Cardio Flashcards
What do each of these give rise to?
Truncus arteriosus Bulbus cordis Endocardial cushion Primitive atrium Primitive ventricle Primitive pulmonary vein Left horn of sinus venosus Right horn of sinus venosus Right common cardinal vein and right anterior cardinal vein Right common cardinal vein and right anterior cardinal vein
Truncus arteriosus = Ascending aorta and pulmonary trunk
Bulbus cordis = Smooth parts (outflow tract) of left and right ventricles
Endocardial cushion = Atrial septum, membranous interventricular septum; AV and semilunar valves
Primitive atrium = Trabeculated part of left and right atria
Primitive ventricle = Trabeculated part of left and right ventricles
Primitive pulmonary vein = Smooth part of left atrium
Left horn of sinus venosus = Coronary sinus
Right horn of sinus venosus = Smooth part of right atrium (sinus venarum)
Right common cardinal vein and right anterior
cardinal vein = Superior vena cava (SVC)
Dextrocardia
Occurs during cardiac looping
Primary heart tube loops to establish left-right
polarity; begins in week 4 of gestation.
Defect in left-right dynein (involved in L/R
asymmetry) can lead to dextrocardia, as seen
in Kartagener syndrome (primary ciliary
dyskinesia).
Steps of chamber formation (atria)
pg 268
1. Septum primum grows toward endocardial
cushions, narrowing foramen primum.
2. Foramen secundum forms in septum
primum (foramen 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. (Not shown) Septum secundum and septum
primum fuse to form the atrial septum.
7. (Not shown) Foramen ovale usually closes
soon after birth because of increases LA pressure.
Patent foramen ovale—caused by failure of
septum primum and septum secundum
to fuse after birth; most are left untreated.
Can lead to paradoxical emboli (venous
thromboemboli that enter systemic arterial
circulation), similar to those resulting from
an ASD.
Steps of ventricular formation (embryo)
- Muscular interventricular septum forms.
- Opening is called interventricular foramen.
- Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing
interventricular foramen.
*This requires neural crest cells. - Growth of endocardial cushions separates
atria from ventricles and contributes to both atrial septation and membranous portion of the interventricular septum.
Ventricular septal defect—most common congenital cardiac anomaly, usually occurs in
membranous septum.
-not cyanotic at birth due to L>R shunt
How are outflow tracts formed and what abnormalities are associated with failure of neural crest cells to migrate?
Neural crest and endocardial cell migrations:
forms > truncal and bulbar ridges that spiral
and fuse to form aorticopulmonary septum
forms > ascending aorta and pulmonary trunk.
Conotruncal abnormalities associated with
failure of neural crest cells to migrate:
Transposition of great vessels.
Tetralogy of Fallot.
Persistent truncus arteriosus.
Describe the 3 major shunts in fetal circulation.
“Blood in umbilical vein has a Po2 of ≈ 30 mm Hg
and is ≈ 80% saturated with O2. Umbilical
arteries have low O2 saturation. “
And then what happens at birth?
Mnemonic: kEEp PDA open
3 important shunts:
1. Blood entering fetus through the
umbilical vein is conducted via the ductus
venosus into the IVC, bypassing hepatic
circulation.
2. 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.
3. Deoxygenated blood from the SVC
passes through the RA > RV > main
pulmonary artery > Ductus arteriosus
> Descending aorta; shunt is due to high
fetal pulmonary artery resistance (due
partly to low O2 tension and nonfunctioning lungs).
At birth, infant takes a breath; decrease resistance
in pulmonary vasculature > increased left atrial
pressure vs right atrial pressure; foramen ovale
closes (now called fossa ovalis); increase in O2 (from
respiration) and increase in prostaglandins (from
placental separation) > closure of ductus
arteriosus.
Indomethacin helps close PDA and forms ligamentum
arteriosum (remnant of ductus arteriosus).
Prostaglandins E1 and E2 kEEp PDA open.
What are the remnants of each of these fetal structures
AllaNtois - urachus Ductus arteriosus Ductus venosus Foramen ovale Notochord UmbiLical arteries Umbilical vein
AllaNtois - urachus > MediaN umbilical ligament (Urachus is part of allantoic duct between
bladder and umbilicus.)
Ductus arteriosus > Ligamentum arteriosum
Ductus venosus > Ligamentum venosum
Foramen ovale > Fossa ovalis
Notochord > Nucleus pulposus
UmbiLical arteries > MediaL umbilical ligaments
Umbilical vein > Ligamentum teres hepatis (round ligament) (Contained in falciform ligament.)
pg271
What supples the SA and AV nodes
What does it mean if there is right, left and codominant circulation.
Where does occlusion of the coronary arteries usually occur.
When does coronary blood flow peak.
SA and AV nodes are supplied by branches of
the RCA. Infarct may cause nodal dysfunction
(bradycardia or heart block).
(dominance refers to which coronary artery supplies the posterior wall)
Right-dominant circulation (85%) = PDA arises
from RCA.
