Block 13 Flashcards
Briefly explain concept of Cor pulmonae
pulmonary vessels constrict to shunt blood away from damaged alveoli to healther alveoli to maintsain gas exchange
increases pulmonary vascular resistance -> pulmonary hypertension -> increases backflow of blood to R side of heart, R side of heart enlarges overtime to compensate => R sided HF
Type of HF where ventricles can’t pump hard enough during systole
Systolic HF or HF w reduced ejection fraction
Type of HF where not enough blood fills ventricles during diastole
Diastolic HF or HF w preserved EF
Adverse effects of HF
- increased preload and afterload
- reduced coronary + renal perfusion due to decreases CO
- fluid accumulation — pulmonary oedema
- increased K+ excretion
- cardiomyocyte necrosis + arrhythmias
Impact of HF on kidneys
decreases CO → decreases renal blood flow → decreased GFR → RAAS activated → increased Na+ and water reabsorption
Age-related changes to heart
- Interstitial collagen within the myocardium increases
- myocardium stiffens
- myocardial relaxation is prolonged
Symptoms of HF
- dyspnoea
- orthopnoea — SOB that’s worse when lying down
- SOB that wakes patient up at night
- pedal oedema
- fatigue
- tachycardia
- tachypnoea
- elevated JVP
2 key complications of COPD
Cor pulmonae
Type II respiratory failure
Type II respiratory failure
alveolar ventilation is insufficient to excrete the carbon dioxide being produced:
low oxygen
high CO2
Cardinal symptoms of CVD
Chest pain
Breathlessness
Palpitations
Syncope
Haemoptysis
Oedema
Cough
Fatigue
Key symptoms of angina
substernal pain
exacerbated by emotional stress + exertion
relieved by rest
*worse in cold, lasts 2-10mins
Subjective sign of disease
Symptom
Objective sign of disease discoverable on examination
Sign
Key symptoms of MI
- pain at rest
- builds up over a few mins
- no relief w GTN or rest
- 30mins plus
- SOB
- sweats
- nausea
- fear
Aortic dissection symptoms
tearing intense chest pain
sudden onset
pain radiates to back as well as other sites e.g. arms/legs/neck/head
Cardiac symptoms of Pericarditis
- retrosternal pain
- relieved by sitting forward
- may radiate to neck + shldr
Orthopnea
type of dyspnea only occurs when a person is lying down
*caused by increased pressure in BVs of lungs
Paroxysmal nocturnal dyspnea
SOB that wakes patient at night
Site of ANP release
myocytes of RA + RV mainly
Action of ANP
- natriuresis - sodium excretion
- lowers BP
- antagonises actions of angiotensin II, aldosterone
Effect of Beta blockers on renin
inhibit renin release from kidneys
Most common pathogen causing lower respiratory tract infections
Streptococcus pneumoniae
Type of breath sounds caused by consolidation in lobar pneumonia
Bronchial breathing
MoA of Class IV antiarrhythmic drugs
- block voltage-sensitive calcium channels
- slow conduction in the SA and AV nodes
- shorten the plateau phase of the action potential
- reduce force of contraction
MoA of Digoxin
- increases vagal outflow to reduce conduction rate at AV node
- inhibits Na+/K+ ATPase pump which increases intracellular Ca2+ => positive inotropic effect
- increased intracellular Na+ slows extrusion of Ca2+ via the Na+/ Ca2+ exchanger decreasing Ca2+ extrusion and thus increased Ca2+ is stored in the SR and available on release
MoA of Class II antiarrhythmic β1-selective-Adrenoceptor antagonist
e.g. Atenolol
diminishes the Phase 4 depolarisation which:
- suppresses automaticity
- prolongs AV conduction
- decreases HR + contractility
MoA of Dobutamine
β1 adrenoceptor agonist and α1 selective activity with some weak β2 activity
- increases contractility + CO
Why is Verapamil contraindicated in HF?
because it blocks calcium channels and has negative inotropic effect
Site of Spironolactone action
collecting ducts
How does spironolactone help reduce pulmonary oedema in HF?
