Cardiovascular Science Flashcards
Where does the cardiac impulse usually originate?
Sino-atrial node
What is autorhythmicity?
The ability to beat without external stimuli
Which drug may be used in extreme bradycardia? Why?
Atropine - it blocks ACh receptors
Which ions are responsible for cardiac cell depolarisation, and which for repolarisation?
Depolar (more +): Na+, Ca2+. Repolar (more -): K+
In the SAN, cells are never at rest. What is the term for the ‘resting potential’?
Pacemaker potential
Describe the action potential in pacemaker cells.
Phase 4: funny current (Na) slowly increases potential. Once a threshold is reached, transient Ca channels open, which open L-type. Ultrarapid K efflux channels open, repolarising the cell and reopening If channels.
Describe the action potential in non-pacemaker cells.
- Na+ in: a stimulus (disruption of neighbouring cells’ gap junctions) increases Em and triggers fast Na+ channels, rapidly increasing Em (+60mV); at about +30, fast channels inactivate, abruptly ending phase 1
- K+ out: a brief efflux of K+ by transient K+ channels, allowing a short-lived partial repolarisation
- Ca2+ in, K+ out: these two ions ‘balance’ to produce the plateau phase, prolonging the action potential
- K+ out: activation of delayed rectifying K+ channels produces rapid repolarisation
- Em = EK+ (-90mV)
Describe the Vaughan-Williams classification of anti-arrhythmics and how they relate to the non-pacemaker action potential.
- Na+ channel blockers: e.g. procainamide, lidocaine, flecainide - affects phase 0 (Na+ influx)
- Beta-blockers (e.g. propranolol) - affects phase 4 (K+ rectifier channels, prolongs refractory period)
- K+ channel blockers (e.g. amiodarone) - affects phase 3 (K+ out channels)
- Ca2+ channel blockers (e.g. verapamil, diltiazem) - affects phase 2 (plateau phase)
Which feature of ventricular action potential is unique to the heart?
Plateau phase
How does the autonomic nervous system effect the SAN action potential?
NA/symp increases steepness/frequency. ACh/para decreases it
Which receptors does the autonomic nervous system act upon?
NA - B1, ACh - M2
Describe briefly the G protein mechanisms of the autonomic nervous system.
B1/M2 -> Gs/Gi -> adenylyl cyclase catalyses ATP to cAMP (or is blocked), increasing/decreasing [cAMP]ic
What is the chronotropic effect?
Slope of action potential curve. Increased chronotropicity describes increased heart rate
What is the inotropic effect?
Contractility and output. Positive inotropes increase contractility.
What is the dromotropic effect?
Conduction velocity; increased dromotropicity describes increased conduction through the AVN
What is the lusotropic effect?
Myocardial relaxation -> duration of systole (+ decreases systole)
Which two manoeuvres may be used to stimulate the vagus nerve and decrease heart rate?
Valsalva (breathing), massage of bifurcation of carotids
What is the cardiac cycle?
The orderly depolarisation and repolarisation sequence of atrial and ventricular contractions/relaxations.
What are the five stages of the cardiac cycle?
- Passive atrial filling
- atrial contraction; a wave on JVP
- isometric ventricular contraction (ventricular pressure < A+PA pressures),
- ventricular ejection,
- isometric ventricular relaxation
What causes the first and second heart sound?
Closure of the AV then semilunar valves
Describe the normal features of the JVP waveform, and the dicrotic notch.
- A wave = Atrial contraction
- C wave = Closure of the triCuspid valve
- V wave = Ventricular systole
- Aortic valve closure causes transient increase in pressure
Describe the causes of JVP pathology.
- Absent A waves = Atrial fibrillation
- cannon A waves = occur when atria contract against closed valves, e.g. in complete heart block, VT, and ventricular ectopic beats
- large A waves = increased atrial pressure, e.g. in tricuspid stenosis, RVH
- large V waves = ventricular pathology, e.g. tricuspid regurgitation
Why are cellular junctions vital in cardiac cells?
Enable autorhythmicity, provide low resistance, and ensure myocytes are reached.
What is the name of the smallest functional unit of cardiac muscle?
Myofibril
What is the purpose in increased [cAMP]ic?
Opens calcium channels
Describe how calcium is built up in the myocyte and what its purpose is.
Calcium induced calcium release (small ic Ca opens VGICs and ryanodine channels in sarcoplasmic reticulum). Ca breaks troponin and allows myosin and actin to bind
Describe the Frank-Starling law.
What enters the heart must be ejected. Increase in EDV increases stroke volume increases force.
Describe, using the Frank-Starling law, how left ventricular hypertrophy may occur.
Chronic raised EDV increasing venous return. Sympathetic innervation only
What is the refractory period?
A period during which another action potential cannot be started
Describe why the refractory period occurs.
K+ is leaving the cell preventing depolarisation.
Describe the relationship between refractory period and heart rate.
Increased refractory period - decreased heart rate, and vice versa
During diastole, why doesn’t arterial pressure fall to 0?
Due to vasomotor tone and elastic recoil
Describe mean arterial pressure (mAP).
- mAP is the average BP over the period of the cardiac cycle
- mAP = CO x SVR = (SV x HR) x SVR
- mAP should be ~70-105mmHg
What is the need to maintain a narrow range of MAP?
- < 60 to perfuse the organs (below this causes shock)
- > 105 to prevent vascular damage
Why are we concerned primarily about arterial pressure, rather than others?
Arterioles are the primary resistance vessels (due to their ability to vasoconstrict and vasodilate)
Describe the auscultation of blood pressure.