Left-dominant circulation (8%) = PDA arises
from LCX.
Codominant circulation (7%) = PDA arises
from both LCX and RCA.
Coronary artery occlusion most commonly
occurs in the LAD.
Coronary blood flow peaks in early diastole.
A 21-year-old man has a mean arterial pressure (MAP) of 89 mm Hg at rest. After running for 40 minutes, his mean arterial pressure has risen only slightly to 99 mm Hg. A decrease in which of the following during exercise most likely accounts for the observed finding?
A. Systolic blood pressure B. Renal blood flow C. Stroke volume D. Systemic vascular resistance E. Right atrial pressure
D. Systemic vascular resistance. During exercise, muscle tissue receives up to 85% of blood flow due to vasodilation of muscle vascular beds. In most vascular beds, the SNS causes vasoconstriction via a1 adrenergic receptors. The notable exception is the muscle bed where b2 adrenergic receptors predominant. These receptors when bound by catecholamines cause vasodilation.
Patient 1
systolic and diastolic BP elevated, PCWP elevated
Patient 2
Systolic and; diastolic BP elevated, PCWP normal
Patient 1: mitral stenosis or Eisenmengers
Patient 2: pulmonary embolus (large)
A man suffers a stroke caused by partial occlusion of his left internal carotid artery. An evaluation of the carotid artery using magnetic resonance imaging (MRI) shows a 75% reduction in its radius. Assuming that blood flow through the left internal carotid artery is 256 mL/min prior to the occlusion, what is blood flow through the artery after the occlusion?
A 75% reduction in radius means that the radius is now ¼
of the original value. The resistance has therefore
increased 256 fold (r4). If perfusion pressure remains
constant, flow must then decrease by 256-fold to 1 mL/min.
A decrease in which of the following would tend to increase lymphatic flow? A. Hydrostatic capillary pressure B. Interstitial osmotic pressure C. Plasma osmotic pressure D. Capillary filtration constant
C plasma osmotic pressure,
if osmotic pressure goes down that means there is less protein
Normal
EDV = 125 ESV = 50 SV= 75
Patient 1
EDV = 125
ESV = 80
SV= 45
Patient 2
EDV = 125
ESV = 30
SV= 95
Patient 3
EDV = 150
ESV = 50
SV= 100
Patient 1 - increased afterload
Patient 2: increase contractility
Patient 3: increased preload
A 40-year-old male is hospitalized with progressive exertional dyspnea, lower extremity edema and cough. She also describes frequent nocturnal episodes of breathlessness and recent hoarseness. Auscultation reveals a mid-diastolic rumble best heard at the cardiac apex. This patient’s hoarseness is most likely caused by:
A. Laryngeal edema B. Impaired arterial supply C. Nerve impingement D. Epithelial sloughing E. Vocal cord polyps
C. The patient has mitral stenosis resulting in LA enlargement and pressure on the L recurrent laryngeal nerve (see arrow).
This is Ortner’s syndrome
- An 80 year old male with syncope on exertion and weak carotid pulses
- A 26 year old female IV drug user with fever, chills and prominent head bobbing
- A 54 year old male with blood tinged sputum and a history of rheumatic heart disease
- A 39 year old women with nocturnal dyspnea and a systolic blowing murmur
(aortic/mitral, stenosis/regurg)?
- An 80 year old male with syncope on exertion and weak carotid pulses - aortic stenosis
- A 26 year old female IV drug user with fever, chills and prominent head bobbing - endocarditis destroys the valve, head bobbing suggests aortic regurg
- A 54 year old male with blood tinged sputum and a history of rheumatic heart disease - before RHD causes mitral/tricuspid regurg it classically causes mitral stenosis), blood is backing up into the lungs.
- A 39 year old women with nocturnal dyspnea and a systolic blowing murmur - mitral insufficiency (blowing mumur and nocturnal dyspenea)
Alpha -1 receptor functions and alpha 2 receptor functions
alpha 1
- **vasoconstriction (increased peripheral vascular resistance and increased BP) - no effect on heart
- mydriasis (ciliary body contracts, increases intraocular pressure because block outflow tract)
- Bladder sphincter constriction
alpha 2:
- **inhibit NE release (decrease sympathetic activity, decreasing blood pressure)
- inhibit insulin release from beta cells
- decrease aqueous humor production
Beta 1 receptor
Beta 2 receptor
Beta 3 receptor
functions
Beta 1: (heart)
- tachycardia
- increased contractility
- increased renin (increase BP)
Beta 2:
- vasodilation, decrease peripheral vascular resistance (mostly skeletal)
- bronchodilator
- 🌸uterine relaxation
- increase glucose (glycogenolysis, gluconeogenesis)
- 🍌increase potassium uptake (can treat hyperkalemia)
Beta 3: lipolysis
Familial Hypercholesterolemia
Autosomal dominant disorder
-severe elevations in total cholesterol and LDL-C
- (most common) nonsense mutation in the LDL receptor
- APO-B100, inhibits binding of LDL to LDL-R
- PCSK9
- gain of function
- enhances LDL-R degradation
Homozygous FH - severely elevated cholesterol levels (total cholesterol and LDLc levels >600 mg/dL); TAG levels are within normal limits
Heterozygous FH - elevated LDLc levels commonly greater than 250 mg/dL
Hyperchylomicronemia (type 1)
-eruptive xanthoma (as opposed to tendonous xanthoma/LDL-R defect) or (tuberous xanthomas - ApoE defect -don’t take VLDL or IDL) - it looks different, pimples become yellow, not itchy)
- very high serum triglycerides
- cholesterol is usually normal
- deficiency in lipoprotein lipase OR in ApoCII
- associated with pancreatitis
- no increased risk of coronary artery disease
Describe the fetal circulation
Blood in umbilical vein has a Po2 of ≈ 30 mmHg
and is ≈ 80% saturated with O2. Umbilical
arteries have low O2 saturation.
