cardio Flashcards
(34 cards)
Contraindications of ACE inhibitors?
What condition is ACE inhibs good for?
- renal aa stenosis, hyperkalaemia, pregnancy, severe aortic stenosis, severe AKI
- diabetic nephropathy
Side effect of B blockers
bronchospasm, cold hands, fatigue, low blood pressure, masking hypos in DM
What ABG findings do you get in pulmonary oedema
Initially type 1 RF due to hyperventilation
Later type 2 RF due to impaired gas exchange
Causes of pulmonary oedema
Fluid overload
LVF/ valve disease/cardiomyopathy
ARDS (infection, DIC, toxins)
Hypoalbuminaemia
What is the management of acute heart failure causing pulmonary oedema
Sit the patient upright 100% O2 IV diamorphine IV furusomide 40-80mg GTN puffs or buccal
If not improving
- Nitrate IV if >100sbp
- SBP <100 cardiogenic shock and ?ICU
Causes of ARDS
Direct inhalation: smoke, drowning, aspiration
Indirect: sepsis, pancreatitis, transfusion reactions, anaphylaxis
MI in which artery corresponds to this STEMI pattern:
- I, avL, V5, V6
- V1-4
- II, III and avF
- = Circumflex
- = LAD
- = right coronary artery
Why is identifying VSD/ ASD early crucial
Once Eisenmengers syndrome in place cant do structural reversal surgery on heart.
Only treatment is heart and lung transplant
Symptoms if infective endocarditis
- Fever, new murmur
- Malaise, lethargy, anorexia
- Haematuria, splenomegaly
- Oslers nodes, Janeway, Clubbing, Splinter, digital infarcts
- Roth spots
What investigations would you do for infective endocarditis?
- FBC, U+E, CRP
- 3 cultures 3 diff types
- Urinalysis
- ECG
- CXR
- Transthoracic echo
What is DUKES criteria for endocarditis
MAJOR:
+ve cultures (2), endocardial involvement on echo
MINOR:
predisposition (valve disease, congenital defects), fever >38, vascular/immunological signs, culture/ echo not good enough for major,
Need 2 maj OR 1 minor + 3 minor
What signs are indicative of infective endocarditis on echo
- New regurgitation
- Vegetations
- Abscess
Causes of bradycardia
- b blockers
- prev MI
- OD
- medications
- endocrine e.g. hypothyroid
- hypoxia
- hypothermia
Name causes of an inverted T wave
- BBB
- MI
- PE
- raised ICP
- normal in children!!!
What are the causes of AF
- hypertension
- valvular heart disease
- CCF
- IHD
- PE
- thyrotoxicosis
- excess alcohol intake
Post MI compliations
ACUTE
- Acute HF: cardiogenic shock or pulmonary oedema
- Chorda tendon rupture > MR
- VSD > ejection systolic rupture
- Ventricle rupture
- Pericarditis
- Cardiac arrest
LONG TERM
- CCF
- Dresslers syndrome
- Arrthymias: VF/ bradycardias
- Ventricular aneurysm
What is CHADsVASC
CHF 1 point Hypertension 1 point Age >75 2 points 65-74 1 point Dm 1 point Stroke/ VTE prev 2 points Vascular disease e.g. peripheral aa or angina 1 point Sex female 1 point
what is HASBLED
Hypertension 1 Abnormal liver function 1 Abnormal renal function 1 Stroke 1 Bleeding 1 Labile INRs 1 Elderly (Age >65) 1 Drugs 1 Alcohol Alcohol use ≥ 8u / week 1
Difference between 3rd and 4th heart sounds? Name the causes
3rd after S1 - ventricles fill to fast.
- CHF, post MI, mitral regurg, VSD
4th before S1 - ventricle walls stiff.
- LVH
WHat causes torsade de pointes
how do you treat it?
Low magnesium, low potassium. common in alcoholics or malnurished
2mg Mg IV
Describe the treatment of IHD - angina
- GTN
- Lifestyle modification
- Statins
- Aspirin
- BP control if high e.g. ACE
- B blocker OR calcium channel blocker (not verapamil and b blocker)
Last line > Nicurandil or Ivabradine
Describe the treatment of heart failure
- Lifestyle
- Patient education
- ACE inhibitors + Beta blocker
- If cough switch to ARTI
If kidney failure hydralazine + nitrite
These are also second line after Ace+B’s - Last line digoxin or ivabradine
NB//
- Diuretic for symptomatic relief (thiazide if elderly or mild, loop if acute or severe) if fluid overload
- Influenza and pneumococcal vaccine
What are the three main causes of heart failure?
Name other causes
IHD, cardiomyopathy, hypertension
Other causes: valvular disease, Cor pulmonale, alcohol, anaemia, AF
Describe the pathophysiology of heart failure
- Decreased output
- RAAS stimulated
- increasing volume and pre load (good), increasing vasoconstriction and afterload (bad, increases blood pressure and cardiac work) - SNS stimulated > causes myocyte apoptosis and necrosis (desensitisation to SNS, contract less efficiently)
- ANP released by heart - antags RAAS
