CARDIO Flashcards
Non-pharmacological tx of htn
-Should be continued even if drug therapy is started-Regular aerobic exercise (can reduce daytime BP by 3.2/2.7 mmHg) -Reduction of alcohol intake -Moderate sodium restriction -Healthy eating -Weight reduction in overweight patients (5 kg weight loss can reduce BP by 7/3 mmHg)
Pharmacological tx of htn
-Begin with one drug at a low to moderate dose and review patient regularly
-If not reached within 3 months of treatment then add a low dose of a second drug from a different class -First line drugs;
• ACEI-Captopril (12.5-50mg daily) OR Perindopril arginine (4-8 mg)
• ARB-Candesartan (8-32 mg daily) OR Irbesartan (150-300mg daily)
• Dihydroperidone calcium channel blockers-Amlodipine (5-10mg) OR Nifedipine (20-120mg)
• Thiazide diuretic-Hydrochlorothiazide (12.5-50mg)
-Following combinations are effective;
-a thiazide or thiazide-like diuretic with an ACEI, ARB or beta blocker
-an ACEI or ARB with a calcium channel blocker
-a beta blocker with a dihydropyridine calcium channel blocker
-an ACEI or ARB with a dihydropyridine calcium channel blocker and a thiazide or thiazide-like diuretic.
Mx pathway for HTN
Complications of HTN
LVH/Failure–> due to increased pressure in ventricle
-AF–> due to diastolic dysfunction
-Cerebrovascular ischemic events (stroke)à stroke due to carotid atheroma, SAH due to increased pressure
-Hypertensive encephalopathy–> transient disturbance in speech/vision
-Renal failure–> benign nephrosclerosisàarteriosclerotic changes (in efferent and afferent tubules) causes progressive decrease in GFR and tubular dysfunction (mainly affects afferent wall through thickening via hyaline arteriosclerosis)à causes appearance of grain kidney (due to microangiopathy and microinfarcts causing glomerular scarring in the cortex) and protein/haematuria
-Retinopathy;
•Cotton wool exudates – ischemia, infarction, fade in few weeks
•Hard exudates (cholesterol leakages) and dot hemorrhages (microaneurysms or ruptured microvasculature)
•Generalised thickening of the arterioles
-IHD–>MI
-PVD–>due to hyaline arteriosclerosis and atherosclerosis (HTN causes epithelial dysfunction which promotes atherosclerosis)
-AAA/Dissection due to internal elastic lamina thickening, SM hypertrophy, fibrous tissue deposits and vessel dilation/tortuation causes walls to become less compliant
What are the symptoms of ARF
- Subcutaneous nodules–> occur on high pressure areas
- Pancarditis–> often causing cardiomegaly- knees, elbows
- Polyarthritis
- Fever
- Sydenham chorea- due to the attack of the basal ganglia
- Erythema marginatum- due to the attack of membranes
- Weak heart sounds (due to inflammation), pericardial friction rub, murmur and cardiac failure
What are the investigations for ARF
-Why aren’t cultures done
- ASO= titre of Ab against strep lysin O (highly specific for strep)
- Anti DNAase B= Ab titres against strep
- Antistreptokinase= Ab against streptokinase
- Antihyaluronidase= strep produces hyaluronidase (Ab mean past infection)
- ECG= prolonged PR interval
- CRP= elevated
- ESR= elevated
- CXR= LV hypertrophy (in RHD)
- Echo= valve vegetations/stenosis
- -> no culture as the strep infection will have cleared and it will be an autoimmune response causing damage
What is the management for ARF/RHD
- Penicillin prophylaxis for patients who have had acute rheumatic fever–> in order to prevent recurrent attacks of ARF leading to RHD
- Medical management for patients with minor valve disease (eg. anticoagulation, ventricular rate control, diuretics, etc.)
- Valve replacement, balloon valvuloplasty for patients with severe valve disease
What is the aetiology of IE
- *-bad oral hygiene-**oral streptococci or staph aureus- form a plaque layer/biofilm- able to do this due to production of dextrose that aids in adherenceà if pt has dental problems can move into blood stream and travel to heart
- IV drug user-staph aureus, oral strep or gram neg bacteria- cause right sided endocarditis (tricuspid valve)-organisms that have come from the skin or dirty needles
- *-prosthetic valves-** if less than 2 months most likely hospital acquired- coag negative staph
- *-prosthetic valves-** if greater than 2 months most likely environmental causeà
- damaged valves- RHD/high pressure areas (mitral regurg, aortic regurg
What are the examination findings of IE
General signs: weight loss; pallor (anaemia), fever (low grade and persistant in SBE, severe in ABE)
- *Hands:** splinter haemorrhages; clubbing (within six weeks of onset); Osler’s nodes (rare-painful erythematous nodules); Janeway lesions (very rare), petichae and purpura
- *Mouth:** mucosal petechiae
- *Arms:** evidence of intravenous drug use
- *Eyes:** pale conjunctivae (anaemia); retinal or conjunctival haemorrhages—Roth’s spots
- *Heart:** signs of underlying heart disease:
(1) acquired (mitral regurgitation, mitral stenosis, aortic stenosis, aortic regurgitation);
(2) congenital (patent ductus arteriosus, ventricular septal defect, coarctation of the
aorta) ;
(3) prosthetic valves.
Abdomen: splenomegaly.
Peripheral evidence of embolisation to limbs or central nervous system.
Urinalysis: haematuria (a fresh urine specimen will then show dysmorphic red cells and red cell
casts on microscopy).
What investigations would you do for IE
- Blood test- blood culture, FBC, ESR, CRP
- Echocardiogram- detect vegetations and abscesses and look at valvular damage
- CXR- look at cardiomegaly
- ECG- look for infarct or arrhythmia
How is IE managed/treated
-Antibiotics
Empirical therapy;
-gentamicin IV, once daily;
PLUS
-benzylpenicillin 1.8 g (child: 50 mg/kg up to 1.8 g) IV, 4-hourly
PLUS
-flucloxacillin 2 g (child: 50 mg/kg up to 2 g) IV, 4-hourly.
In those with a history of IVDU or fulminant endocarditis substitute benzylpenicillin with vancomycin
- Restoration of damaged valve
- Resolution of preceding factor (ie. Fix immunosuppression)
What is the Jones Criteria- is it used in Aus
- Due to its reduced sensitivity in a high incidence population, only the modified Jones criteria is used in diagnosis of ARF
- It has criteria for low and high risk populations and initial vs recurrent attacks
How is IE diagnosed- what is the criteria
- Diagnosed with Dukes criteria
- Need 2 major clinical criteria or 1 major and 3 minor
How does oedema form
-causes of pedal and pulmonary oedema
- Occurs when excess fluid moves into the tissues for multiple reasons such as; increased ECF (due to CHF, renal failure), high venous pressure (DVT), hypoalbuminaemia (causing loss of oncotic capillary pressureà due to liver failure/nephrotic syndrome), increased cap permeability (infection/inflamm, sepsis)
- Pedal oedema: is oedema occurring in the feet/lower limbs- due to insufficiency of leg venules or CHF causing fluid backflow into the peripheries
- *-Pulmonary oedema:** fluid in the lungs most often caused by CHF in which there is increased pressure in the heart causing backflow into pulm artery or LV heart failure
What is Wells Score
The Wells’ Criteria risk stratifies patients for a pulmonary embolism (PE) and provides an estimated pre-test probability of PE
- Above 6 indicates high probability of PE
- Between 2 and 6 indicates moderate probability
- Below 2 is low probability
- suggests diagnosis of PE