3 important shunts:
1. Blood entering fetus through the
umbilical vein is conducted via the ductus
venosus into the IVC, bypassing hepatic circulation.
2. 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.
3. Deoxygenated blood from the SVC
passes through the RA >RV > main
pulmonary artery >Ductus arteriosus
> Descending aorta; shunt is due to high fetal pulmonary artery resistance (due partly to low O2 tension).
At birth, infant takes a breath; decrease resistance in pulmonary vasculature >increase left atrial
pressure vs right atrial pressure; foramen ovale
closes (now called fossa ovalis); increase in O2 (from respiration) and increase in prostaglandins (from
placental separation) > closure of ductus arteriosus.
Indomethacin helps close PDA > ligamentum arteriosum (remnant of ductus arteriosus). Prostaglandins E1 and E2 kEEp PDA open.
Ostium Secundum Type
Ostium Primum Type
Patent foramen ovale
🌟Ostium Secundum Type (90%) is caused
by abnormal growth (not enough) of the
septum secundum.
• Ostium Primum Type (5%) is where the septum primum doesn’t fuse with the endocardial cushion. Seen in Down
syndrome and associated with AV valve
defects.
• Patent foramen ovale is common (25% of adults) and is caused by failure of septum primum and septum secundum to fuse after birth (there is no true hole in the septum at rest). Not considered a true ASD and treatment (closure) is controversial.
Wolff-Parkinson-White syndrome
Most common type of ventricular pre-
excitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing
AV node >ventricles begin to partially
depolarize earlier > characteristic delta wave with widened QRS complex and shortened PR interval on ECG. May result in reentry circuit
>supraventricular tachycardia.
Right-to-left shunt
Early cyanosis—“blue babies.” Often diagnosed
prenatally or become evident immediately
after birth. Usually require urgent surgical treatment and/or maintenance of a PDA.
The 5 Ts:
- Truncus arteriosus (1 vessel)
- Transposition (2 switched vessels)
- Tricuspid atresia (3 = Tr i)
- Tetralogy of Fallot (4 = Te t r a)
- TAPVR (5 letters in the name)
Persistent truncus arteriosus
Truncus arteriosus fails to divide into
pulmonary trunk and aorta due to lack of
aorticopulmonary septum formation; most patients have accompanying VSD.
Transposition of the great vessels
Aorta leaves RV (anterior) and pulmonary trunk
leaves LV (posterior) > separation of systemic
and pulmonary circulations. Not compatible with life unless a shunt is present to allow mixing of blood (eg, VSD, PDA, or patent
foramen ovale).
Due to failure of the aorticopulmonary septum to spiral.
Without surgical intervention, most infants die within the irst few months of life.
Tricuspid atresia
Absence of tricuspid valve and hypoplastic RV;
requires both ASD and VSD for viability.
Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle. This defect is contracted during prenatal development, when the heart does not finish developing. It causes the heart to be unable to properly oxygenate the rest of the blood in the body. Because of this, the body does not have enough oxygen to live, so other defects must occur to maintain blood flow. ⭐️Because of the lack of an A-V connection, an atrial septal defect (ASD) must be present to fill the left ventricle with blood. Also, since there is a lack of a right ventricle there must be a way to pump blood into the pulmonary arteries, and this is accomplished by a ventricular septal defect (VSD). The causes of Tricupsid atresia are unknown.[1]
Tetraology of Fallot
MnemonicL PROVe
Caused by anterosuperior displacement of the
infundibular septum. Most common cause of early childhood cyanosis
- Pulmonary infundibular stenosis (most important determinant for prognosis)
- Right ventricular hypertrophy (RVH)—boot-shaped heart on CXR
- Overriding aorta
- VSD
Pulmonary stenosis forces right-to-left flow across VSD > RVH, “tet spells” (often caused by crying, fever, and exercise due to exacerbation of RV outlow obstruction).
