Anatomy/Physiology Flashcards
Acute Marginal Artery
supplies right ventricle
Post. descending/interventircular artery
supplies posterior 1/3 of IV septum and posterior walls of ventricles
Left anterior descending artery
supplies anterior 2/3 of IV septum, anterior papillary muscles and anterior surface of left ventricle
Left Circumflex coronary artery
supplies lateral and posterior walls of left ventricle
Blood supply for SA and AV nodes
Right Coronary Artery - infarct can cause nodal dysfx
Right Dominant Circulation
85% population, posterior descending artery arises from RCA
Left Dominant Circulation
8% of population, posterior descending artery arises from LCA
Codominant circulation
7% of population, posterior descending artery arises from both Left Circumflex artery and RCA
Peak of coronary blood flow
Early Diastole
Most posterior part of heart
Left Atrium, enlargment can cause dysphagia or hoarseness (compresses Left reccurrent laryngeal)
Cardiac Output
SV * HR -or-
rate of O2 consumption)/(arterial O2 content-venous O2 content
Mean Arterial Pressure
MAP = CO * TPR
2/3DBP + 1/2SBP
Pulse Pressure
systolic - diastolic
proportional to SV
inversely proportional to arterial compliance
Stroke Volume
EDV-ESV
Cardiac Output during exercise
Early - CO is maintained by increase HR and SV
Late - CO is maintained by increased HR only (SV plateaus)
Causes for increased Pulse Pressure
Hyperthyroidism, Aortic regurgitation, arteriosclerosis, obstructive sleep apnea, transiently with exercise
Causes for decreased Pulse Pressure
aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced heart failure
Causes for increased stroke volume
increased contractility, increased preload, or decreased afterload
anxiety, pregnancy, exercise
Increased intracellular Calcium
increases contractility
Decreased Extracellular Sodium
increases contractility because it decreases the Na/Ca exchanger
Catecholamines effect on Heart
Increases activity of calcium pump in sarcoplasmic reticulum
Digitalis on Contractility
blocks Na/K pump thus increase intracellular Na and decreasing Na/Ca exchanger therefore INCREASING intracellular Calcium
Ways to decrease contractility and stroke volume
beta-1 blockade, HF with systolic dysfunction, acidosis, hypoxia/hypercapnea, non-dihydropyridine CCB
Increase of myocardial O2 demand
increased afterload, increased contractility, increased heart rate, increased ventricular diameter
Preload
depends on venous tone and circulating blood volume
approximated by ventricular EDV
Venodilators
nitroglycerin, decreases preload
Afterload
approximated by MAP
Compensation for increased afterload
LV compensates by thickening (hypertrophy) to decrease wall tension
Drugs that decrease both preload and afterload
ACE-inhibitors and ARBs
Vasodilators
hydralazine, decrease afterload
Wall Tension
Associated with Afterload
Pressureradius) / (2wall thickness
Ejection Fraction
EF = (SV)/(EDV) or (EDV-ESV)/EDV
left ventricular EF is an index of ventricular contractility
Normal EF
> 55%
EF in systolic heart failure
<55%
EF in diastolic heart failure
normal, >55%
Pressure =
Pressure = flow * resistance
Resistance of vessels in series
TR = R1+R2+R3…
Resistance of vessels in parallel
1/TR = 1/R1 + 1/R2 + 1/R3….
Causes of increased viscosity of blood
polycythemia, hyperproteinemic states (multiple myeloma), spherocytosis
Causes of decreased velocity of blood
ANEMIA
Resistance equation
(8(viscosity)length) / (pi*r^4)
Type of vessel that accounts for majority of TPR
arterioles, they regulate capillary flow
Inotropy
Strength of contraction
(+) inotropy
catecholamines, digoxin
negative inotropy
uncompensated heart failure and narcotic overdose
Decreases venous return
acute hemorrhage, spinal anesthesia
Increases venous return
fluid infusion, sympathetic activity
Increases TPR
vasopressors
Decreases TPR
Exercise and AV shunt
S1
mitral and tricuspid valve closure. Loudest at mitral area
S2
aortic and pulmonary valve closure, loudest at left sternal border
S3
Early diastole during rapid ventricular filling phase
associated with mitral regurgitation and CHF
more common in dilated ventricles
Heart sound normal in children and pregnant women
S3
S4
atrial kick - in late diastole, High atrial pressure. associated with ventricular hypertrophy. Left atrium must push against stiff LV wall.
