USMLE CVS

What are 2 types of the coarctation of the aorta?

1.Preductal coarctaion (associated with Turner syndrom)

2. Postductal coarctation

How can you suspect the coarctation of the aorta in a patient?

In an infant - poor weight gain, feeding problems, breathing probems (left ventricle hypethrophy as a reaction to the pressure increased) + hypertensive in the upper body and hypotensive and cyanose with weak pulse in the lower limbs

In adults - hypertensive in the upper body and hypotensive with weak pulse in the lower limbs, as result of the left ventricle hypethrophy - pulmonary hypertension+ costal notching (enlargment of the intercostal arteries, can be seen on X-ray). Dissecting aorta aneurysm + intracerebral hemorrhage.

Velocity

Velocity= Q/CSA (cm/sec), low in capillaries, high in the aorta (turbulence).

What is the cause of the patent foramen ovale?

Failure of septum primum and septum secundum to fuse after birth (right tp left shunt+paradoxical emboly)

Down Syndrom heart defects?

About 80% have an atrial septal defect or ventricular septal defect with the former being more common. Congenital heart disease can also put individuals at a higher risk of pulmonary hypertension, where arteries in the lungs narrow and cause inadequate blood oxygenation. Some of the genetic contributions to pulmonary hypertension in individuals with Down Syndrome are abnormal lung development, endothelial dysfunction, and proinflammatory genes.Mitral valve problems become common as people age, even in those without heart problems at birth. Other problems that may occur include tetralogy of Fallot and patent ductus arteriosus.

Which conditions are most highly to cause holosystolic heart murmur?

Ventricular septal defect, mitral regurgitation or tricuspid regurgitation.

https://www.youtube.com/watch?v=9bjWdJ-dfg0

What embryology defect is present in DeGeorge syndrome?

22q11.2 deletion

Failure to develop 3 and 4 branchial arches - truncus arteriosis, tetralogy of Fallot, thymic hypoplasia, hypoparathyroidism, cleft facial disease

Factors affecting systolic pressure

Factors affecting dyastolic pressure

1. TPR (direct)

2. HR (direct)

3. SV (direct)

Factors affecting pulse pressure

PP=SV/C

1. SV (direct) acute and chronic

2. Compliance(arterial) (inverse) chronic

Mean arterial pressure

A normal MAP is about 90 mmHg.

Factors affecting mean arterial pressure

Influence of the RAP on MAP

Aortic regurgitation, type of murmur?

Early diastolic, decrescendo hight-pitched blowing murmur, best heard along the lower left sternal body 2 intercostal space.

Becks triad (cardiac tamponade)

1. Diminished heart sounds

2. Decreased arterial pressure

3. Increased jugular venosus pressure

Effects of the arterial baroreceptors (aortic arch and carotid sinus)

1. Stimulated by the change (rise) in the intravascular pressure through 9 and 10 nerve to the medulla

2. Stimulates parasympathetis, inhibits sympathetic (BP increase - symp. decrease, parasym. increase and vice versa)

3. Activation inhibits ADH

What heart complication might be expected in the person with Kawasaki syndrom?

Coronary artery aneurysms (20%)

The Poiseuille equation

Q=P1-P2/R, P=QR, pressure, flow, resistance (for arterial circuit)

Effects of the length,viscosity and radius on the resistance

R=8ņ (viscosity)*length/пr4

the greater radius the less resistance ( TPR the most in arterioles)

length is constant, 50% reduce in length - 50% reduce resistance

the greater the viscosity the greater the resistance

Reynold’s number

Diameter*velocity*density/viscosity

>2000 - turbulent flow

Most common adult congenital heart disease?

Atrial septal defect

1.Midsystolic ejection murmur at the pulmonic area

2.Fixed spitting of S2

3. Prominent right ventricular cardiac impulse

4.Right atrial and ventricular hyperthrophy

Pericarditis

1. Sharp stabbing pain that varies with breathing

2. Often positional and relieved by leaning forward

3. Diffuse ST elevations with upright T-waves

The most common reason for aortic stenosis?

Bicuspid aortic valve (systolic click)

Surface projections of the heart

Heart chambers projections on the chest wall

Murmurs projections

+tricuspidal stenosis - 5 intercostal space on the left

dyastolic murmurs - tricuspial, mitral stenosis + aortic and pulmonary valves insufficiency

systoic murmurs - tricuspial, mitral insufficiency+ aortic and pulmonary valves stenosis

Projections of the normal heart sounds

Embryology tissue of the heart

splanchnic mesoderma 3,5-4 weeks of development + migration of the neural crest cells - heart tube (truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, sinus venosus)

Types of the atrial septum defects

1. Primum ASD (less common, endocardial cushion defect, might be associated with atrioventricular septum defect (membranosus part) and defect of the atrioventriculat valves)

2. Secundum (more common, excessive apoptosis)

If too sever might evolve into Eisenmenger complex (pulmonary hypertension + right to left shunts). The same is with the ventricular septal defect.

