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Flashcards in Cardio Deck (84):

Where are the auscultation points for normal valve sounds

1) Aortic --> over aorta (R 2nd intercostal space at the right sternal border)
2) Pulmonic --> over pulmonary trunk (L 2nd intercostal space at the left sternal border)
3) Tricuspid --> over right ventricle (L 5th intercostal space at the left sternal border)
4) Mitral --> over left ventricle (L 5th intercostal space at midclavicular line (3 inches to left of the sternum) ie the apex of the heart)


Where are the auscultation points for valvular murmurs

Aortic stenosis (systolic) --> aorta (R 2nd intercostal space at sternal border)
Aortic regurgitation (diastolic) --> left ventricle (L 5th intercostal space at apex of heart)
Pulmonic stenosis (systolic) --> pulmonary trunk (L 2nd intercostal space at sternal border)
Pulmonic regurgitation (diastolic) --> right ventricle (L 5th intercostal space at sternal border)
Tricuspid stenosis (diastolic) --> right ventricle (L 5th intercostal space)
Tricuspid regurgitation (systolic) --> right atrium (R 5th intercostal space at sternal border, to the right of the auscultation point for tricuspid)
Mitral stenosis (diastolic) --> left ventricle (L 5th intercostal space)
Mitral regurgitation (systolic) --> left atrium (L upper border of axilla, since left atrium is mostly posterior heart)


What is the blood supply of the heart?
What is right vs left dominance?
What are the anastamoses?

1) Blood supply: Ascending aorta --> R and L coronary artery (holes in walls of R and L aortic sinuses)
Right coronary artery - supplies R atrium, R ventricle, AV node, SA node, interatrial septum
-posterior interventricular artery - supplies R and L ventricles
-marginal artery - supplies R ventricle
Left coronary artery - v short
-left anterior interventricular artery - supplies R and L ventricles and interventricular septum
-circumflex - supplies L atrium and L ventricle

2) Right dominance - posterior interventricular artery branches from right coronary artery (80%)
Left dominance - PDA branches from circumflex branch of Left coronary artery (20%)

3) Right coronary artery and circumflex branch of left coronary artery -- pathway of collateral flow for tissues


What is the venous drainage of the heart?

Great + middle + small cardiac veins --> great cardiac vein becomes coronary sinus --> Drains into Right atrium
anterior cardiac veins --> directly into right atrium
least cardiac veins --> directly into underlying chamber --> explains why blood in left ventricle is not 100% saturated


What is the structure of the pericardium and its relation to cardiac tamponade

1) Visceral pericardium - covers external surface of heart and roots of the vessels
Parietal pericardium - continuous with visceral at roots of the vessels --> Creates sinuses
transverse sinus - open at both ends, anteriorly bounded by pulmonary trunk and ascending aorta, posteriorly bounded by SVC
oblique sinus - blind recess, bounded by IVC and 4 pulmonary veins
fibrous pericardium - fused with parietal pericardium, inelastic tough layer
2) Cardiac tamponade: accumulation of fluid in pericardial space --> cavity cannot expand outwards bc of fibrous pericardium so it expands inwards --> compresses the heart --> restricts filling during diastole --> reduces cardiac output (need to do pericardiocentesis to remove fluid)


Explain the cardiac conduction system

Composed of Purkinje fibers, NOT nerve cells/nervous tissue
SA node: located in wall of right atrium near where SVC comes in; pacemaker of the heart
fibrous skeleton: layer of dense collagenous connective tissue running across heart at atrioventricular boundary -- layer of insulation between atrial muscles and ventricular muscles
AV bundle: defect in fibrous skeleton -- only electrical connection between atria and ventricles
AV node: located in wall on right side of interatrial septum; retards the wave of depolarization
0.15 second gap between atrial and ventricular depolarization