PROVe. Squatting: increases SVR, decreases right-to-left shunt, improves cyanosis.
Treatment: early surgical correction.
Total anomalous pulmonary venous return
Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc);
associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO
Ebstein anomaly
Characterized by displacement of tricuspid
valve lealets downward into RV, artiicially
“atrializing” the ventricle. Associated with tricuspid regurgitation and right heart failure. Can be
caused by lithium exposure in utero.
Left-to-right shunts
eaRLy
LateR
Acyanotic at presentation; cyanosis may occur
years later.
Frequency: VSD > ASD > PDA.
Right-to-Left shunts: eaRLy cyanosis. Left-to-Right shunts: “LateR” cyanosis.
Ventricular septal defect
Most common congenital cardiac defect.
Asymptomatic at birth, may manifest week later or remain asymptomatic throughout life.
Most self resolve; larger lesions may lead to LV overload and HF.
O2 saturation increase in RV and pulmonary artery
Atrial septal defect
Defect in interatrial septum; loud S1; wide,
fixed split S2. Ostium secundum defects
most common and usually occur as isolated findings; ostium primum defects rarer yet usually occur with other cardiac anomalies.
Symptoms range from none to HF. Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.
O2 saturation increases in RA, RV, and pulmonary artery. May lead to paradoxical emboli
(systemic VENOUS emboli use ASD to bypass lungs and become systemic arterial emboli).
Patent Ductus Arteriosus
ENDomethacin
PGE
In fetal period, shunt is right to left (normal).
In neonatal period, decrease pulmonary vascular
resistance > shunt becomes left to right > progressive RVH and/or LVH and HF.
Associated with a continuous, “machine-like murmur. Patency is maintained by PGE synthesis and low O2 tension. Uncorrected PDA can eventually result in late cyanosis
in the lower extremities (differential cyanosis).
Endomethacin” (indomethacin) ends patency of PDA; PGE keeps ductus Going (may be necessary to sustain life in conditions such as transposition of the great vessels). PDA is normal in utero and normally closes only
after birth.
Eisenmenger syndrome
Uncorrected left-to-right shunt (VSD, ASD, PDA) > increase pulmonary blood flow >pathologic
remodeling of vasculature >pulmonary
arterial hypertension. RVH occurs to
compensate > shunt becomes right to
left. Causes late cyanosis, clubbing D , and polycythemia. Age of onset varies.
Coarctation of the aorta
Infantile:
Preductal coarctation - (Turner Syndrome, FA p585) - constriction is proximal to the DA. Before birth, blood flows through the DA to the descending aorta for distribution to the lower body. Collaterals DO NOT NEED develop in utero. For this reason, preductal coarctation can be life-threating in neonate. Cyanosis from birth immediately symptomatic
Adult: there is no PDA, the coarctation is after the major branches of the aorta so intercostals have to form. Blood can’t flow well so instead more are forced out into the major branches leading to hypertension in upper extremities and hypotension in lower extremities. Intercostals will try to bypass the coarctation and lead to rib notching. The renals are in the hypotense region so they think there is hypotension and activate the RAAS.
______________________________
FA: Aortic narrowing near insertion of ductus arteriosus (“juxtaductal”). Associated with bicuspid aortic valve, other heart defects, and Turner syndrome.
Hypertension in upper extremities and weak, delayed pulse in lower
extremities (brachial-femoral delay). With age, intercostal arteries enlarge due to collateralcirculation; arteries erode ribs > notched
appearance on CXR.
Complications include HF,risk of cerebral hemorrhage (berry
aneurysms), aortic rupture, and possible endocarditis.
Aortic arch derivatives
Aortic arch derivatives
1st: Part of maxillary artery (branch of external
carotid).
1st arch is maximal
2nd: Stapedial artery and hyoid artery.
Second = Stapedial
3rd: Common Carotid artery and proximal part of internal Carotid artery
C is 3rd letter of alphabet
4th: On left, aortic arch; on right, proximal part of right subclavian artery. 4th arch (4 limbs) -systemic
🌈6th: Proximal part of pulmonary arteries and (on left only) ductus arteriosus
*6th arch = pulmonary and pulmonary -to systemic shunt (ductus arteriosus
*Right recurrent laryngeal nerve loops around right subclavian artery
4th
Left recurrent laryngeal nerve loops around aortic arch distal to ductus arteriosus
Measurements of blood oxygen are taken in a fetus. The highest value is most likely recorded in which of the following vessels?
A. Ductus arteriosus B. Superior vena cava C. Inferior vena cava D. Pulmonary trunk E. Ascending aorta F. Descending aorta G. Umbilical artery
C. inferior vena cava
A 5-year-old male with a bounding pulse has a thrill best palpated over the upper left sternal edge. A continuous murmur is heard over the area on cardiac auscultation and caused by the lack of closure of fetal bypass channel. This channel is a derivative of which of the following embryologic structures?
