Heart Flashcards
preload
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction
4 things that increase stroke volume e
Cardiac size, contractility, preload and afterload are the 4 factors affecting stroke volume
Increased central venous pressure would increase venous return, hence increasing preload.
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to
strain
Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.
Effects of BNP
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
4 uses of BNP
Diagnosing patients with acute dyspnoea
a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis
NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure
Prognosis in patients with chronic heart failure
initial evidence suggests BNP is an extremely useful marker of prognosis
Guiding treatment in patients with chronic heart failure
effective treatment lowers BNP levels
Screening for cardiac dysfunction
not currently recommended for population screening
Varicose veins are dilated, tortuous, superficial veins that occur secondary to incompetent venous valves, allowing blood to flow back, away from the heart. They most commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein. Whilst extremely common, the vast majority of patients do not require any intervention.
risk factors
ncreasing age female gender pregnancy the uterus causes compression of the pelvic veins obesity
symtpoms
aching
throbbing
tihing
complications of varicose viens
Other patients may present with complications of varicose veins:
a variety of skin changes may be seen:
varicose eczema (also known as venous stasis)
haemosiderin deposition → hyperpigmentation
lipodermatosclerosis → hard/tight skin
atrophie blanche → hypopigmentation
bleeding
superficial thrombophlebitis
venous ulceration
deep vein thrombosis
A 2-month-old baby is diagnosed with a ventricular septal defect. This is due to a failure in embryological development of which cardiovascular structure?
endocardial sinus
Development of the heart begins at about day 18 in the embryo from the mesoderm from a group of cells from the cardiogenic area. Signals from the underlying endoderm result in the formation of a pair of elongated strands known as the cardiogenic cords. These cords fuse together resulting in the primitive heart tube.
At day 22, there is the development of five regions in the primitive heart tube: beginning superiorly, the 1) truncus arteriosus, 2) bulbus cordis, 3) primitive ventricle, 4) primitive atrium and the 5) sinus venosus. These later become the 1) ascending aorta and pulmonary trunk, 2) right ventricle, 3) left ventricle, 4) anterior atrial walls and appendages, and the 5) coronary sinus and sino-atrial node respectively.
Over the next week, the embryo’s heart undergoes morphogenesis where it loops and twists from a vertical tube into the premature heart with atrial and ventricular orientation present by day 28. Thickenings of mesoderm in the inner lining of the heart walls (called endocardial cushions) appear and grow towards each other. They fuse and divide the atrioventricular canal into left and right sides. Failure of the endocardial cushions to develop properly will result in a ventricular septal defect.
By the end of the 5th week, the four heart chamber positions are complete. The atrioventricular and semilunar valves form between the 5th and 9th weeks.
failure of endocardial cushions to develop rest in what
ventricular septal defect
Aetiology of VSD ( ventricular septal defects)
congenital VSDs are often association with chromosomal disorders Down's syndrome Edward's syndrome Patau syndrome cri-du-chat syndrome congenital infections acquired causes post-myocardial infarction
pan systolic mumur which is louder in smaller defects
management of VSD
small VSDs which are asymptomatic often close spontaneously are simply require monitoring
moderate to large VSDs usually result in a degree of heart failure in the first few months
nutritional support
medication for heart failure e.g. diuretics
surgical closure of the defect
left ventricular ejection fraction =
stroke volume/end diastolic LV volume
stroke volume = end diastolic volume - ends systolic volume
systemic vascular resistance =
mean arterial pressure/cardiac output
A teenage boy collapses while playing tennis and is pronounced dead in hospital. The post-mortem reveals heart abnormalities. What is the most likely abnormality?
hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy is the only condition listed above that typically presents with sudden death, which rules out the other options.
Acute myocarditis may present with chest pain, fever, palpitations, tachycardia and dyspnoea.
Dilated cardiomyopathy may present with right ventricular failure, dyspnoea, pulmonary oedema, and atrial fibrillation.
Restrictive cardiomyopathy presents similarly to constrictive pericarditis, where right heart failure signs predominate: raised JVP, hepatomegaly, oedema, ascites.
Atrial myxoma may present with dizziness, fainting and palpitations, due to obstruction of the conductive pathway.
Hypertrophic cardiomyopathy (HCM)
HCM results in obstruction of the left ventricular outflow tract due to asymmetric septal hypertrophy.
signs and symptoms
sudden death; angina, dyspnoea, palpitations, syncope.
typically following exercise
double apex beat
Tests: ECG (will show high Q waves due to left ventricular hypertrophy), echocardiogram (shows hypertrophy)
treatment
Treatment: bed rest, diuretics, digoxin, ACE-inhibitors, anticoagulation, biventricular pacing, implantable cardioverter-defibrillator, cardiac transplantation
cause of HCM
the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output
characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy
A teenage boy collapses while playing tennis and is pronounced dead in hospital. The post-mortem reveals heart abnormalities. What is the most likely abnormality?
hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy is the only condition listed above that typically presents with sudden death, which rules out the other options.
Acute myocarditis may present with chest pain, fever, palpitations, tachycardia and dyspnoea.
Dilated cardiomyopathy may present with right ventricular failure, dyspnoea, pulmonary oedema, and atrial fibrillation.
Restrictive cardiomyopathy presents similarly to constrictive pericarditis, where right heart failure signs predominate: raised JVP, hepatomegaly, oedema, ascites.
Atrial myxoma may present with dizziness, fainting and palpitations, due to obstruction of the conductive pathway.
