CVASC4 Flashcards
(46 cards)
Patient presents with systolic hypertension in the upper extremeties, Diminished or delayed femoral pulses (radio-femoral delay), and low or unobtainable blood pressure in the extremities. What is the likely diagnosis?
Screening test?
Confirmation of Dx?
Co-arctation of the aorta
Screening Test is Xray - look for notching of ribs or the “3” sign
Diagnosis is confirmed by two dimensional and doppler transthoracic echocardiography.
Claudication can also occur
Patient presents with hypertension AND episodic headache, sweating and tachycardia. Diagnosis?
Phaeochromocytoma
Hypertension and a low serum potassium - what are you concerned about?
May also have muscle cramps, tetany, paraesthesiae
Primary hyperaldosteronism.
- Hypervolaemia and Hypokalaemia
- DO ALDOESTERONE: Plasma Renin Activity ratio
- This will be HIGH in primary hyperaldosteronism ( because renin level will be low ) -(Do abdominal CT to differentiate tumour from adrenal hyperplasia)
In secondary - it will be NORMAL - think of Bilateral renal artery stenosis (Do a doppler u/s of renal arteries)
Which investigations would you consider to rule out END ORGAN DAMAGE in Hypertension?
- Kidney (proteinurea +/- CKD) - UEC, ACR
- Eye - retinopathy (papilloedema & haemorrhages) - fundoscopy /eye review
- Heart - LVH/Heart Failure (Rare- dissection) - ECG/TTE/CXR based on symptoms
- PAD - ABPI (Doppler u/s of limbs)
What are the causes of secondary hypertension?
Renal: Diabetic nephropathy, Chronic glomerulonephritis, Tubular interstitial nephritis, kidney stones, reflux nephropathy, PCKD, Renal artery stenosis.
Endocrine: Conns, Cushings, acromegaly, Phaeo,
Coarctation of Aorta
Inflammatory - Polyarteritis Nodosa
MEDS - OCP, NSAID, Steroid, Appetite Suppresant, Ethanol
What broad categories of investigations would you consider in hypertensive patient?
- Exclude end organ damage
- Secondary hypertension
- Cardiovascular risk (fasting lipids and Glucose)
What investigation would you consider to work out whether a patient had bilateral renal artery stenosis
They would have secondary hyperaldosteronism because of increased renin and aldosterone.
Therefore: NORMAL aldesterone:plasma renin activity ratio.
Follow up with doppler ultrasound of renal arteries
Investigations to consider to exlude secondary hypertension?
Urine ACR, Serum aldosterone: Plasma renin activity ratio, 24hour urinary fractionated metanephrines and catecholamines, Overnight
What is your management approach to a patient who presents with hypertension?
- Detailed medical history and examination.
- Accurately diagnose.
- Decide severity according to guidelines.
- Organise appropriate investigations.
- Calculate and Document Cardiovascular Risk.
- Address cardiovascular risk factors
exercise/nutrition/smoking status/employment/stress
In what settings is a CV risk calculation appropriate?
As PRIMARY PREVENTION only
Not in established CV disease.
Recommended for Non ATSI > 45
for ATSI > 35
Use CLINIC BP measures (must be within the last five years) for CV risk calculation.
What examination findings do you look for in hypertension?
Bedside urinalysis for blood and protein (renal disease)
Listen for carotid artery bruits
Examine the fundi for hypertensive changes
Examine the peripheral vascular system for evidence of PAD
Record and ECG - to look for ventricular hypertrophy and ischaemic changes
Examine the abdomen - evidence of arterial disease (Eg Abdominal aortic aneurysm, or renal bruits which may indicate renal artery stenosis) and ballot the kidneys (Enlarged in polycystic kidney disease)
Major clinical manifestations of pericarditis?
- Pleuritic chest pain - typically sharp and pleuritic worse lying down, improved by sitting up and leaning forward.