Describe innervation to the heart

Heart can function without innervation but it has nerve supply that modulates cardiac cycle
1) Parasympathetic: slow down SA node, lengthen interval of AV node
-preganglionic - vagus nerve
-postgang- cardiac plexus in wall of the heart
2) Parasympathetic sensory: afferent limb of cardiac reflexes (not conscious levels)
-enter CNS at medulla
-cell bodies in inferior vagus ganglion
3) Sympathetic: speed up SA node, reduce interval of AV node
-preganglionic - upper thoracic spinal cord
-postgang - cervical and upper thoracic ganglia
4) Sympathetic sensory: reach conscious levels eg ischemia
-enter CNS at upper thoracic spinal cord levels
-cell bodies in dorsal root ganglia
-brain perceives pain/angina from upper thoracic dermatomes (T1-T4) --> upper chest and medial arm


Describe the SNS system of neurotransmission

Input at spinal cord (T1-L2)
Preganglionic SNS fiber: cholinergic = acetylcholine neurotransmitter
short preganglionic neurons synapse at ganglia in paravertebral column
Postganglionic SNS fiber: synapse at cholinergic-nicotinic receptor (N2-R); noradrenergic = norepi neurotransmitter (synthesized in axon termini of postgang fibers)
Adrenergics diffuse across synapse and bind to adrenoreceptors on post synaptic membrane of effector(/target) tissue: synapse at type alpha and beta adrenergic receptors


Describe how specificity of effector response is achieved within the SNS and PSNS.
Identify the isoforms of adrenoceptors, and major tissues that express these isoforms.

1) specific receptor isoforms expressed on target effector tissue determines specificity of response to adrenergic stimulation (can have different effects from a single compound)
2) Alpha: alpha1 (vascular smooth muscle), alpha2
Beta: beta1 (SA node, ventricular myocytes, renal JG cells)
beta2 (myocardium heart muscle, bronchial smooth muscle, vascular smooth muscle of skeletal muscles meaning smooth muscle of blood vessels that supply skeletal muscle)


Describe the function of COMT, MAO, and cholinesterase.

COMT and MAO- degrade adrenergics (eg norepi at synapse of SNS effector postsynaptic membrane); alternatively norepi can diffuse back across presynaptic membrane for recycling
Cholinesterase- degrades ACh at synapse of PSNS effector postsynaptic membrane; alternatively choline form of ACh can be reuptaken by presynaptic membrane


Describe the basic histology and function of the adrenal gland in the context of ANS physiology

Adrenal gland sits on top of kidneys, supports upfront, quick SNS response when SNS is activated
outer cortex
inner medulla: pregang SNS fibers (ACh) synapse with chromaffin postganglionic fibers at cholinergic-nicotinic receptors--> secretes catecholamines--> epi (and a little norepi) into circulation
epi supports norepi secreted from local postganglionic SNS fibers


Which of the following responses are DECREASED during elevated SNS activity?
1) arterial BP due to increased cardiac output, vasoconstriction
2) blood flow to contracting skeletal muscle
3) glycolysis in liver and skeletal muscle
4) gluconeogenesis in liver, plasma glucose level
5) insulin secretion
6) muscle contractility
7) mental activity, awareness
8) rate of blood coagulation, release of RBCs from spleen
9) GI motility
10) lipolysis in adipocytes

5) insulin secretion decreases
9) GI motility and secretion decreases


Describe the PSNS system of neurotransmission

Input at brainstem, sacral spinal cord
preganglionic PSNS fiber: cholinergic = ACh
Postganglionic PSNS fiber: synapse at N2-R, cholinergic = ACh neurotransmitter
Effector(/target) tissue: synapse at cholinergic-muscarinic (CM) receptors - 5 isoforms, including one in SA node (CM2-R)


Describe the autonomic control over cardiac function (blood pressure)

Receptor: high pressure baroreceptors in carotid sinus, aortic arch; low pressure baroreceptors in right atrium and pumonary arteries
signal carried on afferent fibers (CN IX and X) to medulla (cardioinhibitory, cardioaccelatory, and vasomotor centers)
interneurons release neurotransmitters - activation of SNS is accompanied with inhibition of PSNS and vice versa
Preganglionic efferents synapse with postganglionic efferents
Sympathetic efferents - increase heart rate (beta1), vasoconstriction (alpha1) --> increase blood pressure
Parasympathetic efferents - (CM2-R in SA node)--> decrease heart rate


