Basic Sciences Flashcards
Cardiac Output (CO)
Cardiac Output = Stroke Volume x Heart Rate
Stroke Volume: the volume of blood pumped by the left ventricle in a single heartbeat. Defined as end-diastolic volume (EDV) minus end-systolic volume (ESV). Increases with increased contractility, increased preload, and decreased afterload.
Factors that contribute to cardiac output
- Heart Rate
- Preload
- Afterload
- Contractility
- Heart Rate
(+) : sympathetic stimulation (adrenaline) atropine
(-) : parasympathetic stimulation (acetylcholine), adenosine
2. Preload (end diastolic volume) Volume entering the ventricle influenced by: - Venous return - Fluid volume - Atrial contraction
3. Afterload Resistance ventricles must overcome to circulate blood Factors increasing afterload: - Atherosclerosis - Vasoconstriction - Advanced AS, uncontrolled severe HTN
- Contractility
How hard the myocardium contracts for a given preload
(+): sympathetic stimulation –> noradrenaline
Drugs: dobutamne
(-): parasympathetic stimulation –> acetylcholine
Drugs: B blockers, calcium channel blockers
Familial hypercholesterolemia
- Autosomal DOMINANT
- Corneal arcus –> xanthelasma –> tendon xanthoma
PCSK9
What is QP:QS?
QP:QS signifies ratio of pulmonary to systemic flow
Large shunts (eg: big VSD, ASD) = large QP, QS
As high shunt flow continues, pulmonary resistance may increase (Eisenmenger’s) and QP:QS “normalises”
A 50yo woman has had worsening shortness of breath and oedema. An echo shows a secundum atrial septal defect. Qp:Qs ratio is 2. This implies:
A. She may experience progressive right heart failure due to a chronic reduction in right ventricular preload
B. She may experience progressive right heart failure due to chronic increase in right ventricular preload
C. She may experience progressive left heart failure due to chronic reduction in left ventricular preload
D. She may experience progressive left hear failure due to chronic increase in right ventricular preload.
E. She is unlikely to have any worsening o symptoms over time.
B
▪ Atrial septal defect - left atrial pressures > right atrial pressure
▪ Flow from left atrium to right atrium
▪ Qp:Qs - pulmonary circulation vs systemic circulation
▪ Twice as much blood in right ventricle vs left ventricle
▪ Increased preload and right heart failure and pulmonary HTN
▪ Would intervene if Qp: Qs ratio > 1.5
ASD can be asymptomatic
A 60yo woman has increasing shortness of breath. She has a history of ischaemic heart disease, htn and rheumatic valvular disease. At right and left heart cath:
- Mean PA pressure: 36mmHg (normal 9-19)
- Pulmonary wedge pressure: 29mmHg (normal 4-12)
- LVEDP: 10mmHg (normal 4-12)
- Cardiac output: 5.6L/min
Her symptoms are most likely due to
A. Pulmonary HTN secondary to pulmonary emboli
B. Pulmonary HTN secondary to primary pulmonary HTN
C. Mitral stenosis
D. Aortic stenosis
E. Left heart failure and diastolic dysfunction
Mitral stenosis
▪ Pulmonary wedge pressure = left atrium
▪ Left atrial pressure high
▪ Left ventricular pressure is normal
▪ The gap between the left atrium and left ventricle indicates a mitral stenosis
A 68 year old lady with limited scleroderma with calcinosis, oesophageal dysmotility and sclerodactyly presents with palpitations. The most appropriate management is?
Answer: H) Verapamil
ECG: Atrial Flutter with Variable Block
Scleroderma is associated with Cardiac Disease
- Pericarditis, pericardial effusion, myocardial fibrosis, heart failure, myocarditis, microvascular disease, myocardial infarction (MI), conduction disturbances, and arrhythmias
- Conduction system disease and arrhythmias are common. They are likely to result from fibrosis of the myocardium and conduction system. Many deaths among SSc patients are sudden, and some may result from a ventricular arrhythmia.
B-blockers in Scleroderma
- Vasodilating B-blockers aggravate Raynaud symptoms and may not be tolerated
- B-blockers with b-1 selectivity (metoprolol) less likely to cause vasoconstriction
Amiodarone
- Interstitial lung disease
Calcium channel blockers
- Beneficial in terms of Raynauds + HF in scleroderma
What are the compensatory mechanisms that are activated in heart failure
Compensatory mechanisms that are activated in heart failure include:
• Increased ventricular preload with ventricular dilatation and volume expansion
• Peripheral vasoconstriction, which initially maintains perfusion to vital organs
• Myocardial hypertrophy to preserve wall stress as the heart dilates
• Renal sodium and water retention to enhance ventricular preload
• Activation of the adrenergic nervous system, which increases heart rate and
contractile function
Which is the most common origin of idiopathic ventricular tachycardia in the absence of structural heart disease? A. Aortic annulus B. Aortic sinuses C. Great cardiac vein D. Epicardium E. Right ventricular outflow tract
E. Right ventricular outflow tract
- Idiopathic ventricular tachycardia must be distinguished from ventricular
tachycardia with structural heart disease, because the latter often warrants an
implantable cardioverter defibrillator (ICD).
Detection of ventricular scar on cardiac imaging can be helpful. - Although idiopathic monomorphic ventricular tachycardia can cause syncope, sudden death is rare.
- Beta-blockers, calcium-channel blockers or catheter ablation are often effective.
ECG and their corresponding
p wave: atrial depolarisation
QRS: ventricular depolarisation
T wave: ventricular repolarisation
Perhexiline
- Perhexiline has been used in the treatment of congestive heart failure and refractory
angina. It relieves symptoms of angina, improves exercise tolerance and
increases workload needed to induce ischemia. - MOA: modifying myocardial substrate utilisation from fatty acids to carbohydrates, which is energetically more efficient for the heart to metabolise, thus reducing myocardial oxygen consumption.
SE: hepatotoxicity, peripheral neuropathy and hypoglycaemia.
- Perhexiline is metabolised by cytochrome P450 2D6. Drug level monitoring is essential to identify patients who are slow metabolisers, which occurs in about 7–10% of Caucasians who harbour mutations in CYP2D6.
Carvedilol
A non-selective beta-blocker with α1-adrenoreceptor blocking activity.
B1 selective - nebivolol, bisoprolol, metoprolol XR
A selective β1-adrenoreceptor blocker with nitric-oxide potentiating vasodilatory
effect.
nebiviolol
Dabigatran inducers and inhibitors
Dabigatran is given as the prodrug dabigatran etexilate, and this prodrug is a
substrate for efflux by the p-glycoprotein transporter.
INHIBITORS of p-glycoprotein, such as below can increase dabigatran plasma concentration by decreasing the efflux of the drug into the gastrointestinal lumen.
- ketoconazole (most azoles),
- protease inhibitors
- macrolides
- calcineurin inhibitors
- amiodarone
- verapamil
INDUCERS Strong inducers of p-glycoprotein, such as below can reduce plasma concentrations - rifampicin - carbamazepine - phenytoin,
During pregnancy, which one of the following heart diseases is associated with the highest maternal mortality? A. Aortic stenosis B. Atrial septal defect C. Coarctation of aorta D. Eisenmenger syndrome E. Mitral stenosis
D. Eisenmenger syndrome
