Cardiovascular Flashcards
Derivatives of truncus arteriosus
Ascending aorta and pulmonary trunk
Derivatives of bulbus cordis
Smooth parts (outflow tract) of left and right ventricles.
Derivatives of primitive atrium
Trabeculated part of left and right atria
Derivatives of primitive ventricle
Trabeculated part of the left and right ventricle
Derivatives of primitive pulmonary vein
Smooth part of left atrium
Derivatives of left horn of sinus venosus
Coronary sinus
Derivatives of right horn of sinus venosus
Smooth part of the right atrium (sinus venarum)
Derivatives of right common cardinal vein and right anterior cardinal vein
Superior vena cava (SVC)
Heart development
It is the first functional organ in vertebrate embryos; beats spontaneously by week four of development.
Cardiac looping
Primary heart tube loops to establish left-right polarity; it begins in week four of gestation. Defect in left-rigth dynein (involved in L/R asymmetry) can lead to dextrocardia, as seen in Kartagener syndrome (primary ciliary dyskinesia).
Septation of the atria
- Septum primum grows toward endocardial cushions, narrowing foramen primum. 2. Foramen secundum forms in spetum primum (formen primum disappears). 3. Septum secundum develops as foramen secundum maintains right-to-left shunt. 4. Septum secundum expands and covers most of the foramen secundum. The residual foramen is the foramen ovale. 5. Remaining portion of septum primum forms valve of foramen ovale. 6. Septum secundum and septum primum fuse to form the atrial septum. 7. Foramen ovale usually closes soon after birth because of an increase in LA pressure.
Patent foramen ovale
It is caused by failure of septum primum and septum secundum to fuse after birth; most are left untreated. It can lead to paradoxical emboli (venous thromboemboli that enter systemic arterial circulation), similar to those resulting from an ASD.
Septation of the ventricles
- Muscular ventricular septum forms. Opening is called the interventricular foramen. 2. Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen. 3. Growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of the interventricular septum.
Ventricular septal defect
VSD most commonly occur in the membranous septum.
Outflow tract of the heart formation
Truncus arteriosus rotates. Neural crest and endocardial cells migrate to the truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum, which becomes the ascending aorta and pulmonary trunk. Possible conotruncal abnormalities include transposition of great vessels, tetralogy of Fallot, and persistent truncus arteriosus.
Valve development
Aortic/pulmonary valves are derived from the endocardial cushions of the outflow tracts. Mitral/tricuspid valves are derived from fused endocardial cushions of the AV canal. Valvular anomalies may be stenotic, regurgitant, atretic (eg tricuspid atresia), or displaced (eg Ebstein anomaly).
Fetal erythropoiesis
Fetal erythropoiesis occurs in the yolk sac from weeks 3-8, liver from 6 weeks to birth, spleen from weeks 10-28, bone marrow from 18 weeks to adulthood. Young Liver Synthesizes Blood.
Embryonic globins
ζ and ε. During yolk sac fetal hematopoiesis, the hemoglobin formed is embryonic hemoglobin, subunits ζ2ε2.
Fetal hemoglobin (HbF)
During fetal hematopoiesis within the liver, the predominate hemoglobin form is fetal hemoglobin (HbF) with subunit α2γ2. Compared to maternal hemoglobin, fetal hemoglobin has a higher affinity for oxygen secondary to a lack of interaction between fetal hemoglobin and 2,3-BPG. This allows HbF to extract O2 from maternal hemoglobin (HbA1 and HbA2) across the placenta. From fetal to adult hemoglobin: Alpha Always; Gamma Goes, Becomes Beta.
HbA
Under the influence of increasing cortisol production by the fetal kidneys, hematopoiesis shifts to the bone marrow. In the absence of increased cortisol production, hematopoiesis remains in the liver. During bone marrow hematopoiesis HbA (α2β2) is synthesized gradually and replaces fetal hemoglobin.
Fetal circulation
Blood in umbilical vein has a PO2 of about 30 mmHg and is about 80% saturated with O2. Umbilical arteries have low O2 saturation. There are three important shunts: ductus venosus, foramen ovale, patent ductus arteriosus. At birth, infant takes a breath leading to decrease resistance in pulmonary vasculature causing an increase in left atrial pressure vs right atrial pressure. The foramen ovale now closes (becoming fossa ovalis). There is also now an increase in O2 (from respiration) and a decrease in prostaglandins (from placental separation) leading to closure of ductus arteriosus.
Ductus venosus
Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the IVC, bypassing hepatic circulation.
Foramen ovale
Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the aorta to supply the head and body.
