FA Cardiology- Anatomy & Physiology

What factors affect stroke volume?

*S*troke *v*olume is affected by *c*ontractility, *a*fterload and preload. SVCAP. Increased SV with: -increased contractility (anxiety, exercise, pregnancy) -increased preload -decreased after load A failing heart has decreased SV (systolic and/or diastolic function)

Cardiac receptors transmit signals via which nerves?

1) Aortic arch transmits vis *vagus* nerve to *solitary nucleus of medulla* 2) Carotid sinus, the dilated region at carotid artery bifurcation) transmits via *glossopharyngeal* nerve to *solitary nucleus of medulla* BOTH respond to changes in blood pressure.

What are the variables that affect cardiac output?

1) Stroke volume 2) Contractility 3) Myocardial oxygen demand 4) Preload 5) Afterload 6) Ejection fraction

What is Pulmonary Capillary Wedge Pressure (PWCP)?

A good measure of left atrial pressure. *In mitral stenosis, PCWP > LV diastolic pressure.* Measured with pulmonary artery catheter (Swan-Ganz catheter).

What factors affect phase 4 of pacemaker action potential?

ACh/adenosine decrease the rate of diastolic depolarization and decrease HR. Catecholamines increase depolarization and increase HR. Sympathetic stimulation increases the chance that If channels are open, therefore increasing HR.

What factors affect afterload?

After load is approximated by MAP (mean arterial pressure; i.e. how much the system is entering back on the heart that the ventricle has to pump against). Increased afterload --> increased pressure --> increased wall tension per LaPlace's law. LV compensated for increased after load by hypertrophy in order to *decrease* wall tension. I.e. longterm high BP can cause LV hypertrophy. Vasodilators (ex hydralazine) decrease *arterial* afterload ACE inhibitors and ARBs decreased both preload and afterload.

How do cardiac baroreceptors respond to hypotension?

Decreased arterial pressure --> decreased stretch --> decreased afferent baroreceptor firing --> increased efferent sympathetic firing and decreased effect parasympathetic stimulation --> *vasoconstriction, increased HR, increased BP*. Important response to severe hemorrhage.

What is a vasovagal response?

Diaphoresis, vomiting, low BP, low pulse pressure, due to stimulation of vagal nerve; vagal stimulation of SA node. No reflex tachycardia to HTN. Treat with *atropine*. HF due to reduced cardiac output. A reflex of the involuntary nervous system that causes the heart to slow down (bradycardia) and that, at the same time, affects the nerves to the blood vessels in the legs permitting those vessels to dilate (widen). As a result the heart puts out less blood, the blood pressure drops, and what blood is circulating tends to go into the legs rather than to the head. The brain is deprived of oxygen and the fainting episode occurs.

How does the pressure gradient work?

Drive blood flow from high pressure to low pressure.

What is ejection fraction?

EF = SV/EDV or (EDV-ESV)/EDV Left ventricular EF is an index of ventricular contractility; normal EF >/= 55% EF decreased in systolic HF. EF is *normal* in diastolic HF.

What are the causes of edema?

Edema = excess fluid outflow into interstitium commonly caused by: - increased capillary pressure (ex. HF) - decreased plasma protein (ex. nephrotic syndrome, liver failure) - increased capillary permeability (ex. toxins, infections, burns) - increased interstitial fluid colloid osmotic pressure (ex. lymphatic blockage)

What is the Starling Curve?

Force of contraction is proportional to end-diastolic length of cardiac muscle fibers (preload). In other words, as a larger volume of blood flows into the ventricle, the blood will stretch the walls of the heart, causing a greater expansion during diastole, which in turn increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during systole.

What is a pressure-volume loop?

Graphical representation of the phases of the *left ventricle*. 1) Isovolumetric contraction. Period between mitral valve closing and aortic valve opening. Period of highest O2 consumption. 2) Systolic ejection. Period between aortic valve opening and closing. 3) Isovolumetric relaxation. Period between aortic valve closing and mitral valve opening. 4) Rapid filling. Period just after mitral valve opening. 5) Reduced filling. Period just before mitral valve closing.

What factors determine autoregulation?

Heart- Local metabolites (vasodilatory): adenosine, NO, CO2, decreased O2 Brain- Local metabolites (vasodilatory): CO2 (pH) Kidneys- Myogenic (ANP and BNP) and tubuloglomerular feedback Lungs- Unique in that *hypoxia causes vasoconstriction* so that only well-ventilated areas are perfused. In other organs, hypoxia causes vasodilation. Skeletal muscle- Local metabolites during exercise: lactate, adenosine, K+, H+, CO2 Skin- sympathetic stimulation most important mechanism: temperature control

What factor has the greatest effect of blood viscosity?

Hematocrit Viscosity is increased in hyperproteinemic states (ex. multiple myeloma) and polycythemia Viscosity is decreased in anemia

What is autoregulation?

How blood flow to an organ remains constant over a wide range of perfusion pressures.

In which states is pulse pressure increased?