Describe the formation of the embryonic heart tube

When: 3rd week of devlpt
Where: splanchnic mesoderm, induced by endoderm
What: angiogenic clusters
medial --> dorsal aortae
lateral --> R and L endocardial tubes --> heart tube (4th week)
aortic arch = communication between heart tube and dorsal aorta


What are the regions of the heart tube and what are their adult derivatives?

Blood flows caudally to cranially
caudal end: sinus venosus - receives venous return from placenta, yolk sac, embryo --> becomes sinus venarum (smooth-walled part of right atrium where veins enter)

primitive atrium --> becomes trabeculated parts of right and left atria (ie pectinate muscle)

primitive ventricle --> becomes trabeculated part of left ventricle (trabeculae carnae)

bulbus cordis:
-proximal third --> becomes trabeculated part of right ventricle (trabeculae carnae)
-conus cordis --> becomes smooth parts of the right and left ventricles
-truncus arteriosus --> roots of ascending aorta and pulmonary trunk


Describe the development of the smooth portion of the left atrium

primitive atrium = rough-walled section of LA (pectinate muscle)
pulmonary veins = smooth-walled section of LA
the pulmonary vein grows out of the atrium towards the lungs
then starts getting resorbed back into the wall of the left atrium
end result: 4 pulmonary veins branching from left atrium and v large smooth wall portion


Describe the effects of heart tube folding

heart tube folds on itself:
atrium becomes cranial to the ventricle
veins enter on posterior wall of heart (back wall of right atrium)
arteries leave from anterior wall of heart (front wall of left ventricle)


What are the 2 major functional requirements for heart tube septation?

1) need communication between R and L sides of the heart in the fetus
oxygenated blood is coming from placenta --> IVC --> R atrium, so it needs to go to left side to distribute to body
2) Communication needs to be closed when baby is born
since oxygenated blood is now coming from L side (lungs)


Describe the formation of the atrial septum (end of 4th week -- beg of 6th week)

1) Septum primum grows from wall of atrium towards the 4 atrioventricular endocardial cushions (comprised of neural crest cells)
2) Foramen primum - narrowing gap between septum primum and endocardial cushions
3) Foramen secundum - perforation in septum primum formed due to apoptosis, before closure of foramen primum
4) Septum secundum forms on right side of septum primum covering foramen secundum --> is thicker and more rigid
(-part of septum primum not covered by septum secundum --> becomes fossa ovalis
-free edge of septum secundum --> becomes limbus of fossa ovalis)
5) R-->L pressure gradient in the fetus --> blood flows through tunnel called foramen ovale
6) When fetus is born, pressure gradient becomes L-->R (lungs start working) --> closure of foramen ovale


Describe the two types of atrial septal defects and whether they are cyanotic

1) Primum type: failure of septum primum to fuse with the endocardial cushions (neural crest migration defect, association with valvular defects) --> persistent opening in foramen primum
results in L to R shunt --> acyanotic
2) Secundum type: septum secundum doesnt completely cover foramen secundum --> incomplete closure of foramen ovale
results in L to R shunt --> acyanotic


What is Eisenmenger's syndrome?

when an acyanotic L to R shunt caused by a congenital heart defect overloads pulmonary circuit over time --> causes pulmonary hypertension --> shunt reverses to R to L shunt --> becomes cyanotic


Describe the formation of the ventricular septum (end of 5th week -- beg of 7th week)

1) embryonic ventricular septum- formed from cardiac muscle --> becomes muscular septum in adults
2) aorticopulmonary/spiral septum - ingrowth of neural crest cells that divides the truncus arteriosus in half (R side pulmonary trunk and L side aorta) --> becomes membranous septum in adult


