Cardiovascular Flashcards
Types of angina?
Stable angina-
chest pain resolves during rest but returns on exertion (paroxysmal) caused by transient myocardial ischemia.
Pain relieved by analgesics
Variant angina-
Prinzmetal’s Angina / Vasospastic Angina- different to other anginas as it occurs during sleep caused by sudden vasospasm of the coronary arteries. > women
Silent angina/ischaemia-
asymptomatic and without chest pain. Patients are unaware they have a heart problem and have not usual warning signs. Leads to heart muscle damage and MI. Makes up a significant portion of STEMIs in the elderly (OSCE!!!)
- Types of acute coronary syndrome? -> causes
- Symptoms?
- Cardiac biomarkers for each type
- Unstable angina- chest pain constant even at rest and unprovoked that lasts for >20mins.
Caused by ruptured plaque within lumen wall leading to thrombus formation + occlusion
No serum cardio biomarkers = -ve troponin -> Unstable Angina
Detectable cardio biomarkers= +ve troponin -> NSTEMI
NSTEMI- affects inner third of the myocardium as it is the furthest away from the artery and predisposed the most to higher pressures from blood flow.
Show ST-segment depression and absent Q-wave on ECG due to PARTIAL infarct of the wall.
STEMI- the necrosis extends through entire wall thickness this leads to transmural infarct.
Shows up at ST-segment elevation and present Q-wave on ECG due to FULL infarction of the wall.
Symptoms of STEMI:
Crushing central chest pain -> jaw + arm
Diaphoresis
SOB
Fatigue
N&V
Not relieved by analgesics
Epigastric pain- DM, elderly, women
Management for STEMI?
MONAC
Types of revascularisation
Management for STEMI: MONAC
M- morphine
O- oxygen but <94% (avoid hyperoxia)
N- nitrates (GTN spray)
A-aspirin 300mg
C- clopidogrel/ aspirin- antiplatelet (fibrinolytic therapy)
Revascularisation
PCI: is offered within 12 hours and delivered within 120 min of then thrombolysis could be given (radial access)
Thrombolysis: offered within 12 hrs if PCI cannot be given
What is pericardial effusion?
Complication of pericardial effusion?
What is cardiac tamponade?
Pericardial effusion-
accumulation of fluid (blood, pus, serous) in pericardial sac (between parietal and visceral pericardium) surrounding the heart.
Can lead to cardiac tamponade if fluid volume exerts pressure on the heart and impairs function.
Acute- fluid accumulates quickly -> cardiac tamponade
Chronic- fluid accumulates gradually and may increase in compliance before symptoms develop
Cardiac tamponade-
increased pressures from fluid (blood, pus, serous) accumulation cause chambers of the heart become compressed due to increased pressure from fluid leading to reduced stroke volume/ cardiac output. Result of pericardial effusion.
Risk factors for pericardial effusion and cardiac tamponade?
Trauma- blunt trauma
Pericarditis- viral/ bacterial
Medical- catheterisation, pacemaker
Cancer- lung/breast cancer metastasis to pericardium
Autoimmune- lupus -> inflammation -> fluid accumulation
Radiation therapy
Hypothyroidism Trauma- blunt trauma
Investigations for pericardial effusion and cardiac tamponade?
Effusion:
Medical history- AMPLE
A-allergies
M- medications
P- PMH
L- last ate/drank
E- event leading to admission
Bloods- FBC, U&E, LFT, glucose, coagulation screen, troponin
12-lead ECG
ECHO
X-RAY
Potential causes for tamponade- trauma, infection, medical, cancer, autoimmune (acute/chronic)
Tamponade:
Bloods- FBC, U&E, LFT, glucose, coagulation screen, troponin
12-lead ECG
ECHO
X-RAY
Management for pericardial effusion and tamponade?
Effusion:
Treat underlaying cause- trauma/ infection
Pericardiocentesis
ABCDE + iv fluid/ abx + NSAIDs
Tamponade:
Pericardiocentesis- drainage of fluid using needle/ catheter at xiphoid process with echo guidance
Iv fluids and abx
Treat underlaying cause- trauma/ infection
Acute heart failure management?