Patent ductus arteriosus
Deoxygenated blood from the SVC passes through the RA to the RV to the main pulmonary artery through the patent ductus arteriosus and into the descending aorta. The shunt is due to high fetal pulmonary artery resistance (due partly to low O2 tension). Indomethacin helps to close PDA, which becomes the ligamentum arteriosum (remnant of ductus arteriosus). Prostaglandins E1 and E2 kEEp the PDA open.
Derivative of allantosis
becomes the urachus, which is part of the allantoic duct between bladder and umbilicus. The umbilicus becomes the median umbilical ligament.
Derivative of ductus arteriosus
Ligamentum arteriosum
Derivative of ductus venosus
Ligamentum venosum
Derivative of foramen ovale
Fossa ovalis
Derivative of notochord
nucleus pulposus
Derivative of umbilical arteries
Medial umbilical ligaments
Derivative of umbilical vein
Ligamentum teres hepatis. It is contained in falciform ligament.
Coronary arteries
There are two main coronary arteries, the left coronary artery (LCA) and right coronary artery (RCA). Coronary blood flow peaks in early diastole.
Left coronary artery (LCA)
LCA originates from the left aortic sinus and bifurcates into: LAD (left anterior descending) artery, which gives off superficial (diagonal) and multiple deep (septal perforator) branches. LCX (left circumflex) artery
Right coronary artery (RCA)
RCA originates from right aortic sinus and splits into: Right marginal branch. PDA (posterior descending artery). SA nodal artery
Coronary dominance
The artery that supplies the posterior descending artery (PDA) determines the coronary dominance: Right dominant: the RCA supplies the PDA (85% of population). Left dominant: the LCX (Left circumflex branch of LCA) supplies the PDA (8% of population). Co-dominant: the PDA arises from both the LCX and the RCA (7% of population)
Left Circumflex Branch (LCX)
The Left Circumflex Branch (LCX) of the Left Coronary Artery (LCA) supplies: Posterolateral wall of left ventricle and anterolateral papillary muscle
Left anterior descending branch (LAD)
The Left anterior descending branch (LAD) of the left coronary artery (LCA): Anterior wall of left ventricle, anterior 2/3 of the interventricular septum, anterolateral papillary muscle. This is the most common site for occlusion.
Right coronary artery (RCA)
In most people, the right coronary artery (RCA) supplies: Right atrium and ventricle (inferior walls), left ventricle (diaphragmatic surface), posterior 1/3 of the interventricular septum, SA node, and AV node (in right-dominant individuals). Infarct may cause nodal dysfunction (bradycardia or heart block).
Posterior descending/interventricular artery (PDA)
The posterior descending/interventricular artery (PDA) supplies: Posterior 1/3 of interventricular septum, posterior walls of ventricles, and posteromedial papillary muscle
Posterior part of heart
the most posterior part of the heart is the left atrium; enlargement can cause dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve, a branch of the vagus).
Cardiac output
CO = SV x HR. Whereby: CO = cardiac output, SV = stroke volume. SV is a function of contractility and preload. HR = heart rate. Using Fick’s principle: CO = (VO2) / (Ca – Cv)
Whereby: CO = cardiac output, VO2 = oxygen consumption (ml/min), Ca = oxygen content of arterial blood, Cv = oxygen content of mixed venous blood. During the early stages of exercise, CO is maintained by an increase in HR only (SV plateaus). Diastole is preferentially shortened with an increase in HR, leading to a decrease in filling time, decreasing CO (eg ventricular tachycardia).
Mean arterial pressure (MAP)
MAP = CO x TPR. Technically, MAP = (CO x TPR) + CVP. However, CVP is usually quite low compared to MAP, so this can be approximated as MAP = CO x TPR. MAP = mean arterial pressure; TPR = total peripheral resistance; CVP = central venous pressure. MAP ≈ diastolic pressure + 1/3 pulse pressure or, alternatively, MAP ≈ 2/3 diastolic pressure + 1/3 systolic pressure
Pulse pressure
Pulse pressure = systolic pressure – diastolic pressure. Pulse pressure is directly proportional to stroke volume. A higher stroke volume, such as in aortic regurgitation, will exhibit a high pulse pressure (high systolic and low diastolic measurements). An increase in pulse pressure occurs in hyperthyroidism, aortic regurgitation, aortic stiffening (isolated systolic hypertension in the elderly), obstructive sleep apnea (an increase in sympathetic tone), exercise (transient). A decrease in pulse pressure is seen in aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure.
Stroke volume
SV=end-diastolic volume (EDV) - end stystolic volume (ESV). Stroke volume is affected by contractility, afterload, and preload (SV CAP). There is an increase of SV with an increase in contractility (eg anxiety, exercise, and pregnancy), an increase in preload, and a decrease in afterload. A failing heart has a decrease in SV (systolic and/or diastolic dysfunction).