Describe the following types of ventricular septal defects and whether they are cyanotic:
1) Tetralogy of Fallot
2) Persistent truncus arteriosus
3) Transposition of the great arteries
4) Patent ductus arteriosus

1) Tetralogy of Fallot - aorticopulmonary septum displaced to the right (pulmonary side)
-pulmonary stenosis
-overriding aorta
-ventricular septal defect - failure of fusion of aorticopulmonary septum with embryonic ventricular septum
-right ventricular hypertrophy
results in R to L shunt --> cyanotic (most common)
2) Persistent truncus arteriosus - aorticopulmonary septum doesnt form at all
-also membranous ventricular septal defect
-bc deoxy blood and oxy blood is mixed when blood enters systemic and pulmonary circuits --> cyanotic
3) Transposition of the great arteries - spiral septum is not spiral --> aorta and pulmonary trunk positions are reversed
right ventricle (deoxy) --> aorta
left ventricle (oxy) --> pulmonary trunk
babies must have other septal defects to survive
4) Patent ductus arteriosus - connects pulmonary artery to descending aorta in fetus
reversal of pressure gradient at birth results in L to R shunt: 02 blood shunted from aorta to pulmonary artery--> acyanotic (putting more oxy blood back into the lungs unnecessarily)
more common in preemies (prostaglandin decreases at 9 mos devlpt, needed to close ductus arteriosus)


Describe the differences in prenatal and postnatal circulation

1) Prenatal circulation:
-oxygenated blood from umbilical vein --> ductus venosus (shunt to bypass liver) --> IVC (mixes with deoxy blood)--> right atrium --> foramen ovale shunt --> left atrium --> ascending aorta --> (supplies brain) --> Descending aorta --> umbilical arteries
-deoxy blood from SVC --> right atrium --> tricuspid valve --> right ventricle --> pulmonary trunk --> pulmonary artery --> ductus arteriosus shunt --> descending aorta --> umbilical arteries
2) postnatal circulation:
umbilical vein closes --> becomes ligamentum teres
umbilical arteries close --> become medial umbilical ligaments
ductus venosus closes --> becomes ligamentum venosum
reversed L to R gradient closes foramen ovale
increased 02, decreased prostaglandin (around 9 mos devlpt)--> ductus arteriosus closes --> becomes ligamentum arteriosum


What is the clinical significance of cardiac-specific troponin and creatine kinase?

elevated plasma levels of cardiac specific troponin (cTnI, cTnT) and to a lesser extent creatine kinase (CK-MB) are reliable markers of myocardial injury eg MI


What are the properties of cardiomyocytes that allow for greater contractile force compared to skeletal muscle?

1) slight stretch from resting position L0 signals cardiomyocyte to release intracellular Ca2+ from SR and mitochondria --> increased contractile force
2) cardiomyocytes develop more tension from stretch than other types of muscle --> increased filling = more forceful contraction


(myocardial biomechanics) Explain what happens during diastole and systole in left ventricle. What is the clinical impact of hypertension?

1) Diastole: myocardium is relaxed, low intraventricular pressure and low arterial BP
Early diastole: aortic valve closed, mitral valve ready to open; fibers have no load
mitral valve opens due to increased left atrium filling (/pressure)
filling --> stretch from L0 --> preload --> increased wall tension (since T = p x r)
mitral valve closes when ventricular pressure > atrial pressure
2) Systole: myocardium contracts, high intraventricular pressure and high arterial BP
LV muscle fibers stretched to optimal length --> increased intracellular Ca2+
Early systole = isovolumetric contraction; mitral and aortic valves closed, increase in LV blood pressure
afterload=opposing aortic blood pressure (ie systemic BP)
preload (contractile force) > afterload (aortic pressure) --> aortic valve opens --> LV ejects blood into aorta --> systolic contraction ends
3) Hypertension = increased aortic/systemic blood pressure
heart esp LV has to work much harder to pump blood


What is the function and mechanism of Digitalis (digoxin)?