Hyperthyroidism Aortic regurgitation Aortic stiffening (isolated systolic hypertension in elderly) Obstructive sleep apnea (increased sympathetic tone) Exercise (transient)

How does cardiac muscle a.p. differ from skeletal muscle a.p.?

In contrast to skeletal muscle: - cardiac muscle a.p. has a plateua, which is due to Ca2+ influx and K+ efflux - myocyte contraction occurs due to Ca2+ induced Ca2+ release from the sarcoplasmic reticulum - Cardiac nodal cells spontaneously depolarize during diastole, resulting in automaticity due to If channels ("funny current" channels responsible for a slow, missed Na+/K+ inward current) - cardiac myocytes are electrically coupled to each other by gap junctions.

When does coronary blood flow peak?

In early diastole

What happens in phase 3 of pacemaker action potential?

Inactivation of the Ca2+ channels and increased activation of K+ channels, leading to increased K+ efflux.

What factors affect myocardial oxygen demand?

Increased Myo*CARD*ial O2 demand with increased: - *C*ontractility -*A*fterload (proportional to arterial pressure) - heart *R*ate - *D*iameter of ventricle (increased wall tension)

How do cardiac baroreceptors contribute to Cushing reaction (triad of HTN, bradycardia, respiratory depression)?

Increased intracranial pressure constricts arterioles --> cerebral ischemia --> increased pCO2 and decreased pH --> central reflex sympathetic increase in perfusion pressure (HTN) --> increased stretch --> peripheral reflex baroceptosr induced-bradycardia.

What is the effect of carotid massage?

Increased pressure on carotid sinus --> increased stretch --> increased afferent baroreceptor firing --> *increased AV node refractory period --> decreased HR*

What is the hemodynamic effect of an organ removal (ex. nephrectomy)?

Increased total peripheral resistance and decreased cardiac output.

What happens in phase 1 of myocardial action potential?

Initial repolarization due to inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open.

What is the value of the intersection of curves on cardiac and vascular function curves?

Intersection of curves is the operating point of the heart in which venous return and CO are equal. Changes often occur in tandem, and may be reinforcing. For example, exercise increased isotropy and decreases TPR to maximize CO. Changes may also be compensatory. For example, in HF, inotropy decreases leading to fluid retention to increase preload in order to maintain CO.

What happens to diastole with increased HR?

It is preferentially shortened when HR increases. Less filling time decreases CO (ex. ventricular tachycardia).

What area of the heart is supplied by the left circumflex coronary artery (LCX)?

Lateral and posterior walls of the LV, anterolateral papillary muscle.

What is atrial natriuretic peptide?

Released from *atrial myocytes* in response to increased blood volume and atrial pressure. Acts vis cGMP. Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to "aldosterone escape" mechanism.

What is B-type (brain) natriuretic peptide?

Released from *ventricular myocytes* in response to increased tension in the ventricles. Similar physiologic action to ANP, with *longer half-life*. BNP blood test used for diagnosing HF (very good negative predictive value). Available in recombinant form (*nesiritide*) for treatment of HF.

What happens in phase 4 of myocardial action potential?

Resting potential. High K+ permeability through K+ channels.

The SA and AV nodes are supplied by which coronary artery?

Right coronary artery. Infarct of the RCA may cause nodal dysfunction leading to bradycardia or heart block.

The right (acute) marginal artery supplies which area of the heart?

Right ventricle

How is stroke volume measured?

SV = end-diastolic volume (EDV) - end-systolic volume (ESV) I.e. How much is left after pumping, minus how much is left after filling I.e. How much blood is being ejected per heart beat

What happens in phase 4 of pacemaker action potential?

Slow spontaneous diastolic depolarization as Na+ conductance increases. Accounts for automaticity of SA and AV nodes. *The slope of phase 4 in the SA node determines HR*.

What forces determine fluid movement through capillary membranes?

Starline forces Pc = capillary pressure (pushes fluid out of capillary) Pi = interstitial fluid pressure (pushes fluid into capillary) πc = plasma colloid osmotic pressure (pulls fluid into capillary) πi = interstitial fluid colloid osmotic pressue (pulls fluid out of capillary) Jv = net fluid flow = Kf [(Pc-Pi)-ζ(πc-πi) Kf = permeability of capillary to fluid ζ = permeability of capillary to protein

What is the role of central chemoreceptors?

Stimulated by changes in pH and PCO2 of *brain interstitial fluid*, which in turn are influenced by arterial CO2. Central chemoreceptors *do not directly respond to PO2* (peripheral chemoreceptors do).

What is cardiac output?

Stroke volume times heart rate CO = SV x HR During the early stages of exercise, CO is maintained by increased HR and SV. During the late stages of exercise, CO is maintained by HR only, as SV has a maximum plateau.

What is pulse pressure?

Systolic pressure minus diastolic pressure. Pulse pressure is proportional to stroke volume, inversely proportional to arterial compliance. The greater the SV, the greater the PP. The greater the arterial compliance, the "weaker" the PP.

How do you calculate total resistance of vessels in series versus in parallel?