Jugular venous pulse - a wave
atrial contraction
Jugular venous pulse - c wave
RV contraction (close tricuspid valve)
Jugular venous pulse -x descent
atrial relaXation and downward displacement of close tricuspid valve during ventricular contraction
absent in tricuspid regurg
Jugular venous pulse -v wave
increased right atrial pressure due to filling against closed tricuspid valve
Jugular venous pulse - y descent
blood flow from Rt Atria to Rt Ventricle
Normal Heart Split
delayed closure of pulmonic valve during inspiration
from decreased intrathoracic pressure so more blood returns
Wide Splitting
Seen in conditinos that dela right ventricular emptying
pulmonic stenosis, RBBB
Exaggeration of normal splitting
Fixed Splitting
Seen in ASD which causes left-to-right shunt
regardless of breath, pulmonic valve is greatly delayed due to increased blood flow
Paradoxical Splitting
Conditions that delay LV emptying
aortic stenosis, LBBB
P2 closes before A2 and on inspiration, no split
Auscultation over aortic area
Systolic murmurs like: aortic stenosis, flow murmur, aortic valve sclerosis
Auscultation over Left Sternal Border
Diastolic murmurs: aortic regurgitation, pulmonic regurgitation
Systolic murmurs: hypertrophic cardiopathy
Auscultation over Pulmonic Area
Systolic ejectino murmur: pulmonic stenosis and physiologic murmur
Auscultation over tricuspid area
Pansystolic murmur: tricuspid regurgitation, VSD
Diastolic Murmur: tricuspid stenosis, ASD
Auscultation over Mitral Valve Area
Systolic Murmur: mitral regurgitation
Diastolic Murmur: mitral stenosis
Inspiration
increases intensity of right heart sounds
Hand Grip
increases intensity of MR, AR, VSD murmurs
MVP: increases murmur intensity and later onset of click/murmur
Valsalva, Standing
increases hypertrophic cardiomyopathy murmur
MVP: decreases murmur intensity, earlier onset of click/murmur
Rapid Squating
increases intensity of aortic stenosis murmur
MVP: increases murmur intensity and later onset of click/murmur
Systolic Heart Sounds
aortic/pulmonic stenosis, AV regurgitation, VSD
Diastolic Heart Sounds
Aortic/Pulmonic Regurgitation, AV stenosis
Holosystolic, high-pitched “blowing murmur” at apex and radiates toward axilla
Mitral Regurgitation
Holosystolic, high-pitched “blowing murmur” loudest left sternum 5th intercostal space to right sternal border
Tricuspid regurgitation
Crescendo-decrescendo systolic ejection murmur
loudest at heart base; radiates to carotids
Aortic Stenosis
“pulsus parvus et tardus”
pulses are weak with a delayed peak, aortic stenosis
can lead to syncope, angina and dyspnea on exertion
Holosystolic, harsh-sounding murmur. Loudest at tricuspid area, accentuated with hand grip
VSD
Late systolic Crescendo with midsystolic click
MVP
Cause of midsystolic click
due to sudden tensing of chordae tendinae
High-pitched “blowing” early diastolic decrescendo murmur. Bounding pulses and head bobbing
Aortic Regurgitation (wide pulse pressure is chronic)
Aortic Root dilation, bicuspid aortic valve, endocarditis, or rheumatic fever
Aortic Regurgitation
Follows opening snap. delayed rumbling diastolic murmur
Mitral Stenosis
Continuous machine-like murmur, loudest at S2, left infraclavicular area
PDA, often due to congenital rubella
ACh/adenosine on Heart
decrease the rate of diastolic depolarization and HR (longer for depolarization to occur)
P wave
atrial depolarization (repolarization of atria in QRS)
PR interval
conduction delay through AV node (normally <200msec)
QRS complex
ventricular depolarization
QT interval
Mechanical contraction of ventricles
T wave
Ventricular repolarization
T wave inversion
recent MI
ST segment
Isoelectric, ventricles depolarized
U wave
caused by hypokalemia, bradycardie
Speed of conduction
Purkinje > Atria > ventricles > AV node
Pacemakers
SA > AV > bundle of His/Purkinje/Ventricles
