HSF 2 T3

What is the functional result of a large Patent Foramen Ovale (PFO)?

Oxygenated blood is shunted to the right atrium (L->R shunt)

The second heart sound (dub) occurs during which phase of the cardiac cycle?

Beginning of diastole (closure of semilunar valves)

The coronary arteries are the only systemic arteries that perfuse during which phase?

Ventricular diastole

Visceral pain fibers (nociceptive) from the heart typically follow which pathway back to the CNS?

Sympathetic cardiopulmonary splanchnic nerves

During a transesophageal echocardiogram (TEE), the ultrasound probe is passed into the esophagus. Which cardiac chamber is most clearly visualized immediately anterior to the probe?

Left atrium

If an electrical signal fails to reach the anterior papillary muscle of the right ventricle, which specific anatomical structure within that ventricle might be damaged?

Septomarginal trabecula

A narrowing or obstruction in the smooth-walled outflow tract of the left ventricle just inferior to the aortic valve would be located in the:

Aortic vestibule

A surgeon reaches into the pericardial sac and slides their fingers into a 'blind' sac posterior to the left atrium, bounded by the pulmonary veins. Which sinus are they in?

Oblique pericardial sinus

During cardiac surgery, you can stop circulation in this are by making a stitch through the sinus and pulmonary trunk and ascending aorta to diver blood through a bypass machine. You reach by placing a finger posterior to the pulmonary trunk and aorta and anterior to the SVC, what have you just entered?

Transverse pericardial sinus

Prolonged PR Interval

AV node block

Shortened PR interval

Supraventricular arrhythmias

QRS complex is tall because of

Hypertrophy

QRS complex is short because of

Damaged muscle from MI

Typical, wide QRS is from

Bundle branch blocks

Abnormal, wide QRS

PVCs

Long QT is due to

Hypocalcemia

Short QT is due to

Hypercalcemia

If the first area to depolarize is the first area to repolarize (like an electrical wire), we get a/an

Inverted T wave

Causes of Inverted T wave

Coronary ischemia, hypertrophy, BBB

Mean axis of depolarization

59 degrees

Right shift deviation of axis of depolarization is from

Deep inspiration, standing up

Left shift of axis of depolarization is due to

Deep expiration, lying down, obesity

How to differentiate between left ventricular hypertrophy and left BBB when both cause left shift?

Hypertrophy causes increased QRS magnitude, BBB causes increases QRS duration

How long is a normal QRS interval?

0.1s.

Slow HR

Bradycardia, AV/SA block, BBB

What causes increased HR?

Premature contraction of atrium, AV node/junctional, ventricles; sinus tach, SVT, Vtach

Sinus Bradycardia is

Vagal nerve stimulation to slow HR

SA node block is missing a

P wave prior to next QRS

AV block causes

Vagal stimulation, ischemia, calcification, inflammation, drugs

2nd Degree AV Block Types

Type 1: increasing PR interval until dropped beat with a P wave. Type 2: regular PR interval with random missed beats with a P wave.

3rd degree AV block

Complete blockage; P waves and QRS at mutually exclusive intervals; intervals are regular

RBBB EKG changes

V1 M, V6 W

LBBB EKG changes

V1 W, V6 M

Premature Atrial Contractions

Accelerated rate, shortened PR interval, P wave right before QRS

AV node premature complex (premature junctional complex)

Accelerated rate, inverted P wave, normal QRS

Premature ventricular contractions

Accelerated rate, nonexistent PR, hidden P wave, widened QRS

Tachycardia

Accelerated rate

SVT

Accelerated rate, shortened or nonexistent PR interval, normal QRS

How to treat SVT

Adenosine (open K+, hyperpolarization, inhibit cAMP, slows conduction) and Vagal Maneuvers (baroreceptor reflex)

SVT vs Junctional Tach

Junctional Tach is a type of SVT. High junctional origin=inverted P wave before QRS. Mid-junction=hidden P wave. Low junctional=P wave after QRS

VTach

Accelerated rate, nonexistent PR interval, widened QRS (especially in lead II and V5)

Multiple PVCs can lead to

Vtach

>3 consecutive PACs=

Non-sustained atrial tachycardia

>30 seconds of PACs=

Sustained atrial tachycardia

Torsades

Twisting of the QRS complexes, associated with LQTS/Vtach/Vfib

Wolff-Parkinson-White Syndrome EKG

Delta wave (slanting up QRS+shortened PR). Accessory pathway may allow for SVT.

Wolff-Parkinson-White syndrome is from

Bundle of Kent present at birth causing extra electrical pathway allowing depolarization to spread to ventricle without AV node pause

Dehydration can lead to

Afib

What can lead to Afib?

PACs > Atach > Afib

Which arrythmia is associated with blood clots

Afib

Afib EKG

Irregular rate, nonexistent P wave, normal QRS

In Vfib,

Fatal, various areas of the ventricle become hyperexcited, no real contraction of the ventricles occurs

Which medication explicitly targets and reduces the funny current (If) without directly changing myocardial contractility?