TR = R1 + R2 + R3... 1/TR = 1/R1 + 1/R2 + 1/R3...

What is preload?

The volume of blood in the ventricles at the END OF DIASTOLE. Could also be defined as the amount of stretch placed on the heart between each beat. How much blood is loaded in the ventricle, ready to be ejected.

What happens in phase 1 of pacemaker action potential?

There is no phase 1 of pacemaker action potential.

What happens in phase 2 of pacemaker action potential?

There is no phase 1 of pacemaker action potential.

What happens in phase 0 of pacemaker action potential?

Upstroke due to opening of voltage-gated Ca2+ channels. *Fast voltage-gated Na2+ channels are permanently inactivated because of the less negative resting voltage of these cells.* This results in a *slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.*

Which blood vessels account for most blood storage capacity?

Veins

What is LaPlace's law?

Wall tension = pressure x radius/ 2 x wall thickness

In which states is pulse pressure decreased?

Aortic stenosis Cardiogenic shock Cardiac tamponade Advanced heart failure

Which blood vessels account for most of total peripheral resistance?

Arterioles.

Where is the pulmonic valve?

Between right ventricle and pulmonary artery.

Where is the mitral valve?

Between the left atrium and left ventricle - carries oxygenated blood.

Where is the tricuspid valve?

Between the right atrium and right ventricle - carries deoxygenated blood

What is the Fick Principle?

CO = rate of O2 consumption/ arterial O2 content - venous O2 content. Calculates cardiac output by determining how much blood must flow thru pulmonary or systemic circulation to account for difference in O2 content between arterial and venous circulations

Which blood vessels have the highest total cross-sectional area and lowest flow velocity?

Capillaries

What is the role of peripheral chemoreceptors?

Carotid and aortic bodies are stimulated by decreased PO2 (<60mmHg), increased PCO2 and decreased pH of blood.

How does a change in total peripheral resistance affect cardiac output?

Changes in TPR lead to altered CO at a giver RA pressure, however, mean systemic pressure (x-intercept) is unchanged. - Vasopressors increased TPR - Exercise, AV shunt decrease TPR

How does a change in venous return affect cardiac output?

Changes in circulating volume or venous tone lead to altered RA pressure (preload) for a given CO. Mean systemic pressure (the x intercept on the cardiac function curve) changes with volume/venous tone. - Fluid infusion and sympathetic activity increase venous return - Acute hemorrhage, spinal anesthesia decrease venous return

How does a change in inotropy affect cardiac output?

Changes in contractility lead to altered CO for a given RA pressure (preload). - Catecholamines and digoxin increase contractility (inotropy) - Uncompensated HF, narcotic overdose decrease contractility (inotropy)

What factors affect contractility?

Contractility (and SV) increase with: -Catecholamines (increased activity of Ca2+ pump in sarcoplasmic reticulum) -Increased intracellular Ca2+ -Decreased extracellular Na+ (decreased activity of Na+/Ca2+ exchanger) -*Digitalis* (blocks Na+/K+ pump --> increases intracellular Na+ --> decreases na+/Ca2+ exchanger --> increased intracellular Ca2+) Contractility (ad SV) decrease with: -*β-blockers (decreased cAMP) -HF with systolic dysfunction (ejection dysfunction) -Acidosis -Hypoxia/hypercapnia (dec. PO2/ inc. PCO2) -*Non-dihydropyridine Ca2+ channel blockers*

Coronary artery occlusion occurs most commonly in which artery?

Left anterior descending (LAD). It supplies the anterior 2/3 of the inter ventricular septum, anterolateral papillary muscle and anterior surface of the LV.

What is mean arterial pressure?

MAP = CO x TPR TPR is total peripheral resistance Average arterial pressure during a single cardiac cycle MAP = 2/3 diastolic pressure + 1/3 systolic pressure

Where does pacemaker action potential occur?

Occurs in the SA and AV nodes.

Where is the aortic valve?

Opening between left ventricle and aorta.

What happens in phase 2 of myocardial action potential?

Plateau. Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.

What are of the heart is supplied by the posterior descending/interventricular artery (PDA)?

Posterior 1/3 of inter ventricular septum, posterior walls of ventricles and posteromedial papillary muscle.

What factors affect preload?

Preload is approximated using EDV (end diastolic volume). Preload depends of venous tone and circulating blood volume. Venodilators (ex. hydralazine) decrease preload (i.e. system holds more blood to take preload off of heart) ACE inhibitors and ARBs decreased both preload and afterload.

How do you calculate volumetric flow rate?

Q = flow velocty (v) x cross-sectional area (A) Q = v x A

What happens in phase 3 of myocardial action potential?

Rapid repolarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels.

What happens in phase 0 of myocardial action potential?

Rapid upstroke and depolarization due to voltage-gated Na+ channels opening.

What in inotropy?

The force of a muscular contraction.

What is the most posterior part of the heart?

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).

What is afterload?

The resistance against which the heart contracts and is clinically reflected by systolic blood pressure. The pressure of "the door" the blood has to break through to get out of the ventricle.