- Pericardial friction rub - superficial scratchy sound best heard over left sternal border (With diaphragm)
- ECG changes - widsespread ST elevation or PR depression
- Pericardial effusion
- If viral - preceding URTI sx, if systemic infection - you can get fever and leukocytosis, If autoimmune (RA,SLE) or uraemic or post MI - patients will have symptoms of the underlying cause
Remember Tamponade would present as Decreased BP, elevated JVP and muffled heart sounds
How would you differentiate an ECG of a patient with acute pericarditis from a patient with Acute MI?
- MI - tends to be ST segment changes in regions of heart being infarcted (In MI - localised to a coronary vascular territory) - Peri its widespread.
MI - you can get convex large st elevation over 5mm
Peri u_sually normal concavity and less than 5mm_
MI - reciprocal leads get ST depression ( you dont tend to see that in Peri)
T wave inversion with ST elevation in MI - you dont tend to see that in pericarditis UNLESS myopericarditis
PERI - PR elevation AVR and depression in most/all other leads!
How do ECG changes evolve in pericarditis
Starts with diffuse ST elevation and PR depression
THEN
ST and PR segments normalise
THEN
widespread T wave inversion
THEN
T waves normalise
How would you identify a pericardial effusion on CXR?
A globular cardiac sillhouette with CLEAR LUNG FIELDS - greater than 0.5 cardiothoracic ratio
AT LEAST 200ml of pericardial fluid must be present before the cardiac sillhouete enlarges
What are the causes of pericarditis?
- VIRAL - most common, can be preceded by URTI - Don’t forget HIV!
- Bacterial - less common
- TB - exposure? uncommon
- Fungal - uncommon
- AUTOIMMUNE - rheuamatoidm, SLE (might check ANA in your investigations)
- MALIGNANCY - common in patients with breast, lung and heam malignancies
- Post - MI - more common in large infarcts - delayed presentation
8 Uraemic - suspect in patients with CRI - esp peridialysis period
- Drugs - rare
Negative troponin in Pericarditis?
Reassuring - but will be positive in 30% of patients.
Will be pos in myocarditis too
Investigations of Pericarditis?
ECG
CXray
Troponin
ESR/CRP
Transthoracic Echo - this needs to be urgent if signs of effusion/tamponade
Then look for underlying cause depending on hx
ANA
HIV
Blood culture
TUberculin skin test
etc
Admission criteria for pericarditis?
High fever - over 38 degrees celsius
Subacute course - symptoms over several days without a clear cut acute onset
Large pericardial effusion
Caridac tamponade
Failure to respond within 7 days to NSAIDS or Aspirin
Management approach for Pericarditis
- Treat underlying cause - connective tissue - immunemodulators, Purulent - antibiotics, Uraemic - dialysis
- Restriction of EXERCISE
-
Colchicine (3 months) PLUS Aspirin or Ibuprofen (2 weeks or more depending on sx)
* If 70 kg or more - 500mcg bd for three months*
* If less than 70kg (or renal impairment) - 500mcg orally daily for three months*
AND
Ibuprofen 600mg 8hrly for one week then decrease by 200mg every week until stop.
- Recurrent pericarditis - seek cardiologist advice
What are the complications of pericarditis?
- Constrictive pericarditis
(Scarring and consequent loss of elasticity of pericardial sac, typically chronic - but rarely can be subacute, transient or occult)
- Pericardial effusion
- Cardiac tamponade (Triad of muffled heart sounds, increased JVP and decreased BP)
How would you identify a pericardial effusion without tamponade? What’s the clinical significance?
Its only on ECHO (no physical signs of it)
IF pericardial effusion with HAEMODYNAMIC COMPROMISE - immediate drainage (therapeutic and diagnostic)
IF no haemodynamic compromise - don’t need it drained immediately
What is pulsus paradoxus?
Its an abnormally large DECREASE in systolic blood pressure on inspiration (over 10mm/Hg)
It’s commonly found in tamponade an it’s a sign of ventricular independence
Clinical Signs of Tamponade
TRIAD - muffled heart sounds, elevated JVP and decreased Blood pressure
PLUS
Pulsus paradoxus (decreased BP on inspiration)
Sinus Tachy
Pericardial rub (due to inflammatory pericarditis)