- blood flow is heard when turbulent and not laminar
- BP is measured by auscultating the Korotkoff sounds; the first sound (K1) is heard when flow is initially maximally restricted (turbulent; systolic BP) and K5 when maximally relaxed (laminar; diastolic BP)
Name the types of short-term and long-term control of BP.
- short-term: baroreceptors (pressure), chemoreceptors (O2, CO2, pH), muscle receptors (metabolic activity), higher brain centres (temperature, exercise, emotion), and methods of extrinsic control (nervous system/ adrenaline (sympathetic-induce release from adrenal medulla); constrictors such as angiotensin II and TXA2 and dilators such as histamine, bradykinin and NO)
- both short- and long-term: ANP (atrial natriuretic peptide) is a powerful vasodilator released in response to atrial stretch; ‘natriuretic’ refers to Na+ excretion (H2O follows Na+, BP is decreased)
- long-term: ADH (vasopressin), RAAS system
Describe the RAAS system and its primary result of activation.
- Renin in kidney converts angiotensiongen to angiotensin I in liver,
- then ACE converts this to angiotensin II in the lungs. This causes vasoconstriction and Na/H2O retention, increasing BP
- aldosterone is a mineralocorticoid which also results in renal Na+/H2O retention and increased BP
Describe the natriuretic peptide system and its primary result of activation.
- (Pre-pro BNP -> pro-BNP ->) BNP + ANP (ventricular and atrial) decreasing renin production, causing vasodilation and increased excretion
- long-term, the ‘natriuretic’ refers to Na+ excretion (followed by H2O)
Describe the ADH/vasopressin system and its primary result of activation.
Precursor in the hypothalamus activates the posterior pituitary gland, through osmoreceptors (detecting osmolality). Activates re-absorption of water, increasing BP and ECF
What is the main factor affecting blood flow?
- Radius
- Poiseuille’s law (blood flow, Q, is directly proportional to the radius of the vessel ^4)
- Very small alterations in radius have profound effects on resistance and blood flow (radius x2 = blood flow x16)
Which humoural agents cause vasodilation and which cause vasoconstriction?
- Vasodilation: nitric oxide (NO), bradykinin, and histamine
Vasoconstriction: angiotensin II, serotonin, TXA2, leukotrienes, endothelin
Describe the mechanism underpinning nitric oxide vasodilating the vessels.
- NO is synthesised by vascular endothelial cells and diffuses through the vascular smooth muscle cell membrane
- L-arganine -> ENOS -> NO
- Activates guanylate cyclase, generating cGMP and resulting in vasodilatation
- cGMP is broken down by phosphodiesterase (PDE); blockade of PDE-5 is the MOA of sildenafil (Viagra)
Describe how cerebral autoregulation protects against small changes to cerebral blood flow.
Automatic vasoconstriction/dilation to maintain pressure
Describe the control of venous return through the body.
- venous pressure depends on posture; when supine, all veins are abount the level of the heart and venous pressure ~0, whereas when standing venous pressure in the feet can be as high as 100mmHg
- venous return is driven by the arterial-venous pressure gradient, forcing flow to the veins from behind (‘vis a tergo’). this is assisted by three pump mechanisms;
- cardiac pump: the RV ‘sucks’ blood from the right atrium and vena cava
- respiratory pump: inspiration results in decreased intrathoracic and increased intrabdominal pressures, augmenting the pressure gradient
- skeletal muscle pump: contraction of skeletal muscle displaces blood in the veins towards the heart
Describe the effects of exercise on the physiology.
Increased HR, CO, sympathetic discharge, vasoconstriction, and flow
What is the name of the sac surrounding the heart and its layers?
- The pericardium
- Visceral serous
- Parietal serous
- Pericardial cavity
Describe the branches of the coronary supply.
Left -> left marginal (and circumflex), left anterior descending (and diagonal/lateral). Right -> marginal and posterior intervascular
What is an auricle?
Extensions of the atria which allow extra filling
Describe superior vena cava vein supply.
jugular -> subclavian + brachial -> brachiocephalic -> SVC
Which structural landmark seperates the atria from the ventricles?
The coronary sulcus
Describe the venous return of the coronary blood itself.
Sinus venosus -> coronary sinus -> right atrium
Which congenital heart defect results in hypoxaemia?
Septal defect (hole)
What is the purpose of the oval fossa’s crista terminalis?
It seperates smooth and rough muscle
Describe, anatomically, how the AV and semilunar valves differ.
Semilunar valves have pockets which collect blood and prevent backflow. AV valves have tendinous cords which connect them to papillary muscles
How do the papillary muscles contract simultaneously?
Moderator band connects the two valves
Describe the anatomical location of the thoracic duct.
Between the azygous vein and the oesophagus (a duck between two gooses)
Describe the boundaries and contents of the mediastinal divisions.
- superior: thoracic outlet (T1) to the transverse thoracic plane (T4-5)/sternal angle (angle of Louis). contains aortic arch and its branches, SVC and azygous arch, thoracic duct, vagus + recurrent laryngeal + phrenic nerves
- anterior: pericardium (posterior) to sternum (anterior). contains the thymus, internal thoracic arteries, and parasternal nodes
- middle: formed by the borders of the pericardial sac. contains the heart and its great vessel roots, trachea and main bronchi
- posterior: pericardium (anterior) to bodies of T5-12 (posterior). contains the oesophagus, descending thoracic aorta, vagus, splanchnic and sympathetic chains