Contractility
Contractility is the intrinsic ability of cardiac muscle to develop force at a given muscle length. Also know as inotropism. Contractility is related to the intracellular Ca2+ concentration and can be estimated using the ejection fraction (stroke volume/end-diastolic volume). An increased HR leads to an increase in action potential frequency. This leaves less time for the Na/K ATPase to pump Na out of the cell and the Na/Ca exchanger becomes less effective. As a result, more Ca enters the myocardial cells during the plateau and more Ca is released from the sarcoplasmic reticulum, resulting in greater myocardial contractility. Cardiac glycosides (digitalis) -> increase the force of contraction by inhibiting Na+, K+-ATPase in the myocardial membrane. An increase in intracellular Na+ leads to decreased activity of the Na+-Ca2+ exchanger which is responsible for bringing sodium ions into the cell and removing Ca2+. This leads to increased Ca2+ and thus increased contractility. Contractility (and SV) decrease with beta 1 blockade (a decrease in cAMP), HF with systolic dysfunction, acidosis, hypoxia/hypercapnia (a decrease in PO2/an increase in PCO2), non-dihydropyridine Ca channel blockers.
Myocardial oxygen demand
Myocardial O2 demand increases with an increase in contractility, afterload (proportional to arterial pressure), heart rate, diameter of ventricle (increase in wall tension).
Wall tension
Wall tension=(pressure x radius)/(2 x wall thickness).
Preload
Preload is approximated by ventricular EDV. It depends on venous tone and circulating blood volume. vEnodilators (eg nitroglycerin) decreases prEload.
Afterload
Afterload is approximated by MAP. An increase in afterload causes there to be an increase in pressure, which increases wall tension. LV compensates for an increase in afterload by thickening (hypertrophy) in order to decrease wall tension. vAsodilators (eg hydrAlAzine) decrease Afterload (Arterial). ACE inhibitors and ARBs decrease both preload and afterload. Chronic hypertension (an increase in MAP) causes LV hypertrophy.
Ejection fraction
EF=SV/EDV=(EDV-ESV)/EDV. Left ventricular EF is an index of ventricular contractility. Normal EF is greater than 55%. EF decreases in systolic HF. EF is normal in diastolic HF.
Starling curve
The Starling curve describes the increase in cardiac output (or stroke volume) in response to increase in venous return/preload or end-diastolic volume. The Starling Curve is based on a length – tension relationship. Increased end diastolic volume causes an increased ventricular fiber length, with resultant increase in developed tension/pressure. Up and left shift of Starling curve (increase in contractility): Increased HR (due to exercise, etc.); Sympathetic stimulation or ß1 sympathomimetic agonists; Increased intracellular calcium. Downward shift of the Starling curve is caused by negative inotropes such as beta blockers (carvedilol, metoprolol) and calcium channel blockers (verapamil, diltiazem). Congestive heart failure shifts the Starling curve down and to the right.
Mathematical explanation of resistance, pressure, and flow
ΔP = Q*R, where P = pressure, Q = blood flow, R = resistance. Flow (Q) remains constant, so the equation can be rearranged to: Q = ΔP/R. (In this case, ΔP represents the difference in arterial blood pressure before and after the arterioles.) Since flow is constant, ΔP must increase when resistance increases
Total resistance of vessels in series
TR=R1+R2+R3…
Total resistance of vessels in parallel
1/TR=1/R1+1/R2+1/R3…
cardiac function curve
The cardiac function curve depicts the Frank-Starling relationship for the ventricle, and shows that cardiac output is a function of end-diastolic volume. The vascular function (venous return) curve depicts the relationship between blood flow through the vascular system (venous return) and right atrial pressure. When combining the cardiac output and venous return curves the intersection is known as the equilibrium, or steady state point. This is the operating point of the heart.
Changes of inotrope affect on cardiac function curve
Positive inotropic agents result in a shift of the curve to a higher cardiac output and a correspondingly lower right atrial pressure. Negative inotropic agents or pathological conditions such as heart failure lead to decreased cardiac output and a higher right atrial pressure.
Changes in blood volume affect on cardiac function curve
Changes in blood volume or venous capacitance change the venous return curve, and causes an increase in both cardiac output and right atrial pressure. An increase in blood volume or decrease in venous capacitance, such as a transfusion or exercise, increase mean systemic pressure, shifting the venous return curve to the right. A new equilibrium point is reached, and both cardiac output and right atrial pressure are increased. A decrease in blood volume or increase in venous capacitance, such as hemorrhage, decrease mean systemic pressure, and the venous return curve shifts to the left. At the new equilibrium point both cardiac output and right atrial pressure are decreased.