Function: positive inotrope - use for impaired cardiac function eg decreased ejection fraction
increases contractile force (inotropy)
increases end diastolic volume
increases contraction velocity
increases cardiac output
also slows SA and AV nodal conduction (used in heart failure)
sensitizes baroreceptors - reduces SNS afferent activity (downregulates SNS tone)

-Normally, the NA+/K+ ATPase pumps Na+ out and K+ in
-NCX takes advantage of the gradient to pump Na+ in and pump Ca2+ out --> decrease in sarcoplasmic Ca2+ --> relaxation
-Digoxin inhibits Na+/K+ ATPase --> increased sarcoplasmic Na+ --> NCX inhibited --> increased sarcoplasmic Ca2+ --> increased contractility --> increased cardiac output


Describe the effect of SNS and PSNS tone on SA pacemaker activity and the mechanism behind this effect

Mechanism: increase in positive charge in an electrogenic cell (eg Na+ influx) increases resting membrane potential (from its resting -85 mV) --> decreases time to reach threshold, and vice versa

SNS: increased Na+ permeability at AV and SA node --> decreased time to reach depolarization threshold --> increased rate of rise of depolarization --> increased heart rate (decreased interval between peaks) compared to basal HR

PSNS: increased K+ permeability at AV and SA node --> decreased rate of rise of depolarization (time to reach threshold) --> increased interval between peaks compared to basal rate --> decreased heart rate


Describe arrhythmias associated with the SA node:
*what are the characteristics of sinus rhythm? Normal sinus rhythm?
1) Sinus tachycardia
2) Sinus bradycardia

*Sinus rhythm: rhythm set by the SA node (P waves)
Normal sinus rhythm: P before QRS, regular P-P intervals and QRS-QRS intervals (regular rhythm), HR 60-100 bpm
1) Sinus tachycardia: HR >100 bpm
decreased P-P interval
2) Sinus bradycardia: HR


Describe arrhythmias associated with the AV node:
1) primary heart block
2) second degree heart block
3) tertiary/complete heart block

1) primary heart block - delayed conduction through AV node/bundle of His
-prolonged PR interval
-still 1 P before QRS
2) second degree heart block - increased refractory period for AV node
-not every P wave is followed by QRS interval
3) tertiary/complete heart block - no atrial impulses reach the ventricles
-P and QRS are at regular intervals separately but not coordinated with each other
-escape rhythm: junctional escape (if block is at AV node, around 50 bpm) or ventricular escape (if block is distal to AV node, around 30 bpm by His-Purkinje pacemaker)


Describe circus rhythms caused by the phenomenon of reentry.

What is the clinical abnormality that results?
How does afib manifest on EKG? What are the types of afib? What is one serious risk associated with afib?

1) Normal: unidirectional spread of action potential (depolarization) through the myocardium; retrograde conduction prevented by effective refractory period
Reentry: results in formation of ectopic pacemaker (outside of SA node) because damaged cells allow retrograde conduction
if time for retrograde conduction is longer than effective refractory period -- AP hits myocytes when they are active again --> creates circus rhythm circuit --> self-sustaining ectopic pacemaker
-abnormal circus rhythm can spread to myocytes in relative refraction period and doesnt self-terminate

2) fibrillation - twitches of myofibrils but no coordinated contractions of the entire muscle
atrial fibrillation - no recognizable P wave (bc no uniform atrial depolarization), irregularly irregular interval
ventricle doesnt beat at 200+ beats/minute bc of AV nodal delay
generally localized to left atrium
Types: Recurrent (resolves itself), paroxysmal (in and out of sinus and afib)
Risk: atrial thrombus --> PE or stroke


What is the meaning of "atrial fibrillation with rapid ventricular response"

Usually ventricle is spared the extremely increased (200+) bpm bc of AV nodal delay
Lot of impulses getting through AV node and HR is 80-100 bpm
*always do thyroid panel, problem for hyperthyroid


What is atrial flutter?