3 cyanotic congenital heart abnormalities (aorticopulmonary septum defects)

1. Truncus arteriosus (no APS)

2. Tetralogy of Fallot ( APS more on the right side)

3. Transposition of great vessels (does not goes spiral)

Compliance

C=V/P, mostly for venosus system

Wall tension (LaPlace relationship)

T is directly proportional to Pr (pressure, radius)

Aortic aneurysm (due to high velocity) increase wall tension - might burst

Dilated heart failure - increased wall tension

Systolic performance (pressurises and ejects) is determined by?

1. Preload

2. Contractility

3. Afterload

Preload

Load or prestretch on ventricular muscle at the end of diastole.

LV preload - LVEDV (60-110 ml/m2), LVEDP (3-12 mmHg) (Directly measured in the ventricle ); CVP (4-12 cmH2O/3-8 mmHg), PCWP (estimates left atrial pressure) (4-12 mmHg), RAP (2-6 mmHg) ( measured in the venous system)

Contractility and heart rate effects on the heart

Systolic interval decreased: contractility effect

Diastolic interval decreased: heart rate effect

Afterload is increased?

1. Aortic pressure is increased

2. SVR is increased

3. Aortic stenosis

Frank-Starling curve

Rise in ventricular performance as preload increases

Ventricular volumes

End-diastolic volume

End-systolic volume

Stroke volume = EDV - ESV

Ejection fraction = SV/EDV more than 55% in a normal heart

Pressure overload

1. Increased contractility, increased performance-normal CO(initially)

2. Chronically- concentric hypertrophy, increase in wall thickness.

3. Decreased compliance, diastolic dysfunction followed by systolic dysfunction

Volume overload

1. Well tolerated if developed slowly

2. Chronically- eccentric hypertrophy, compliance is not compromised, diastolic function is maintained

3. Systolic dysfunction

Cardiomyopathy

1. Dilated (diastolic function remains intact, increased sympathetic stimulation, systolic dysfunction, mitral and tricuspidal failure)

2. Restrictive - decreased ventricular compliance with diastolic dysfunction and a decrease in a ventricular cavity size (increased filling pressure, ventricular hypertrophy +-, systolic close to normal

3. Hypertrophic (septal or left ventricular hypertrophy is unrelated to a pressure overload, diastolic dysfunction due to muscle stiffness, HOCM. Сrescendo-decrescendo systolic murmur heard best at the apex

Factors that cause vasoconstriction

1. Norepinephrine (binds alpha-1-receptors to activate Gq (heterotrimeric G protein alpha, activate beta-type phosholipase C-release Ca into cytoplasm, activate protein kinase C)- vasoconstriction, releases from sympathetic postganglionic neurons.

2. Epinephrine released from the adrenal medulla activates alpha-1-receptors.

3. Angiotensin 2 via the AT1 receptor (Gq)

4. Arginine vasopressin (AVP, ADH) via the V1 receptor (Gq).

Vasodilation mechanisms

1. Decreased sympathetic activity

2. NO released from the vascular endothelium

3. Adenosine, CO2, K+, H+

4. EPI stimulates vascular beta-2-receptors (Gs-cAMP)

Venous return

1. Determines preload

2. Pressure flow resistance

3. RAP is downstream pressure for VR, mean systemic filling pressure (Psf) - upstream pressure

4. Increase in blood volume increases Psf and VR

5. Decrease in blood volume decreases Psf and VR

6. Decrease in venous compliance (sympathetic stimulation, muscle pump) increases Psf and VR

7. Increase in compliance (sympathetic inhibitions, venodilators, alpha block) decreases Psf and VR

Determinants of the CO

1. HR

2. Contractility

3. Afterload

4. Preload

CO

CO=HR*SV

High HR decreases filling time for the ventricles - can decrease SV

Exercise - sympathetic activation: decreases systolic intervals, increases contractility, venoconstrict, increases conduction velocity, skeletal muscle pump - maintain SV.

Contractility

Direct relation between CO

Afterload to CO

Inverse relation between afterload and CO

Preload in CO

Direct relation between preload and CO

VR determines preload

CO/VR curve

Resistance in CO

If arterioles vasodilate VR increases

Arteriolar vasodilation decrease afterload

If arterioles vasoconstrict VR falls, CO falls (F-S curve)

Arteriolar vasoconstriction increases afterload

Psf: increasing vascular volume

1. Increase vascular volume (infusion, RAAS) of decreasing venous compliance (sympathetic stimulation, muscle pump, exercise, lying down) increases Psf

2. Increases CO (F-S)

Psf: decreasing vascular volume

1. Decreasing vascular volume Haemorrhage, burn trauma, vomiting, diarrhea) or increasing venous compliance ( inhibit sympathetics, alpha block, venodilators, standing up right) decreases Psf