A. Sinus venosus B. Bulbus cordis C. Primitive atria D. Fourth aortic arch E. Sixth aortic arch
E. sixth aortic arch - ductus arteriosus
Rapid fire
- What defines dominance of circulation
- What is supplying the SA and AV node
- Where does coronary artery occlusion most commonly occur
- What are some consequences of left atrial enlargement
1) Right-dominant circulation=85%; defined by which artery supplies the PDA - supplies posterior 1/3 of interventricular septum, AV node and posterior wall of ventricles
2) SA and AV node usually supplied by RCA
3) Coronary artery occlusion most commonly occurs in the LAD
4) Left atrium enlargement can cause dysphagia (compression of the esophagus) or hoarseness (compression of the left recurrent laryngeal nerve, a branch of the vagus).
Myocardial/Ventricular Action Potential
Phase 0-4
In contrast to skeletal muscle:
Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux.
Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from sarcoplasmic reticulum (Ca2+-induced Ca2+ release)
.
Cardiac myocytes are electrically coupled to each other by gap junctions.
Phase 0 = Rapid upstroke – Voltage-gated (VG) Na+ channel open.
Phase 1 = Initial repolarization – inactivation of VG Na+ channels. VG K+ channel begins to open.
Phase 2 = Plateau – Ca2+ influx through VG Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction
Phase 3 = Rapid repolarization – massive K+ efflux due to opening of VG slow K+ channels and closure of VG Ca2+ channels.
Phase 4 = Resting potential – high K+ permeability through K+ channels
Equations for:
CO
SV
EF
Wall tension
MAP
Resistance of arterioles
Fick’s principle
Pulse pressure
- CO = SV x HR (ml or L/min)
- SV = EDV-ESV
- EF = SV/EDV normal is >55%
- Wall tension = (Pressure x radius)/(2 x thickness)
- MAP = CO x TPR (aka SVR), MAP = 2/3 diastolic + 1/3 systolic
- Resistance - viscocity x length / radius ^4
- Fick’s principle: CO = (rate of O2 consumption)/
(arterial O2 content − venous O2 content - Pulse pressure = systolic pressure – diastolic pressure
*Pulse pressure is proportional to SV, inversely
proportional to * arterial compliance.
What are the steps to catecholamine induced increase in inotropy
- Phosphorylation of Ca2+ channels causes the Ca2+ channels to remain open ⏱longer. - increase contractility with increase intracellular calcium
- Phosphorylation of proteins in the SR enhances release of Ca2+. - increase contractility with increase intracellular calcium
- Phosphorylation of myosin increases myosin ATPase which increases the speed of cross-bridge cycling.
- Phosphorylation of Ca2+ pumps in the SR increases the speed of calcium re-uptake, and relaxation.
What is the NCX? Sodium calcium exchanger
How is this involved in the effects of digitalis (digoxin)
The sodium-calcium exchanger (often denoted NCX) removes calcium from cells, using the electrochemical gradient of sodium (Na+). Calcium out, sodium in. When the exchanger works poorly, calcium accumulates in the myocyte leading to enhanced contractility.
First of all digitalis increases inotropy and SV. It does this not by directly affecting the NCX.
Digitalis competes with K+ for binding to the Na+/K+ ATPase. (Potassium in, sodium out) Therefore hypokalemia increases risk of drug toxicity.
Therefore sodium builds up intracellularly and the NCX can’t bring sodium in and calcium out so calcium builds intracellularly
myoCARDial oxygen consumption
increased by Contractility, Afterload, heart Rate, and ventricular Diameter
Why do you think an increase in preload (reflected by SV) increases MVO2 less than an increase in afterload (reflected by MAP)?
D. Radius increases by the 3rd root of volume assuming the LV is a sphere
Eccentric and concentric hypertrophy
Cardiomyocytes grow in both length and width by addition of sarcomeres. Physiological stimulation (such as pregnancy or endurance training) can induce eccentric hypertrophy. Here sarcomeres are added to increase length but cellular width also increases somewhat.
Physiologic concentric hypertrophy is seen in isometric exercise training, such as weight-lifting (increase in sarcomere width only).
Pathologic eccentric hypertrophy features increases in sarcomere but cells shrink in width (e.g. valvular regurgitation).
Pathologic concentric hypertrophy arises in chronic hypertension or aortic stenosis.
Using Laplace’s equation which hypertrophy strategy or strategies would be most effective in reducing O2 consumption?
A. Concentric because wall tension would increase
B. Concentric because wall tension would decrease
C. Eccentric because wall tension would increase
D. Eccentric because wall tension would decrease E. Both strategies because wall tension would increase with either F. Both strategies because wall tension would decrease with either
B> concentric because wall tension would decrease
A 21-year-old man has a mean arterial pressure (MAP) of 89 mm Hg at rest. After running for 40 minutes, his mean arterial pressure has risen only slightly to 99 mm Hg. A decrease in which of the following during exercise most likely accounts for the observed finding? A. Systolic blood pressure B. Renal blood flow C. Stroke volume D. Systemic vascular resistance E. Right atrial pressure
D. Systemic vascular resistance. During exercise, muscle tissue receives up to 85% of blood flow due to vasodilation of muscle vascular beds. In most vascular beds, the SNS causes vasoconstriction via a1 adrenergic receptors. The notable exception is the muscle bed where b2 adrenergic receptors predominant. These receptors when bound by catecholamines cause vasodilation.