Tx of Torsades de Pointes
Magnesium Sulfate
Drugs that prolong QT
Sotalol, Risperidone, Macrolides, Chloroquine, Protease inhibitor (-navir), quinidine, Class Ia and III antiarrhythmics, thiazides
Romano-Ward Syndrome
autosomal dominant, pure cardiac phenotype (no deafness) congenital long QT syndrome
Jervell and Lange-Nielsen Syndrome
Autosomal Recessive, Sensorineural deafnes, congenital long QT syndrome
Delta wave
Wolff-Parkinson-White Syndrome; abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) to bypass the rate-slowing AV node so ventricles depolarize earlier
Prolonged PR interval (>200msec)
1st Degree AV block
Progressive lengthening of PR interval until a beat is dropped
2nd degree Mobitz Type I (Wenckebach)
Chaotic and erratic baseline (irregularly irregular) with nodiscrete P waves inbetween irregularly spaced QRS complex
Atrial fibrillation
“saw tooth” appearance of flutter waves
Atrial flutter
Tx for Atrial Flutter
Class IA, IC, or III antiarrhythmics
Rate Control use beta-blocker or CCB
Definitive tx: catheter ablation
completely erratic rhythm with no identifiable waves
Ventricular arrhythmia (tx with CPR and defibrillation)
Dropped QRS beats, no change in PR interval
(2 more P waves than QRS)
(3 more P waves than QRS)
2nd degree AV block; Mobitz type II
2: 1
3: 1
2nd degree AV block; Mobitz type II
Pacemaker
Atria and ventricle beat independently of each other
3rd Degree heart block or complete heart blood, tx with a pacemaker
Lyme disease
can result in 3rd degree heart block
“aldosterone escape” mechanism
ANP
Release from atrial myocytes in response to increase blood volume and atrial pressure
ANP
Cause vasodilation and decrease sodium reabsorption at renal collecting tubues. Constricts efferent arterioles and dilates afferent arterioles
ANP
Released from ventricular myocytes in response to increased tension
B-type (brain) natriuretic peptide
longer t1/2 than ANP, with similar mechanism
BNP
Nesiritide
recombinant form of BNP for treatment of heart failure
Aortic Arch Receptors
vagus nerve to solitary nucleus of medulla responds to increased BP only
Carotid sinus receptors
glossopharyngeal nerve to solitary nucleus of medulla, responds to increase and decreased BP
Baroreceptors
respond to hypotension, decrease of afferent firing increase efferent sympathetic firing and decrease parasympathetic leading to vasoconstriction. Important in hemorrhage
Carotid Massage
increased pressure on carotid sinus will increase AV node refractory period and decrease HR
Cushing Reaction
hypertension, bradycardia and respiratory depression
increased ICP contricts arterioles leading to cerebral ischemia and sympathetics thus HTN and reflex bradycardia
Peripheral Chemoreceptors
carotid and aortic bodies stimulated by decreased oxygen when pO2 is <60mmHg
Central Chemoreceptors
stiulated by changes in pH and pCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2
Organ with largest blood flow
Lung
Largest share of systemic cardiac output
Liver
Highest blood flow per gram of tissue
Kidney
Largest AV O2 difference because O2 extraction is ~80%
Heart
Increased oxygen demand for heart is met by
increase coronary artery flow
PCWP in mitral stenosis
PCWP > LV diastolic pressure
normal <12
Autoregulation blood flow in heart
Local metabolites (vasodilatory) - CO2, adenosine, NO
Autoregulation blood flow in Brain
Local metabolites (vasodilatory) - CO2 (pH)
Autoregulation blood flow in Kidneys
Myogenic and tubuloglomerular feedback
Autoregulation blood flow in Lungs
Hypoxia causes vasoconstriction
Autoregulation blood flow in Skeletal Muscle
Local Metabolites - lactate, adenosine, K, H, CO2
Autoregulation blood flow in Skin
Sympathetic stimulation most important mechanism - temperature control
Whose head is on a rat?
Molly’s!!! (weird punch bowl)