2. Reduce CO (F-S)

Fick principle of blood flow

1. Used to calculate blood flow

2. Flow=uptake (consumption)of oxygen/A-V (oxygen content difference across the organ

3. Can calculate oxygen consumption (VO2)

   VO2=CO*(CaO2 (total arterial oxygen content )-CvO2 (total venous oxygen content))

   Pulmonary venous O2 content - 0,2 ml O2 per ml blood

4. For any given O2 consumption, a decrease in delivery results in increased lactic acid production and possible hypoxia damage, decrease in the amount of the venous O2

Intrinsic blood flow regulation

1. Metabolic mechanism (flow is regulated by constricting and dilating smooth muscle around arterioles)

   tissue produces a vasodilators metabolite that regulates flow (K, H, CO2, adenosine) - dilation of arteriolew when concentration increases and vice versa

2. Myogenic mechanism

   arteriolar stretch and surrounding muscles ( change in pressure)

Extrinsic regulation

EPI can cause vasodilation via B2 receptors

Cerebral circulation

If arterial PO2 is normal or above cerebral blood flow is regulated via arterial PCO2

A large decrease in arterial O2 increases cererbal flow (high attitude pulmonary edema)

Baroreceptors don’t affect flow

Fetal circulation system

55% of CO goes to the umbilical cord, highest O2

Fetal Hb has a very hight affinity to O2

CVS stress: exercise

In the arterial system:

1. PO2 normal, Hb fully saturated

2. PCO2 normal

3. Oh stable or decrease due to production of lactic acid

4. MAP slight increase

5. Temperature slight increase

6. TPR large decrease, dilation of the skeletal muscle

Exercise and systemic venous circulation

Normal cardiac cycle

Heart sounds

S1-mitral and tricuspid valves closure

S2- closure of the aortic and pulmonic valves ( during inspiration-physiological splitting, right heart delayed)

Heart sounds

S3-After opening of the AV valves during rapid filling of ventricle. Normal in kids. Pathological - volume overload.

S4 - atrium contracts against a stiff ventricle ( concentric hypertrophy, aortic stenosis, MI)

Auscultation

Venous pulse

a-atrial systole

c-bulging of the tricuspid valve

x-atrial diastole

v-venous return during systole of the ventricle

y-opening of the tricuspid valve

Abnormal venous pulses

Pressure-volume loops

S3 heart tone

Volume overload, appears in diastole due to high ventricle compliance, can be heard at children, pregnant women in normal, in pathology indicates heart failure due to volume overload (severe regurgitation, VSD). Gallop rhythm.

Digoxin

1. Na/K ATPase inhibitor - increases contractility

2. Adverse effects: hyperkalemia, nausea, vomiting, diarrhoea, blurry yellow vision, arrhythmias, AV block

Hydralazine

Increases cGMP-smooth muscle relaxation ( arterioles vasodilation is more the veins - afterload reduction). Prevents oxidation of nitric oxide and thereby lowering systemic vascular resistance and mean arterial pressure.

Can be used in pregnant women (sever hypertension, HF), can be administered with B-blockers to prevent reflex tachycardia

Side effects- tachycardia, agina, drug-induced lupus(+procainamide, isoniazide, methyldopa)

Alpha receptors

There are two types of alpha-adrenergic receptors; alpha-1 and alpha-2. Both are G-protein coupled receptors (GPCR); however, the downstream effects of the two are different. The alpha-1 receptor is of the Gq type, resulting in activation of phospholipase C, increasing IP3 and DAG, and ultimately increasing the intracellular calcium concentrations leading to smooth muscle contraction and glycogenolysis.The alpha-2 receptor acts as an allosteric inhibitor through Gi function, leading to an inhibition of adenylyl cyclase, decreasing the formation of intracellular cAMP.  It also leads to a reduced amount of cytoplasmic calcium, which decreases neurotransmitter release and central vasodilation.Epinephrine and norepinephrine have relatively equal affinities for both types of alpha-receptors, with other drugs used in shock having a higher selectivity for the alpha-1 receptor.  

Mitral stenosis murmur

Mid-diastolic rumble with an opening snap at the apex, loud S1. Better heard at the apex.

https://m.youtube.com/shorts/kpnuyFuQXjk

Beta-receptors

1- fat, heart, kidney ( raise contractility, heart rate, conduction)

2-arterial and bronchus smooth muscle (relaxation)

Equilibrium potentials of important ions

K-95mV

Na+70mV

Cl-76mV

Ca+125mV

The only receptor both voltage and ligand-gated

NMDA

Ligands-aspartate and glutamate

Memory and pain transmission

Pulmonary regurgitation murmur

Diastolic, decrescendo murmur best heard at the left second intercostal space, increasing with inspiration