Changes in total peripheral resistance affect on cardiac function curve
Changes in total peripheral resistance alter both curves simultaneously, however the mean systemic pressure remains constant. Increasing total peripheral resistance causes a decrease in both the cardiac output and venous return curves. A counterclockwise rotation of the venous return curve occurs. The increased total peripheral resistance leads to decreased venous return as the blood is retained on the arterial side. A downward shift of the cardiac output curve is a result of increased aortic pressure (increased afterload) as the heart has to pump against a higher pressure. Decreasing total peripheral resistance causes an increase in both cardiac output and venous return. A clockwise rotation of the venous return curve occurs. Decreased total peripheral resistance results in more blood being able to flow back to the heart from the arterial side. An upward shift of the cardiac output curve is caused by the decreased aortic pressure (decreased afterload).
Isovolumetric contraction in pressure-volume loop
Isovolumetric contraction (3 to 5). At point 3, the cycle is at end diastole with the mitral valve closed; LV has been filled by the EDV. The ventricles begin contraction when the mitral valve closes and before the aortic valve opens (point 5), the period of highest O2 consumption.
Systolic ejection in pressure-volume loop
Systolic ejection (5 to 7). At point 5, aortic valve opens and the total stroke volume is ejected into the aorta. The ventricle volume decreases, but the ventricular pressure continues to increase until near the very end of this phase. At point 7 , the pressure drop causes the aortic valve to close. The width of the pressure-volume loop is measured graphically to represent the stroke volume. The volume remaining in the LV at point 7 is end systolic volume.
Isovolumetric relaxation in pressure-volume loop
Isovolumetric relaxation (7 to 1). After point 7, the ventricle begins to relax. Since all the valves are closed again, the ventricular volume is constant (isovolumetric) in this phase.
Ventricular filling in pressure-volume loop
Ventricular filling (1 to 3). At point 1, the mitral valve opens and the filling of the ventricles begins. Initially, a rapid filling period begins which is followed by a reduced filling.
Effect of preload on pressure-volume loop
Increased preload leads to an increase in ventricular end-diastolic volume and results from increased venous return. This, in turn, results in an increase in stroke volume based on the Frank-Starling relationship. Since increased preload causes increased stroke volume, this results in an increased width of the pressure-volume loop.
Effect of afterload on pressure-volume loop
Increased afterload requires the ventricle to pump against a higher pressure, decreasing stroke volume. This decreased stroke volume leaves more blood left in the heart after each contraction, and results in an increase in end-systolic volume. The decrease in stroke volume from increased afterload is reflected in decreased width and increased height of the pressure–volume loop.
Effect of contractility on pressure-volume loop
With increased contractility the ventricle is able to develop greater tension than usual during systole, causing an increase in stroke volume. This results in a decrease in end-systolic volume.
cardiac cycle
The cardiac cycle is the process of cardiac filling and ejection, and is often visualized with electrocardiography or jugular venous pressure readings. Atrial systole is the activation of the atria, pumping atrial blood into the ventricles. Isovolumetric ventricular contraction happens when the ventricles contract before the aortic and pulmonic valves open; it is the period of highest O2 consumption. Rapid ventricular ejection is the period of ventricular contraction after the aortic and pulmonic valves have opened, when the ventricles are ejecting blood into the pulmonic and systemic circulations. Reduced ventricular ejection follows rapid ventricular ejection and results from decreased ventricular volume. This follows the length-tension relationship described by the Frank-Starling equation, where contraction strength is directly related to the load; therefore, a decreased volume would translate into a decreased load, which means less contraction strength and reduced ventricular ejection. Isovolumetric ventricular relaxation is the period between the aortic valve closing and the mitral valve opening. Rapid ventricular filling happens when the atrial pressure equals the ventricular pressure. It starts when the mitral and tricuspid valves open.
The first heart sound (S1)
The first heart sound (S1) is the sound of the atrioventricular (tricuspid and mitral) valves closing; it occurs at the beginning of isovolumetric ventricular contraction.
The second heart sound (S2)
The second heart sound (S2) is the sound of the aortic and pulmonic valves closing. Normally, the aortic valve closes before the pulmonic, which may result in “splitting” of the second heart sound, typically during inspiration.
The third heart sound (S3)
The third heart sound (S3) results from blood sloshing against the ventricular walls during the middle third of diastole. In children and pregnant women the third heart sound may be normal. In adults it is associated with increased filling pressure from a dilated ventricle, and is considered pathological.