What increases pulse pressure
What decreases pulse pressure
FA. 272
Increased pulse pressure in…
-hyperthyroidism,
-aortic regurgitation (drops diastolic because blood has another route),
-aortic stiffening (arteriosclerosis in elderly - can’t absorb pressure
-exercise (transient) increases BP and decreases SVR)
-obstructive sleep
apnea (increases sympathetic tone)
Decreased pulse pressure in
- aortic stenosis,
- cardiogenic shock,
- cardiac tamponade
- advanced heart failure (HF).
hydrostatic pressure vs osmotic pressure
and what does net filtration pressure mean?
Hydrostatic pressure - is about fluid movement OUT
Osmotic pressure - is about solute concentration drawing fluid IN
Net filtration pressure, the higher it is, the higher the movement OUT of capillaries
What are causes of edema?
1) Increased capillary pressure (increased Pc, heart failure)
2) Decreased plasma proteins (decreased πc, nephrogenic syndrome, liver failure)
3) Increased capillary permeability (increased Kf, toxins, infections, burns)
4) Increased interstitial fluid colloid osmotic pressure (increased π lymphatic blockage)
*What are the heart sounds
S1- mitral and tricuspid valve closure. Loudest at mitral area
S2- aortic and pulmonary valve closure. Loudest at left upper sternal border
S3 (abnormal)- in early diastole during rapid ventricular filling phase. Associated with increased filling pressures (e.g. CHF) and more common in dilated ventricles. Can be normal in children and pregnant women.
S4 (abnormal)(“atrial kick”) – in late diastole. High atrial pressure. Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall. - “stiff noncompliant ventricle during left atrial contraction).
Heart sound splitting
Normal splitting – Inspiration > drop in intrathoracic pressure > increased venous return to the RV > increased RV stroke volume and ejection time > delayed closure of pulmonic valve (P2).
Also decreased pulmonary impedance and therefore increased capacity of the pulmonary circulation
Wide splitting –Delay in RV emptying causes delayed P2 (regardless of breath but especially on inspiration). An exaggeration of normal splitting.
-Right bundle branch block, pulmonary stenosis
Fixed splitting – Left to right shunt, increased RA and RV volume, regardless of breath. P2 will always be greatly delayed.
*Atrial septal defect
Paradoxical splitting – Delay in LV emptying. Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound.
-left bundle branch
-aortic stenosis
Therefore on inspiration,
P2 closes later and moves closer to A2, thereby
“paradoxically” eliminating the split (usually
heard in expiration).
Heart murmurs
MR/TR
AS
VSD
Mitral valve prolapse
[Systolic]
Holosystolic, high-pitched “blowing murmur.”
Mitral—loudest at apex and radiates toward axilla. MR is often due to ischemic heart disease (post-MI), mitral valve prolapse, LV dilatation.
Acute: endocarditis, papillary muscle rupture, trauma, chordal rupture)
Chronic: myxomatous, RF, healed endocarditis, radiation)
Tricuspid—loudest at tricuspid area. TR commonly caused by RV dilatation.
Rheumatic fever and infective endocarditis can cause either MR or TR.
Aortic stenosis (AS): Crescendo-decrescendo systolic ejection murmur (ejection click may be present). LV >> aortic pressure during systole. Loudest at heart base; radiates to carotids. “🌌Pulsus parvus et tardus”—pulses are weak with a delayed peak. Can lead to Syncope, Angina, and Dyspnea on exertion (SAD). Most commonly due to agerelated calcification in older patients (> 60 years old) or in younger patients with early-onset calcification of bicuspid aortic valve.
VSD Loudest at tricuspid area with a L to R shunt. Harsh holosystolic murmur in physical exam.
Mitral Valve prolapse (MVP) Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae). **Most frequent valvular lesion. Best heard over apex. Loudest
just before S2. Usually benign. Can predispose to infective endocarditis. Can be
caused by myxomatous degeneration (1° or 2° to connective tissue disease such as
Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture.
