Cardiovascular Flashcards
What’s the management of hypertension for a Caucasian 45 year old man?
Lifestyle changes
1st: ACEi or ARB
2nd: Add Ca-channel blocker
3rd: Add thiazide-like diuretic
4th: Add further diuretic or A or B-blocker
What’s the management of hypertension for a Black Afro-Caribbean 60 year old lady?
Lifestyle changes
1st: Ca-channel blocker
2nd: Add ACEi or ARB
3rd: Add thiazide-like diuretic
4th: Add another diuretic, A or B-blocker
What’s the management of hypertension for a Caucasian 75 year old lady?
1st: Ca-channel blocker
2nd: Add ACEi or ARB
3rd: Add thiazide-like diuretic
4th: Add another diuretic, A or B-blocker
Name some:
- ACEi
- ARB
- B-blockers
- A-blockers
- Ca channel blockers?
ACEi: Lisinopril, ramipril
ARB: Candesartan, losartan
B-Blocker: Bisoprolol
A-blocker: Doxazosin
CCB: amlodipine
What are the 3 types of diuretics? Give an example of each type.
Thiazide-like
- indapamide
Loop
- furosemide
K sparing
- spironolactone
How do thiazide-like diuretics work?
Act on proximal part of distal tubule
Increase sodium excretion from blood to urine
Increase water excretion from blood to urine
This reduces the blood volume and therefore BP
How do loop diuretics work?
Act on the loop of Henle
Causing loss of water from blood to urine
Reducing blood volume and BP
How do K sparing diuretics work?
Inhibit sodium/potassium exchange by blocking aldosterone
So loss of water from blood to urine but no loss of K
Not very effective diuretics
Briefly describe the RAAS pathway.
Liver produces angiotensinogen
Renin, an enzyme, is released by kidney due to low fluid volume in nephron
Renin converts angiotensinogen –> angiotensin 1
In lungs, ACE converts ang-1 –> ang-2
Ang-2 causes adrenal gland to release aldosterone
Aldosterone acts on collecting ducts to retain water
How do CCBs work?
When calcium enters the cells of blood vessels, the blood vessels constrict.
CCBs block Ca entering the cells, so blood vessels don’t constrict and even dilate, so BP doesn’t rise
What’s the management of heart failure?
Lifestyle changes
Drugs:
- diuretics, loop and if required K sparing
- ACEi or ARB
- B blocker
- Spironolactone
- Digoxin
How does digoxin work?
It slows down the heart and allows proper filling of ventricles
List some symptoms of R and L sided heart failure? Explain.
Right:
RV can’t pump blood to lungs quick enough, blood backs up into VC, so there’s peripheral and sacral oedema, ascites
Left:
LV can’t pump blood to aorta very well, blood backs up into lungs causing pulmonary hypertension and oedema, SOB, cough. Also body is hypoperfused: cold peripheries, wasting
What respiratory symptoms are seen in heart failure?
SOB
Cough:
- paroxysmal nocturnal dyspnoea
- orthopnea
Investigations of heart failure?
ECG
Bloods: B natriuretic peptide
CXR
Echo
What would you see on the CXR of a patient in heart failure?
A: Alveolar oedema
B: Kerley B lines
C: Cardiomegaly
D: Dilated prominent upper lobe vessels
E: Pleural effusion
How is hypertension staged?
- Over 135/85
- Over 150/95
Severe: systolic > 180, diastolic > 110
How are stages 1 + 2 hypertension managed?
Stage 1: lifestyle modification, smoking, alcohol, exercise, diet, relaxation
Stage 2: drugs
What is AF?
Abnormal heart rhythm caused by rapid and irregular atrial contraction
Atrial stagnation, blood clots as it’s stagnant in artia
Clots are pumped around body
What are the risk factors for AF?
Hypertension Coronary artery disease Valvular heart disease Sepsis Alcohol PE Thyrotoxicosis
Clinical features of AF?
Palpitations
SOB
Chest pain
Dizziness
Investigations of AF?
ECG
Echo
Management of AF?
Rate control: B blockers, or Ca channel blockers
Rhythm control: cardioversion, amiodarone
Anti-coagulation: warfarin, aspirin, NOAC
When would you use cardioversion to treat AF?
In younger patients with new AF
How would you assess a patient with AF’s risk of having a stroke?
How would you manage depending on risk?
CHA2DS2Vasc
CCF Hypertension Age over 70 (2) Diabetes Stroke/TIA (2) Vascular disease Age 65-74 Sex female C
0 = low risk, no intervention 1 = moderate, consider intervention 2 = high risk, intervene
What’s a NOAC?
Novel anti-coagulant
Apixiban
Rivaroxiban
In a patient taking an anti-coagulant? How could you asses the risk of them having a bleed?
HAS BLED score
Hypertension
Abnormal renal or liver function
Stroke
Bleeding
Labile INR
Elderly (over 65)
Drugs and alcohol
What anti-coagulants can we give? Briefly describe how they work.
NOAC: apixaban, rivaroxiban
They inhibit clot formation
Warfarin: vitamin K antagonist, reducing synthesis of coagulation factors
Aspirin: inhibits platelet aggregation
How is heart failure classified?
New York heart association
- no symptoms or limitation to ADLs
- mild symptoms, slight limitation to ADLs
- marked symptoms, limitation to ADLs, only comfortable at rest
- severe symptoms, uncomfortable at rest
What community support is available to patients with heart failure?
Named GP Advanced nurse practitioners District nurses Charities (BHF) Counselling Palliative services Community mental health teams
What is angina?
Chest pain caused by insufficient blood flow to heart muscles
Often caused by coronary artery disease, arrhythmias, vasospasm
Clinical features of stable angina?
Constricting discomfort in front of chest, neck, shoulders, jaw, arms
Precipitated by physical exertion
Relieved by rest or GTN spray
What’s the difference between stable and unstable angina?
Stable is pain on exertion
Unstable is pain at rest as well
Investigations of angina?
Angiography
Stress echo
Management of angina?
- symptom control: GTN spray
2. prevention of acute coronary syndrome (unstable angina, MI) Aspirin beta-blocker Statin Ca channel blocker ACEi
More severe: ivabradine, nicorandil etc.
What is ivabradine?
Drug that slows down heart rate