The fourth heart sound (S4)
The fourth heart sound (S4) is a low frequency diastolic sound that occurs during the late diastolic filling phase (the atrial kick). It results from an atrial kick filling a ventricle with decreased compliance, often seen in left ventricular hypertrophy. S4 is heard before S1. It is sometimes heard in the elderly due to a stiff ventricle. When loud, it is indicative of a pathological state, generally a hypertrophic left ventricle. The trough is where the aortic valve closed, and the following “bump” in pressure results from aortic pressure recoil against a closed aortic valve. This bump is also known as the dicrotic wave.
a wave
“a” wave — increase in right atrial pressure during atrial contraction (i.e., atrial systole). Absent “a” wave is characteristic of atrial fibrillation due to a lack of coordinated atrial contraction
c wave
“c” wave — increase in right atrial pressure during right ventricular isovolumic systole (contraction); due to bulging of the tricuspid valve into the right atrium.
x descent
“x” descent — decrease in right atrial pressure following the peak of the “c” wave due to atrial relaXation. Absent “x” descent — tricuspid regurgitation. Backflow of blood into the right atrium during systole prevents relaxation of right atrial pressure. (may see a positive wave)
v wave
“v” wave — increase in right atrial pressure during late ventricular systole due to right atrial filling against a closed tricuspid valve. Peak of “v” wave usually corresponds with (or occurs just after) the T wave on EKG.
y descent
“y” descent — decrease in right atrial pressure following the peak of the “v” wave; due to tricuspid valve opening and right atrium emptYing
Normal splitting
Inspiration causes a drop in intrathoracic pressure, increasing venous return. This causes an increase in RV filling, which increases RV stroke volume. This increases RV ejection time and delayed closure of pulmonic valve. A decrease in pulmonary impedance (an increase in capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve.
Wide splitting
This is seen on conditions that delay RV emptying (eg pulmonic stenosis, right bundle branch block). Delay in RV emptying causes delayed pulmonic sound (regardless of breath). It is an exaggeration of normal splitting
Fixed splitting
It is seen in ASD. ASD leads to left to right shunt, which increase RA and RV volumes, causing there to be an increase in flow through the pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed.
Paradoxical splitting
It is seen in conditions that delay aortic valve closure (eg aortic stenosis, left bundle branch block). This causes a reversal of the normal order of valve closure is reversed so that P2 sound occurs before delated A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2, thereby paradoxically eliminating the split.
Auscultation of the aortic valve
The aortic valve is best heard in the 2nd intercostal space at the upper right sternal border. Systolic murmur: aortic stenosis, aortic valve sclerosis. Diastolic murmur: aortic regurgitation (heard best at left lower sternal border at third and fourth intercostal spaces)
Auscultation of the pulmonic valve
The pulmonic valve is best hears in the 2nd intercostal space at the upper left sternal border. Systolic ejection murmur: pulmonic stenosis. Flow murmur: atrial septal defect. Diastolic murmur: pulmonic regurgitation. ASD commonly presents with a pulmonary flow murmur (an increase flow through pulmonary valve) and a diastolic rumble (an increase flow across tricupsid); blood flow across the actual ASD does not cause a murmur because there is no significant pressure gradient. The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of the pulmonary artery.
Auscultation of the tricuspid valve
The tricuspid valve is best heard at the lower left sternal border. Pansystolic murmur: tricuspid regurgitation, ventricular septal defect. Diastolic murmur: tricuspid stenosis, atrial septal defect
Auscultation of the mitral valve
The mitral valve is best heard in the 5th intercostal space at the left midclavicular line. Systolic murmur: mitral regurgitation. Diastolic murmur: mitral stenosis
Effect of inspiration on heart sounds
It increases venous return to right atrium. It increases the intensity of right heart sounds.
Effect of hand gripping on heart sounds
It increases afterload. It increases the intensity of MR, AR, and VSD murmurs. It decreases hypertrophic cardiomyopathy murmurs. MVP will have a later onset of click/murmur.
Effect of valsalva and standing up on heart sounds
This decreases preload. It decreases intensity of most murmurs (including AS). It increases the intensity of hypertrophic cardiomyopathy murmur. It will also cause an earlier onset of click/murmur of MVP.
Effect of rapid squatting on heart sounds
This increases venous return and preload. This decreases the intensity of hypertrophic cardiomyopathy murmur. It also increases the intensity of AS murmur. It also causes there to be a later onset of click/murmur of MVP.
systolic heart sounds
includes aortic/pulmonic stenosis, mitral/tricuspid regurgitation, VSD, and MVP.
Diastolic heart sounds
includes aortic pulmonic regurgitation, mitral/tricuspid stenosis.
