minor]

Major:

Joints- arthritis
O- Carditis- new murmur, Carey coombes mid diastolic mitral vasculitis murmur
N- Subcutaneous nodules
E- Erythema marginatum
S-Sydenham’s Chorea / St Vitas’s dance

Minor:

Fever/pyrexia

Raised ESR/CRP

Prolonged PR [or QT interval]

Arthralgia

Previous rheumatic fever

Investigations

Strep infection- recent- throat culture/high anti-Streptolycin O titres

35
Q

Which of the following does not cause a systolic murmur?

A.Atrial septal defect

B.Ventricular septal defect

C.Hypertrophic obstructive cardiomyopathy (HOCM)

D.Aortic regurgitation

E.None of the above

A

D.Aortic regurgitation

36
Q

You perform a cardiovascular examination on an elderly gentleman who reports episodes of collapsing and often wakes up short of breath at night.

Upon auscultation you discover an ejection systolic murmur, which radiates to the carotids.

Which is the most likely valvular pathology?

A.Aortic stenosis

B.Aortic regurgitation

C.Mitral regurgitation

D.Tricuspid regurgitation

E.Mitral stenosis

A

A.Aortic stenosis

37
Q

A 53-year-old woman with Atrial Fibrillation is reviewed by her cardiologists.

On inspection the patients cheeks appear quite flushed. Auscultation reveals a very loud S1 and a mid diastolic murmur.

Which is the most likely valvular pathology?

a) Mitral stenosis
b) Graham Steele
c) Mitral regurgitation
d) Aortic regurgitation
e) Austin Flint

A

a)Mitral stenosis

38
Q

What produces a Graham Steele murmur?

A

Pulmonary regurgitation

High pitched early diastolic murmur

Heard best at left sternal edge at full inspiration

39
Q

49-year-old women presents with 3 month history of increasing SOB on exertion. She has no chest pain, cough or ankle swelling.

On examination: BP 158/61 and there are crackles at the bases of both lungs.

On auscultation you hear a diastolic decrescendo murmur loudest at the left sternal edge.

Which is the most likely valvular pathology?

a) Aortic regurgitation
b) Aortic stenosis
c) Mitral regurgitation
d) Mitral stenosis
e) Tricuspid regurgitation

A

a)Aortic regurgitation

LHF symptoms

40
Q

Which sign is commonly associated with a valvular condition where the murmur is heard louder during expiration, and softer during the Valsalva manoeuvre, and typically radiated to the carotid?

a) Water hammer (collapsing pulse)
b) Flushed cheek (malar rash)
c) Displaced apex beat
d) Slow-rising pulse
e) Subcutaneous nodules

A

d)Slow-rising pulse

41
Q

What happens to aortic stenosis murmur when valsalva maneouvre is done?

A

Becomes softer

42
Q

Buzzwords summary table

Aortic stenosis

Mitral regurgitation

Aortic regurgitation

Mitral stenosis

Tricuspid regurgitation

A