Hypertrophic cardiomyopathy (HCM)
HCM results in obstruction of the left ventricular outflow tract due to asymmetric septal hypertrophy.
signs and symptoms
sudden death; angina, dyspnoea, palpitations, syncope.
typically following exercise
double apex beat
Tests: ECG (will show high Q waves due to left ventricular hypertrophy), echocardiogram (shows hypertrophy)
treatment
Treatment: bed rest, diuretics, digoxin, ACE-inhibitors, anticoagulation, biventricular pacing, implantable cardioverter-defibrillator, cardiac transplantation
cause of HCM
the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output
characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy
most common cause of typical anginal( pain over sternum and shoulder ) pain
atherosclerosis
The pathological process involved in atherosclerosis begins with thickening of the tunica intima(composed of proteoglycan rich extracellular matrix and acellular lipid pools)
Fatty streak int eh subendotheilal space by Low density lipoprotein can be seen
Fibroatheroma starts which is characterized primarily by infiltration of macrophages & T-lymphocytes, with the formation of a well-demarcated lipid-rich necrotic core.
The appearance of foam cells occur relatively early in the disease process and play a major role in the pathogenesis of atheroma formation.
Further progression leads to a thin cap fibroatheroma, wherein the necrotic core becomes bigger and fibrous cap thins out.
Finally, smooth muscle cells from the tunica media start to proliferative and migrate into the tunica intima.
the aortic arch is a continuation of what and gives rise to what
The aortic arch is a continuation of the ascending aorta. It gives off the right brachiocephalic trunk, the left common carotid artery and the left subclavian artery in that order, before continuing as the descending aorta.
The thyrocervical trunk arises from the
subclavian artery and gives off branches
Inferior thyroid artery
Suprascapular artery
Ascending cervical artery
Transverse cervical artery
CABG - coronary artery bypass surgery used to treat coronary artery disease
what vessel do they use
complications
internal mammary artery increasingly used as opposed to the saphenous vein
AF (40%) and stroke (2%)
Preload = end diastolic volume Afterload = aortic pressure
Starlings law
Increase in end-diastolic volume will produce larger stroke volume- this occurs up to a point beyond which cardiac fibres are excessively stretched.
2 major risk factors for atherosclerosis
smoking and hyperlipidaemia.
ophthalmic artery arises from what
internal carotid
A patient with dilated cardiomyopathy presents to his GP with symptoms of heart failure.
Which of the following explains why his heart condition has lead to heart failure?
ventricular dilation due to Laplace law - pressure in the lumen = wall tension/lumen radius
Atrial stretch receptors
Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors: the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by juxtaglomerular apparatus-Increase in angiotensin II.
Increased atrial stretch will also result in increased release of atrial natriuretic peptide.
Which one of the following pathological explanations best describes the initial pathological processes occurring in an abdominal aortic aneurysm in an otherwise well 65-year-old, hypertensive male?
loss of elastic fibres from the media
starling law
as preload progressively increase , stroke volume increases gradually then decrease suddenly
complications of MI
cardiac arrest cariogenic shock chronic HF tacky or Bradycardia pericarditis left ventricular anerursym left ventricular free wall rupture ventricular spetal defect acute mitral regurgitation
0-24hr post-MI histology findings: early coagulative necrosis, neutrophils, wavy fibres, hypercontraction of myofibrils. High risk of ventricular arrhythmia, HF and cardiogenic shock
1-3 days post-MI histology: Extensive coagulative necrosis, neutrophils (associated with fibrinous pericarditis)
3-14 days post-MI histology: macrophages + granulation tissue at margins. High risk of free wall rupture, papillary muscle rupture and LV pseudoaneurysm
2 weeks to several months post-MI histology: contracted scar complete. Associated with Dressler syndrome, HF, arrhythmias, mural thrombus
post MI findings
A 53-year-old woman is attending her GP for a routine “well-woman check”. At the start of the appointment, the doctor uses an automated sphygmomanometer to measure the patient’s blood pressure, which reads 174/96 mmHg. She is informed that the reading is high, likely because she just walked into the clinic, and will be repeated in a few minutes.
What is the usual physiological mechanism in response to a rise in blood pressure?
Glutamatergic activation of caudal ventrolateral medulla by nucleus tractus solitarii
The vagus nerve regulates the baroreceptor reflex, correcting an acute decrease in arterial blood pressure
what is responsible for the closure of the ductus arteriosus at birth
At birth, there is an increased oxygen tension in the blood, and a reduced level of prostaglandins; both of which allow the patent ductus arteriosus to close.
An increased left atrial pressure allows the foramen ovale (connection between left and right atria) to close.
when do the coronary arteries fill
ventricular diastole
on xray patients with aortic dissection will also have what seen
widened mediastinum
Which nerve directly innervates the sinoatrial node?
no particular node
What is the expected oxygen saturation levels in the right atrium for a healthy individual?
70% ad deoxygenated
atrial flutter characterised by what
sawtooth - narrow complex tachycardia
An 82-year-old lady has just been diagnosed with heart failure after 8 months of increasing breathlessness and ankle swelling. She is started on a number of medications, given some lifestyle advice and counselled on the prognosis. Which two types of valve dysfunction will she be most prone to because of her new diagnosis?
what two conditions is she now more prone too
The most common valve dysfunctions secondary to heart failure are functional mitral and tricuspid regurgitations. This is because the enlarged ventricles cause an incomplete seal at the valves during diastole.
The most common valve dysfunctions secondary to heart failure are functional mitral and tricuspid regurgitations. This is because the enlarged ventricles cause an incomplete seal at the valves during diastole.