Aortic stenosis murmur
Aortic stenosis causes a pansystolic crescendo-decrescendo murmur heard loudest in the second intercostal space at the right sternal border, which often radiates to the carotid arteries or can be auscultated at the clavicles. The murmur increases in intensity with maneuvers that increase preload (e.g. leg-raising) and decreases in intensity with maneuvers that decrease preload (e.g. Valsalva) or increase afterload (e.g. isometric hand-squeezing). Aortic stenosis is associated with an S4 heart sound. Physical exam may reveal pulsus parvus et tardus (weak peripheral pulses with a maximal intensity peak that is late relative to the heartbeat) due to the slowed emptying of left ventricle to the systemic circulation. It can lead to Syncope, Angina, and Dyspnea on exertion (SAD). It is often due to age related calcification or early-onset calcification of bicuspid aortic valve.
Mitral regurgitation murmur
Holosystolic, high-pitched “blowing murmur”. It is the loudest at the apex and radiates toward the axilla. MR is often due to ischemic heart disease (post-MI), MVP, LV dilation. It can also be caused by rheumatic fever and infective endocarditis.
Tricuspid regurgitation murmur
Holosystolic, high-pitched “blowing murmur”. It is the loudest at the tricuspid area and radiates to the right sternal border. TR is commonly caused by RV dilatation. It can also be caused by rheumatic fever and infective endocarditis.
Mitral valve prolapse murmur
On auscultation a mid-to-late systolic click which varies with maneuvers (earlier with decreased left ventricular end-diastolic volume (LVEDV), later with increased LVEDV) and a soft late systolic murmur of mitral regurgitation are appreciated that is the loudest right before S2. Standing and valsalva decrease preload, reducing the LVEDV and relieving the cordae tendinae of some tension. This makes the click occur earlier in systole. Squatting increases preload, augmenting the LVEDV and placing greater tension on the cordae tendinae. This makes the click occur later in systole. It is the most frequent valvular lesion. It is usually benign but can predispose to infective endocarditis. It can be caused by myxomatous degneration (primary or secondary to connective tissue disease such as Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture.
Ventricle septal defect murmur
Holosystolic, harsh sounding murmur. Loudest at the tricuspid.
Aortic regurgitation murmur
Aortic regurgitation causes a high-pitched diastolic murmur, often with a blowing quality, beginning immediately after A2. It may decrescendo or persist throughout diastole, and is enhanced by the patient leaning forward and holding his breath at end-expiration. There is a long diastolic murmur and signs of hyperdynamic pulse when severe and chronic. It is often due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever. It can progress to left HF.
Mitral stenosis murmur
On auscultation a low-pitched diastolic rumble with an opening snap (due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion of leaflet tips) just after the second heart sound is heard best at the fourth intercostal space, midclavicular line, with the patient in left lateral decubitus position. The time between the opening snap and the second heart sound decreases as the stenosis becomes more severe. Patients may have a loud first heart sound by comparison. LA pressure is much greater than LV pressure during diastole. It often occurs secondary to rheumatic fever. Chronic MS can result in LA dilation.
Patent ductus arteriosus (PDA)
A patent ductus arteriosus has a classic “machine-like” continuous murmur that distinguishes it from other heart conditions. It is loudest at S2. It is often due to congenital rubella or prematurity. It is best heard at the left infraclavicular area.
Action potentials in myocytes
Action potentials in myocytes in ventricles, atria, and Purkinje fibers have 5 phases named Phase 0 to 4. These cell types have a resting membrane potentials of about -90 mV. The resting membrane potential is determined by conductance to K+ and it approaches the K+ equilibrium potential.
Phase 0 in cardiac myocytes
Phase 0 is the upstroke of the action potential. It is caused by an increase in Na+ conductance. Fast voltage gated Na+ channels open (Na+ influx) and the membrane potential approaches the Na+ equilibrium potential.
Phase 1 in cardiac myocytes
Phase 1 is the initial repolarization. Na channels have a decrease in conductance, and voltage gated K+ channels begin to open. Activation of voltage gated K+ channels results in transient repolarization that explains the small dip before the plateau. This occurs before the calcium channels open.
Phase 2 in cardiac myocytes
Phase 2 is the plateau of the action potential. It is caused by an increased Ca2+ conductance through L type voltage gated Ca2+ channels, balanced by an K+ efflux through leaky K+ channels. Ca2+ flows into the cell and K+ flows out. Ca2+ influx induces Ca2+ release from the sarcoplasmic reticulum causing myocyte contraction.
Phase 3 in cardiac myocytes
Phase 3 is the rapid repolarization. It is caused by a massive K+ efflux due to the opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Subsequent large outward K+ current hyperpolarizes the membrane.
Phase 4 in cardiac myocytes
Phase 4 is the resting membrane potential. Inward and outward currents are equal again, and membrane potential approaches K+ equilibrium potential again.
