CR Flashcards
P wave
Atrial depolarisation
0.08-0.1s
QRS complex
Ventricular depolarisation
T wave
Ventricular repolarisation
PR interval
Delay at AVN
0.12-0.2s
QT interval
Time when all the ventricular muscle is contracting
0.35-0.43s
Physiology of AF
Atria experience chaotic signals and quiver
Only some APs pass through to ventricles giving irregular ventricular rhythm
Causes of AF
Hypertension Heart attacks Abnormal valves Hyperthyroid Sleep apnoea
Symptoms of AF
Palpitations Reduced ability to exercise Fatigue Dizziness Confusion Shortness of breath Chest pain
ECG evidence for AF
No distinct P wave
Irregular R-R intervals
Treatment for AF
Cardioversion to restore regular sinus rhythm
Thromboprophylaxis
Treatment of underlying cause if possible
Why is there an increased chance of clots with AF?
Pooling of blood in atria
Stagnant blood more likely to clot
Clots can dislodge and be pumped out of the heart
Can block arteries in the circulation
Can cause stroke if reach cerebral arteries
Rivaroxiban mode of action
Direct factor Xa inhibitor
Vitamin K antagonists
Warfarin
Prevent formation of some clotting factors
Heparins
Activate antithrombin III
Inhibits thrombin and factor Xa
Speed of action potential in different parts of the heart
Atria = 0.5m/s
AVN = 0.05m/s
Bundle of his and bundle branches = 2m/s
Purkinje fibres = 4m/s
Atrial contraction and exercise
10% of ventricular filling at rest
40% of ventricular filling in exercise
Less time for atrial filling in exercise
Atrial contractions needed to achieve maximum stroke volume
Normal cardiac output
- 9L/min for females
5. 6L/min for males
Normal stroke volume
70ml in 70kg male
Normal heart rate
60-100bpm
Normal MAP
65-110mmHg
Local mediators controlling vasodilation of arterioles supplying muscles
CO2, H+, K+, AMP, adenosine, NO, bradykinin
Blood distribution to muscles at rest and in exercise
21% at rest
85% in exercise
Mutation in Liddle syndrome
Mutation in C terminus of the ENaC channel
Inability for Nedd4-2 to bind
Channel cannot be marked for degradation
Increased activation of ENaC
Increased sodium retention
Increased water retention
Increased blood volume and therefore pressure
Symptoms of Liddle syndrome
Early onset hypertension
Metabolic alkalosis
Muscle wasting (low potassium)
Diagnosis of Liddle syndrome
Hypokalemia
Elevated bicarbonate
Supressed renin and aldosterone
DNA probes
Liddle syndrome inheritance pattern
Autosomal dominant
Risk factors for hypertension
Old age Smoking Obesity Lack of exercise High salt intake Stress Ethnicity - more common in ACs Family history
Treatment of hypertension
ACEIs Beta blockers CCBs Diuretics Renin inhibitors Angiotensin II receptor antagonists Aldosterone antagonists
Complications of hypertension
Stroke Aneurysm Eye problems Ischaemic heart disease Kidney damage Left ventricular hypertrophy
Amiloride
Potassium sparing diuretic
Targets ENaC channels in distal convoluted tubule
How can hypertension lead to left ventricular hypertrophy?
Leads to increased afterload
Heart has to pump harder to pump same volume of blood
Muscle thickens in response
What does aldosterone target?
ENaC and Na/K ATPase
Why does an increased blood volume lead to increased blood pressure?
Increase in central venous pressure Increased venous return to the heart Increased preload Increased stroke volume and cardiac output Increased BP
How is intrapleural pressure maintained?
Elastic recoil properties of the lung and chest wall
Want to recoil against each other
Creates negative pressure
Surfaces stuck together by pleural fluid
Types of pneumothorax
Primary spontaneous - rupture of bleb in absence of disease
Secondary spontaneous - due to lung disease - COPD
Traumatic - due to penetrating lung injury
Pneumothorax risk factors
Male Tall Marfan syndrome Thin Young Atmospheric changes Lung disease Mechanical ventilation Scuba divers
Pneumothorax symptoms
Chest pain Shortness of breath Tachycardia Tachypnoea Repeated dry coughing Cyanosis
Pneumothorax diagnosis
Absent breath sounds on one side Tracheal deviation Unequal chest expansion JVP distension X ray - lung borders in lung space CT - can show lung collapse
Pneumothorax treatment
Left alone
Aspiration of air
Surgery to close hole in pleura
Why can’t he fly
Cabin pressure reduced
May be lower than intraplerual pressure
Could cause lung to collapse again
Asthma pathophysiology
Hyperactive and hyper-responsive airways Increased IL-4 production IgE production Degranulation of mast cells Inflammatory cytokine release Increased mucous secretion Mucous plugging
Asthma triggers
Dust Pollen Animal hair Mould Smoke Asbestos Chemicals NSAIDs Aspirin Exercise Chest infections
Risk factors for asthma
History of atopic disease Family history Inner city environment Obesity Viral infections in early childhood Smoking Early exposure to broad spectrum antibiotics
Symptoms of asthma
Shortness of breath Coughing Wheezing Chest tightness Hypocapnia
Symptoms of severe asthma attack?
SaO2 25bmp
Unable to complete sentences in one breath
Diagnosis of asthma
Spirometry - reduced FEV1/FVC ratio
Treatment of asthma
Beta2 agonists
Muscarinic antagonists
Inhaled corticosteroids
Normal SaO2
> 95%