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A 40-year-old male is hospitalized with progressive exertional dyspnea, lower extremity edema and cough. She also describes frequent nocturnal episodes of breathlessness and recent hoarseness. Auscultation reveals a mid-diastolic rumble best heard at the cardiac apex. This patient's hoarseness is most likely caused by: A. Laryngeal edema B. Impaired arterial supply C. Nerve impingement D. Epithelial sloughing E. Vocal cord polyps
C. The patient has mitral stenosis resulting in LA enlargement and pressure on the L recurrent laryngeal nerve (see arrow). This is Ortner’s syndrome
- An 80 year old male with syncope on exertion and weak carotid pulses
- A 26 year old female IV drug user with fever, chills and prominent head bobbing
- A 54 year old male with blood tinged sputum and a history of rheumatic heart disease
- A 39 year old women with nocturnal dyspnea and a systolic blowing murmur
AS, AR, MS, MR - heart
- Aortic stenosis
- Aortic regurg
- Mitral stenosis
- Mitral regurg
Describe pacemaker action potential
Phase 0= Upstroke- VG Ca2+ channels open. VG Na+ channels are inactivated at less negative resting voltage.
Phase 1 and 2 = absent
Phase 3= inactivation of the Ca2+ channels and increase activation of the K+ channels resulting in K+ efflux
Phase 4= slow spontaneous diastolic depolarization due to If (“funny current”). If channels
responsible for a slow, mixed Na+/K+ inward current; different from INa in phase 0 of ventricular
action potential. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA
node determines HR. ACh/adenosine decrease the rate of diastolic depolarization and decrease HR, while
catecholamines increase depolarization and increase HR. Sympathetic stimulation increase the chance that If channels are open and thus increase HR.
Name the AV blocks
1st degree – PR interval is prolonged (>200 msec). Benign and asymptomatic. No treatment required.
2nd degree
-Mobitz type I (Wenckebach)- Progressive lengthing of the PR interval until a beat is “dropped”. Usually asymptomatic
-Mobitz Type II – Dropped beats that are not preceded by a change in length of the PR interval (as in type I). May progress to 3rd- degree block. Often treated with pacemaker. (one beat drop 2)
3rd degree (complete) –Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than ventricular rate. Usually treated with pacemaker. Lyme disease and MIs are causes.
Barroreceptor reflex
Baroreceptor Reflex
Aortic arch transmits via CN X. Carotid sinus transmits via CN IX.
High BP activates baroreceptor activity, which the solitary nucleus integrates and then activates the PSNS (and inhibits the SNS) to slow heart rate and reduce BP
Low BP reduces baroreceptor activity, which the solitary nucleus integrates and activates the SNS (and inhibits the PSNS) to increase HR and increase BP
A 20-year-old female presents to the physician following a near syncopal episode. His blood pressure is 90/60 mmHg and his heart rate is 180/min and regular. Gentle neck massage just below the angle of the right mandible produces an immediate reduction in his heart rate to 72 bpm and his BP increased to 110/70. This maneuver (carotid massage) improved the patient’s symptoms by:
This is a patient with paroxysmal supraventricular tachycardia (PSVT), the most common paroxysmal tachycardia. PSVT typically results from a re-entrant impulse traveling through slowly and rapidly conducting segments of the AV node. Simple treatments include maneuvers that increase cardiac PSNS tone, such as carotid sinus massage and the Valsalva maneuver. The PSNS primarily functions to slow the heart rate by slowing conduction through the AV node, which is specifically beneficial for this arrhythmia because it abolishes the re-entrant circuit and the arrhythmia.
What are noncardiac effects of alpha1 stimulation
- 💦Bladder outlet obstruction/smooth muscle constriction aka urinary retention.
- Mydriasis - ciliary body contracts
- Increased intraocular pressure - reduces reuptake of aqueous humor, acute angle closure glaucoma.
Besides inhibiting NE and acetylcholine release from presynaptics, what noncardiac function do alpha 2 receptors play?
They affect pancreatic beta cells and also inhibition of insulin release
They also decrease production of aqueous humor.
Alpha 2, always think blocking release.
What factors increase contractility?
What factors decrease
Contractility (and SV) increase with:
-Catecholamine stimulation via β1 receptor:
-Ca2+ channels phosphorylated >increasedCa2+
entry >increasedCa2+-induced Ca2+ release and increasedCa2+ storage in sarcoplasmic reticulum
-Phospholamban phosphorylation >active Ca2+ ATPase >increased Ca2+ storage in sarcoplasmic reticulum - a protein that negatively regulates SERCA, increasing the uptake and storage of calcium in SR
-increased intracellular Ca2+
-decreased extracellular Na+ (decreased activity of Na+/Ca2+
exchanger)
-Digitalis (blocks Na+/K+ pump
> increased intracellular Na+ > decreased Na+/Ca2+
exchanger activity > increased intracellular Ca2+)
Contractility and SV decrease with:
-β1-blockade (decreased cAMP)
-HF with systolic dysfunction
-Acidosis
-Hypoxia/hypercapnia (decrease Po2/ increase Pco2)
- Non-dihydropyridine Ca2+ channel blockers
What are the function of dopamine receptors in the cardiac system?
- Natriuresis
- Vascular smooth muscle relaxation (renal splanchnic)
What are properties of normal endothelium?