Skeletal vs cardiac action potential
Cardiac muscle action potential has a plateau, which is due to Ca influx and K efflux; myocyte contraction occurs due to Ca induced Ca release from the sarcoplasmic reticulum. Cardiac nodal cells spontaneously depolarize during diastole, resulting is automaticity due to If channels (funny current channels responsible for a slow mixed Na/K inward current). Cardiac myocytes are electrically coupled to wach other by gap junctions.
Action potential in SA and AV nodes
Action potential in SA and AV nodes differ from the ventricular action potential. They have only 3 phases.
Phase 1 and Phase 2 are not present in the SA/AV node action potentials
Phase 0 in SA and AV nodes
Phase 0 – upstroke of action potential. Opening of slow voltage gated Ca channels. This differs from ventricular action potential, which has a fast upstroke that is dependent on Na current. The slower conduction velocity allows AV node time to transmit action potential from atria to ventricles. This delay allows the atria time to empty before ventricles contract.
Phase 3 in SA and AV nodes
Phase 3 – repolarization. Ca channels are inactivated which result in a K efflux from activation of K channels
Phase 4 in SA and AV nodes
Phase 4 – slow depolarization. Accounts for the pacemaker automaticity. In pacemaker cells, phase 4 of the action potential is characterized by spontaneous depolarization due to increased inward Na conductance, known as the pacemaker (“funny”) current. The funny current controls the rate of spontaneous activity of sinoatrial myocytes and hence the cardiac rate. In contrast to phase 4 of pacemaker action potentials, phase 4 of ventricular cardiomyocyte (ie, nonpacemaker) action potentials is characterized by K equilibrium, with no spontaneous inward Na conductance.
P wave
Atrial depolarization. Atrial repolarization is masked by QRS complex.
PR interval
It is the time from start of atrial depolarization to start of ventricular depolarization (normally less then 200 msec).
QRS complex
The QRS complex represents ventricular depolarization, which is normally
QT interval
The QT interval represents ventricular depolarization, mechanical contraction of the ventricles, and ventricular repolarization and is affected by serum Ca2+ levels: Hypocalcemia prolongs the QT interval. Hypercalcemia shortens the QT interval
T wave
The T wave marks ventricular repolarization. T-wave inversion may indicate recent MI.
J point
The junction between the end of QRS complex and start of ST segment.
ST segment
The ST segment is isoelectric in a normal heart since it represents a period where the ventricles are depolarized and there are no currents towards the leads of the ECG.
U wave
It is caused by hypokalemia and bradycardia
Speed of conduction through different muscle fibers
From highest speed to lowest: Purkinje, atria, ventricles, and AV node.
Dominant pacemakers in the heart
SA, than AV, than bundle of his/purkinje/ventricles.
Conduction pathway through the heart
SA node to atria to AV node to commun bundle to bundle branches, to fasicles to purkinje fibers to ventricles.
SA node
SA node is the pacemaker due to inherent dominance with slow phase of upstroke.
AV node
AV node is located in the posterioinferior part of the interatrial septum. Blood supply usually from RCA. 100 msec delay allows time for ventricular filling.
Torsades de pointes
Polymorphic ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG. It can progress to ventricular fibrillation. Long GT interval predisposes to torsades de pointes. It can be caused by drugs, a decrease in K, a decrease in Mg, or other abnormalities. Treament includes magnesium sulfate. Drugs that prolong QT (ABCDE): AntiArrhythmics (Class IA, III), AntiBiotics (e.g., macrolides), Anti”C”ychotics (e.g., haloperidol), AntiDepressants (e.g., TCAs), and AntiEmetics (e.g., ondansetron)
Congenital long QT syndrome
An inherited disorder of myocardial repolarization, typically due to ion channel defects. There is an increase risk of sudden cardiac death due to torsade de pointes. Types include Romano Ward and syndrome Jervell and Lange-Nielsen syndrome.
Romano-Ward syndrome
A congenital long QT syndrome. It is autosomal dominant, pure cardiac phenotype (no deafness).
Jervell and Lange-Nielsen syndrome
A congenital long QT syndrome. It is autosomal recessive with sensorineural deafness.
Brugada syndrome
Brugada syndrome is a genetic disorder of cardiac sodium channels that leads to an increased risk of ventricular tachyarrhythmias and sudden cardiac death. Brugada syndrome is an autosomal dominant disorder most common in Asian males. ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave is the only ECG abnormality that is potentially diagnostic in Brugada syndrome. The only proven therapy for Brugada syndrome is an implantable cardioverter-defibrillator (ICD).
Wolff-Parkinson-White syndrome
Wolff-Parkinson-White syndrome is a pre-excitation syndrome wherein an extra conduction pathway/accessory pathway (aka the bundle of Kent) leads to arrhythmias marked by the characteristic delta wave with shortened PR interval on ECG. Symptoms range from asymptomatic, to palpitations and vague complaints, to sudden death from tachyarrhythmias that prevent ventricular filling. Wolff-Parkinson White syndrome is diagnosed by ECG with a: Shortened PR interval; Widened QRS complex; Delta wave (which signifies early ventricular depolarization).