Ivabradine

Cardiac Output

CO= HR * SR. Men=5.6 L/min, Women 4.9 L/min

Ways to measure Cardiac Output

ECG thru left ventricular outflow tract. Swan Ganz thru balloon in pulmonary artery to measure left atrial pressure. Fick: Q=VO2/(CaO2-CvO2)

Angiotensin II (RAAS) acts thru

AT1 to induce release of Ca2+ in cardiac myocytes, also releases NE from nerve terminals. Inotropic agent

Insulin binds to IR and gives X thru the PI3K pathway

Positive inotropic effects

Glucagon binds to GR to include cAMP and blood glucose, it will have X

Positive chronotropic and inotropic effects

Hypokalemia (Low K+ in the extracellular fluid) gives a lower T wave and

Hyperpolarizes myocytes; arrhythmias; cardiac arrest - Increases RMP, bringing it closer to threshold potential

Hyperkalemia (High K+ in the extracellular fluid) gives a high T wave and

Depolarized membrane potential; muscle weakness; blocks conduction; arrhythmias - Decreases RMP, moving it further from threshold potential

Calcium levels will change the

QT interval

Increased preload means

Greater stress=greater contraction, leads to increased EDV and venous return > opens the stroke volume more to the right

Increased afterload can be caused from hypertension

Force that the contracting myocytes must overcome from large increases in arterial pressure or aortic pressure/aortic stenosis, impairs stroke volume and thus CO > decreases stroke volume by shifting up and to the right

Increased norepinephrine release to the ventricle will cause

LV volume to decrease and LV pressure to increase, shifts to the left and up while opening stroke volume

Digitalis/digoxin

Cardiac glycoside, “arrow poison”, inhibits Na/K pump, increases Ca2+ (inotropic), slows conduction of AV node and depresses SA node to slow HR by vagus nerve, can slow HR and prevent arrhythmias (SVT), can cause arrhythmias due to calcium entry

Dobutamine

B1 adrenergic agonist, increases Ca2+ (inotropic), increases HR, vasodilator, can cause arrhythmias

Milrinone

Phosphodiesterase 3 inhibitor to increase cAMP, increase Ca2+ (inotropic), vasodilator, can cause arrhythmias

Levosimendan

Increases calcium sensitization of troponin C (inotropic) without increasing Ca2+ or HR

Stroke volume

SV=EDV-ESV

Which of the following occurrences alone would increase the width of the P-V loop?

Decreased afterload or increased EDV

Which layer contains the endothelium that lines the lumen of all vessels

Tunica intima

Which layer contains smooth muscle cells and elastic fibers?

Tunica media

Which layer contains collagen fibers?

Tunica adventitia

Sildenafil/Viagra

Inhibit cGMP degradation by phosphodiesterases, inhibiting Ca2+ entry and activating MLC phosphatase by activation of PKC, leading to smooth muscle relaxation/vasodilation

Arteries

Expand to hold blood, compliant, elastic recoil maintains consistent pressure

Arterioles

Lots of smooth muscle and surface area, can change blood flow to different tissues

Capillaries

Only contain endothelial cells, allowing 1 RBC to pass at a time; moves blood slowly to allow for maximal time for nutrient and gas exchange

Veins

Large diameter, reservoir for blood; contains valves to induce one-way blood flow

Left ventricle BP

120/5

Left and right (CVP) atrium BP

2

Aorta and large arteries BP

120/80

Capillary BP

17

Veins and capillaries BP

7

Right ventricle BP

25/2

Pulmonary arteries BP

25/8

Mean arterial blood pressure

2/3 DP + 1/3 SP

Mean arterial blood pressure 2nd equation (SVR=systemic vascular resistance)

MABP = CO * SVR

Arteriosclerosis is the general term for hardening of arteries

Loss of compliance, collagen replaces elastic fibers, increase in systolic pressure and LV hypertrophy

In low risk patients with hypertension, antihypertensive treatment

Did not improve mortality or CV outcomes but instead led to adverse events

Velocity of flow

Flow rate / cross sectional area

Velocity is

Inversely related to cross sectional area

Flow rate

F=delta P/R

Cardiac output

CO=(MABP-CVP)/SVR

Poiseuille’s law (resistance and flow)

R=8nl/πr^4 or F=πΔPr^4/8nl

Radius is controlled by

Local control, circulating hormones, sympathetic reflexes

Resistance equations

In series:Rtotal=R1+R2+… In parallel:Rtotal=1/((1/R1)+(1/R2)+…)

Total blood flow through all the arterioles of the body is equal to

Cardiac output

Variation in blood flow to individual tissues is possible because of

Arterioles in the body are arranged in parallel

Metabolic hyperemia

Increase in metabolic products during tissue metabolism inducing vasodilation which increases blood flow; Increase in Adenosine, CO2, H+, Phosphates; Decrease in O2