First line
* Sit patient up, give high flow oxygen, IV access
* Furosemide 40-120mg IV- diuretic
* (do not offer diamorphine)
* NICE does not suggest IV nitrates but being increasingly used
Second line (special circumstances)
* Non-invasive ventilation
* Mechanical ventilation (tired patient, inability to maintain oxygenation)
* Inotropes/ vasopressors (cardiogenic shock)
* Ultrafiltration
* Mechanical assist devices
* Surgery for valvular disease
After stabilisation
* Beta blocker
* ACE inhibitor
Device therapy
* Cardiac-resynchronisation therapy pacemaker
* Implantable cardio defibrillator
* Heart transplantation
Hypertension investigations?
Blood pressure
Height and weight, BMI / waist
Pulses and radio-femoral delay
Kidneys- Palpable kidneys (ADPKD)
Check bloods (FBC, U&Es, LFT, Lipids, HbA1c)
ECG
Urine ACR- proteinuria, haematuria, glycosuria
Fundoscopy
Renal imaging- deranged U&E
Hypertension causes?
Essential hypertension:
Obesity
Genetics
Alcohol
Salt
Metabolic syndrome (lipids, BMI, T2DM, HTN)
Exercise- naturally increases during but lowers resting
Secondary hypertension:
Renal disease- PCKD
Endocrine- Cushing’s
Pre-eclampsia
Iatrogenic- steroids, NSAIDs
Hypertension complications?
Stroke
Dementia- vascular
Retinopathy
Heart failure
Renal disease
LV failure
What is hypertension?
Classification of HTN?
Reduced elasticity and compliance of large arteries leads to more stiffend vessels
Accumulation of arterial Ca+, collagen and degradation of elastin
Defective Na+ storage leading to retention
Stage 1 hypertension: Clinic blood pressure (BP) is 140/90 mmHg or higher
Management- Ok to monitor lifestyle modification arrange 24 hour monitor
Stage 2 hypertension: Clinic BP 160/100 mmHg is or higher
Management- Lifestyle modification fairly urgent 24 hour monitor. Treat if BP remains high in clinic or on 24 hour BP
Severe hypertension: Clinic BP is 180 mmHg or higher or Clinic diastolic BP is 110 mmHg or higher
Treat immediately may be an emergency
Hypertensive crisis- BP >200/120mmHg (pre-eclampsia, stroke, AAA)
BP overestimation- cuff too small
BP underestimation- cuff too big
Types of vascular occlusion?
Types of occlusion:
- Atheroma (atherosclerosis)- fatty plaque deposits in artery walls (cholesterol, fats, cell debris)
- Thrombus/ embolism- (thrombus- clots that forms and remains at the site where it has developed) (embolism- clot that has broke loose from original site and travels through blood stream to a different location in the body)
- Spasm- narrowing or complete blockage due to sudden, voluntary contraction of vessel. Result in angina or MI
- Vasculitis- inflammation of blood vessels leading to occlusion (autoimmune, infections, drug reactions, genetics)
Difference between:
Ischaemia
Partial occlusion
Complete occlusion
Infarction- occur when there is a sudden and complete blockage of the coronary artery
Heart failure
Ischaemia= inadequate supply of blood to a tissue resulting in insufficient supply of oxygen and other metabolic needs for that tissue. Caused by occlusion of arteries, veins and capillaries -> hypoxia
Partial occlusion= atherosclerotic plaque -> plaque extends into the lumen of muscle -> partial occlusion -> local ischaemia of heart tissue-> stable angina + NSTEMI
Complete occlusion- atherosclerotic plaque -> plaque rupture -> thrombus formation -> complete occlusion-> infarction -> unstable angina + STEMI
Infarction= Cell / Tissue Necrosis (death) caused by an inadequate supply of blood carrying oxygen and other metabolic needs. Occurs when there is a sudden and complete blockage of the coronary artery
Heart failure
Difference between NSTEMI and STEMI?
NSTEMI- affects inner third of the myocardium as it is the furthest away from the artery and predisposed the most to higher pressures from blood flow. This is subendothelial infarct and show ST-segment depression on ECG due to PARTIAL infarct of the wall.
STEMI- after 3-6 hours, the necrosis extends through entire wall thickness this leads to transmural infarct. Shows up at ST-segment elevation on ECG due to FULL infarction of the wall.