Atrial fibrillation
Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes. It is associated with hypertension, coronary artery disease (CAD), rheumatic heart disease, binge drinking (holiday heart), HG, valvular disease, hyperthyroidism. It can result in atrial stasis and lead to cardioembolic events. Treatment includes antithrombotic therapy (eg warfarin), rate control (beta-blockers, non-dihydropyridine Ca channel blocker, digoxin), rhythm control (class Ic or III antiarrhythmics), and/or cardioversion (pharmacological or electrical).
Atrial flutter
A rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the sawtooth appearance of the flutter waves. Management similar to atrial fibrillation (rate contol, anticoagulation, cardioversion). Definitive treatment is catheter ablation.
Ventricular fibrillation
A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.
1st degree AV block
The PR interval is prolonged (over 200 msec). It is benign and asymptomatic. No treatment is required.
2nd degree AV block Mobitz type I (Wenckebach)
There are progressive lengthening of PR interval until a beat is dropped (a P wave is not followed by QRS complex). It is usually asymptomatic. Variable RR interval with a pattern (regularly irregular).
2nd degree AV block Mobitz type II
Dropped beats that are not preceded by a change in the length of the PR interval (as in type I). May progress to 3rd degree block. It is often treated with a pacemaker.
Third degree heart block
The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. Atrial rate is faster than ventricular rate. It is usually treated with pacemaker. Lyme disease can result in 3rd degree heart block.
Atrial natriuretic peptide
It is released from atrial myocytes in response to an increase in blood volume and atrial pressure. It acts via cGMP. It causes vasodilation and a decrease in Na reabsorption at the renal collecting tubule. It dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to aldosterone escape mechanism.
B-type (brain) natriuretic peptide
It is released from ventricular myocytes in response to increase tension. There are similar physiologic action to ANP, with longer half life. BNP blood test used for diagnosing HF (very good negative predictive value). It is available in recombinant form (nesiritide) for treatment of HF.
Peripheral baroreceptors
The two important peripheral locations of baroreceptors in the body are the carotid sinus and the aortic arch. The aortic arch contains both baroreceptors and chemoreceptors, while the carotid sinus contains just baroreceptors. The carotid body is the other location of the peripheral chemoreceptors. The receptors in the aortic arch transmit information via the vagus nerve and those in the carotid sinus via the glossopharyngeal nerve. They both go to the solitary nucleus of the medulla.
carotid massage
The purpose of a “carotid massage” is to decrease heart rate (HR). This is a vagal response to increasing pressure on the carotid sinus, which leads to: Increased stretch; Increased baroreceptor firing; Increased AV node refractory period; and Decreased HR
Cushing reflex
The Cushing reflex is a physiologic response to increased intracranial pressure. The 3 responses are: Increased blood pressure; Bradycardia; Respiratory depression. During the Cushing reflex, the increased intracranial pressure causes compression of cerebral arterioles and cerebral ischemia (increased cerebral PCO2). This leads to an increase in sympathetic stimulation in order to increase perfusion pressure (blood pressure). The baroreceptors sense this increased BP and induce bradycardia.
chemoreceptors
The chemoreceptors in the carotid and aortic bodies respond to: Decreased PO2 (less than 60 mmHg, primary stimulus), Increased PCO2, Decreased blood pH. In response to a decrease in PO2 as seen in respiratory arrest or circulatory shock, firing of peripheral chemoreceptors leads to an increase in sympathetic firing and decrease in parasympathetic output. This is in contrast to local mediators of blood pressure where low PO2 leads to vasodilation. This induces the following cardiovascular responses: Vasoconstriction, Increased sympathetic outflow to the heart, Increased arterial pressure
Normal inferior vena cava and right atrial pressure
Normal inferior vena cava and right atrial pressure is less than 5 mmHg.
Normal right ventricular pressure
Normal right ventricular pressure is ~ 25/5 mmHg.
normal mean pulmonary artery pressure
The normal mean pulmonary artery pressure is ~ 25/10 mmHg. Pulmonary hypertension occurs when the mean pulmonary artery pressure is ≥ 25 mmHg at rest.
Normal left atrial pressure
Normal left atrial pressure is less than 12. PCWP approximates left atrial pressure. It should be measured at end expiration, since this is the closest to zero intrathoracic pressure. In mitral stenosis, pulmonary capillary wedge pressure is greater than left ventricular diastolic pressure.
Normal left ventricular pressure
Normal left ventricular pressure is ~ 130/10 mmHg.