Blocks aldosterone action in CD which:
increases Na+ and water excretion
so decreased fluid volume = decreased pulmonary oedema
Canon ball lesions in all lung fields indicate
Metastatic cancer
Important side effect of ACE inhibitors:
first-dose hypotension
Therapy for NSTEMI
Antiplatelet therapy, LMWH, statins and anti-ischaemics
D-dimers are
biomarkers for ongoing thrombosis
1st Degree heartblock on ECG
- regular QRS complexes
- p waves present BUT delay at AV node, P-R interval prolonged => 1st degree heart block
Slow or blocked conduction through AV node is
HEART BLOCK
Effect of adenosine on AV node
BLOCKS AVN
Effect of atropine on AV node
STIMULATES AV node
Common presentation of atrial flutter on ECG
- 150bpm
- narrow QRS complex
Common causes of tachycardia
- Hyperthyroidism
- Anxiety
- Heart failure
- Hypovolaemia
- Septicaemia
Commonest pathogen causing lower respiratory tract infections in ALL age groups
Streptococcus pneumoniae
Patchy shadowing in lung fields on X-ray
BRONCHO-PNEUMONIA
Antiarrhythmic drugs that:
slow conduction in the SA + AV noded
shorten the plateau phase of the AP
decrease force of contraction
CLASS IV anti-arrhythmic drugs
Beta 1 selective receptor agonist used to treat acute but reversible HF e.g. cardiogenic or septic shock
DOBUTAMINE -> increases cardiac output + contractility
Type of calcium channel receptors that Verapamil acts on
L-type Ca2+ channels
The pathogen that generally causes pneumonia after a preceding viral illness
Staphylococcus aureus
Mechanism of Action of Theophylline
competitively inhibits type III + type IV phosphodiesterase
WHICH prevents cAMP breakdown
LEADING TO: bronchial SM relaxation; bronchodilation
What clinical finding distinguishes L. pneumophilia from other pneumonias?
HYPONATREMIA!
In what pathologies are hyper-inflated lungs normally seen?
COPD - as air gets trapped within the lungs
Typical therapy for NSTEMI
LMWH - inactivates thrombin + activated factor X prevent further thrombin activation and fibrin formation
Statins - maintain plaque stability
Anti-ischaemic medications - maintain perfusion and prevent ischaemia
Anti-platelet therapy - prevent further platelet recruitment to the thrombus
Briefly explain atrial flutter
ATRIA contract v fast
BUT, AV node is refractory so only conducts a proportion of impulses
Torsades de Pointes
specific type of polymorphic ventricular tachycardia:
common cause: decreased K+ AND decreased Mg2+
How to calculate HR in bpm from an ECG?
300 / no. of lrg squares
What is heart block?
slow/blocked conduction through AV node
Sinus Arrest
failure of sinus node discharge ==> no atrial/ventricular depolarisation
3 classes of class I anti-arrhythmic drugs
MODERATE
- Quindine
- Procainamide
WEAK
- Lidocaine
- Phenytoin
STRONG
- Propafenome
- Flecainide
Non-selective beta blockers
Propanolol
Timolol
Nadolol
Cardioselective beta blockers
Atenolol
Carvedilol
Bisoprolol
Metoprolol
MoA of Ca2+ channel blockers
inhibit Ca2+ influx during membrane depolarisation
EFFECTS:
- reduces LV contraction
- dilates BVs
- reduces myocardial oxygen demand
Main aetiological agents of acute bronchitis
VIRUSES: Rhinoviruses Adenoviruses Parainfluenza Influenza A+B
Exacerbation of COPD is usually:
acute bronchitis!!!
Which groups of ppl are more susceptible to bronchopneumonia?
infants AND elderly
Which organisms commonly cause cavitating pneumonia?
S. aureus
Klebsiella
Mycobacteria TB
Majority of community acquired pneumonia is caused by
BACTERIA
70% - 90% caused by Streptococcus pneumoniae
Which class of antibiotic should be used to treat Legionnaire’s?
Macrolides or Quinolones (penicillins don’t work!!!)
Pneumonia occurring 48hrs after hospital admission or discharge
Hospital acquired pneumonia
Where are ACE inhibitors activated in the body?
phase 1 metabolism in liver
Where are baroreceptors located?
Carotid sinus AND aortic arch