Endothelium dependent vasoregulation
- Dilation: NO, Prostacyclin
- Endothelin: strongest vasoconstrictor substances
Antihypertrophic properties
-inhibition of vascular smooth muscle cells proliferation and migration
Modulation of immune response
-resist WBC adhesion and attachment
Anticoagulant, antithrombotic, profibrinolytic function
- heparan sulfate
- thrombomodulin
Steps of atherosclerosis
- damage to endothelium (large,medium sized muscular arteries especially at bifurcations) - disturbed shear features low flow, flow reversal and an altered EC phenotype and behavior
- high EC turnover, poor alignment, inflammatory genes, high permeability, oxidative stress (ROS), prothrombotic - prostacyclin and NO decreased - LDL oxidation
- Scavenger receptor - macrophages take up oxidized LDL becoming foam cell
- Oxidized LDL and damage signals expression of adhesion molecules, monocyte attachment, transmigration, monocyte activation into more macrophages.
- Cell necrosis leaves a lipid pool
- Macrophage cytokines stimulate smooth muscle cells migration and replication, matrix synthesis eventually forming fibrous cap.
- Active macrophages eventually weaken the plaque cap, exposure of matrix to platelets and mural thrombus formation.
Turner syndrome
Female (45, XO)
Short stature (if untreated; preventable with growth hormone therapy), ovarian dysgenesis (streak ovary), shield chest, bicuspid aortic valve, coarctation (femoral < brachial pulse),
lymphatic defects (result in webbed neck or cystic hygroma; lymphedema in feet, hands) horseshoe kidney. Most common cause of 1° amenorrhea. No Barr body.
Menopause before menarche. decrease estrogen leads to increase LH, FSH. Sometimes due to mitotic error - mosaicism (eg,
45,XO/46,XX). Pregnancy is possible in some cases (IVF, exogenous estradiol-17β and progesterone).
Congenital defect: Bicuspid aortic valve, coarctation of aorta, dissection of aorta
Most girls and women with Turner syndrome have normal intelligence. Developmental delays, nonverbal learning disabilities, and behavioral problems are possible, although these characteristics vary among affected individuals.
A man starts taking metoprolol, how would each of the following parameters change
Cardiac myocyte [camp]
JGA cell [camp]
Vascular smooth muscle [cAMP]
Cardiac myocyte [camp] - decreased
JGA cell [camp] decreased
Vascular smooth muscle [cAMP] no change
A 48 yr old woman comes to her physicians office with a 1 month history of dyspena on exertion that resolves with rest. Her other medical problems include hypertension and hypercholesterolemia. An exercise stress test reveals ST segment elevation duringtesting, however the patient is symptom free during that time period. Which condition is likely comorbid
Diabetes mellitus
A 4 month infant presents with repeated episodes of tachypnea, poor feeding and failure to thrive.On PE, the child is pink and her extremities are warm. There is aloud, harsh holosystolic murmur that is herd best at the left sternal border. A systolic throll is palpated over the region .On CXR the heart is enlarged and there are increased pulmonary vascular markings. The most likely diagnosis in this patient is.
And what is the underlying anatomic location?
Ventricular septal defect
Membranous interventricular septum
What indicates the presence of an acute myocardial infarction in this patient
elevated serum troponins and ST elevation
-not:
t wave inversion, ST depression, Q waves
A 13 year old female presents to the office, she has no significant past medical history. ON cardiac auscultation you determine that there is fixed splitting of her second heart sound.
A defect in atrial septum.
A previously healthy 12 year old is brought to ER after being stung by a bee on his right forearm. Fifteen minutes later he complained of shortness of breath and was observed by his parents to be wheezing. On exam he is tachycardiac and hypotensive, repsiratory examination reveals wheezing with mild subcostal retractions,. his capillary refill time is delayed. What drug to give
Epinephrine: first line for anaphalactic shock
A Swan-Ganz Catheter is placed to evaluate a postoperative patient with hyptension and suspected heart failure. The calculated cardiac index is low and the pulmonary artery wedge pressure that is obtained is 2 mm Hg (normal 6-15 mm Hg). What is the msot likely diagnosis in this patient?
Hemorrhage - really low left atrium pressure.
67 year old’s ECG shows a wide QRS complex and broad notched R wave in V6. In addition there are absent R and prominant S waves in V1. What auscultory finding is consistent?
paradoxically split S2
2 year old is brought to office because of poor activity tolerance and increased dyspnea with exertion. In the office as the toddler is crying she appears to be cyanotic. A heave is present anteriorly along the left sternal border. A harsh systolic ejection murmur is heard over the upper left sternal border which decreases as the baby is crying. A single S2 is auscultated. What is the underlying condition and likely mechanism for the systolic murmur that is auscultated
Tetralogy of Fallot
Subvalvular pulmonic stenosis
54 year old with hypercholesterolemia is about toe begin on atorvastatin. Which serum chemistry should be obtained as a baseline
Serum transaminases
Which of the following are platelet P2YI ADP receptor
- enoxaparin
- bivalirudin
- aspirin
- clopidogrel
- tirofiban
Clopidogrel