like atrial fibrillation, arises from reentry
rapid and regular atrial activity ~300 bpm
manifests as sawtooth bumps in EKG --> P waves
at least 1 P before QRS interval
ventricular response depends on extent of AV nodal delay --> most common is 2:1 --> ventricular rate of 150 bpm
generally localized to right atrium (reentry arising from tricuspid)


Describe bundle branch blocks

block causes delay in whatever bundle branch its feeding into
would see widened QRS interval on the EKG in the limb lead from the side of body
eg right bundle block would have widened QRS interval in right limb lead III, left BBB seen in left limb leads I and II


Describe the following abnormalities in ventricular conduction pathways:
1) premature ventricular contraction (PVC)
2) ventricular tachycardia
3) ventricular fibrillation

1) PVC: feeling of heart skipping a beat, arises from irritable focus but heart fixes itself; see on EKG as QRR'S, widened QRS bc myocyte is slow conducting pathway

2) Ventricular tachycardia: normal sinus rhythm before ectopic pacemaker takes over and you see a run of strong closely spaced, widened QRS intervals (which mask P waves); 3+ consecutive PVCs
HR ~300 bpm; cardiac output is impaired because ventricles dont have enough time to fill with blood
can be monomorphic or polymorphic (multiple ectopic pacemakers)

3) Ventricular fibrillation: fibrillations of ventricular myocardium instead of regular coordinated contractions --> zero cardiac output --> fatal if not addressed immediately (defibrillate to allow SA node to establish refractory time)
looks like squiggles on EKG


How do electrolyte imbalances manifest on EKG?

Ca2+: ST and QT intervals affected
hypocalcemic: prolonged QT interval bc Type L Ca2+ channels become sluggish when [Ca2+] is too low--> open too long --> prolonged QT interval and ST segment
*ST segment follows the plateau phase of the cardiomyocyte action potential
hypercalcemic: short QT interval bc Type L channels become irritable and close quickly
hyperkalemia: repolarization anomaly with v high T wave
hypokalemia: flattened T wave, ST depression


Describe function and mechanism of beta blockers

Negative inotropic agents- block B1 adrenergic receptors (atenolol, metroprolol) --> lower heart rate and contractility at SA node--> control angina and reduce hypertension
*type of antiarrythmic medication

increases refractory to prevent circus rhythms


What happens during a myocardial infarction MI? What are associated changes on the EKG?

1) Loss of blood supply (eg vessel occlusion) --> ischemia --> myocardium injured or dies --> cannot conduct electrical impulses
ST segment elevation (in leads II, III, AVF --> inferior MI; in V1-V4 --> anterior MI)
peaked Q waves
new Q waves --> irreversible myocardial death --> direction of current away from damaged myocardium
prominent R wave in lead I --> posterior MI


Myocardial infarction: in which leads would you see MI in different regions of the heart?

Inferior (II, III, AVF) --> Right coronary artery (R atrium + ventricle, diaphragmatic border)
Posterior (V1) --> Right coronary artery *use V1 to look for posterior myocardial infarction
*RCA branches also supply AV and SA nodes
Left lateral (I, AVL, V5, V6) --> Left circumflex artery (L atrium + ventricle)
Anterior (V1-V4) --> Left anterior descending artery (interventricular septum)


1) MAP
2) PCO2

1) Mean arterial pressure - measurement of perfusion pressure (along with blood pressure)
goal is to maintain perfusion pressure to sustain oxygen delivery
2) PCO2- partial pressure of CO2 (dissolved CO2 in blood)
measured by chemoreceptors
indicator of pH (lot of CO2 --> low pH)


What are the two components that endogenously monitor arterial blood pressure?

*only for acute changes in BP

1) baroreceptors
high pressure (carotid sinus and wall of aortic arch)
low pressure (right atrium and pulmonary arteries)
*baroreceptor desensitization in hypertensive patients, cant regulate their MAP by urinating more bc the urine output curve is shifted right for chronic HTN
2) chemoreceptors
peripheral (carotid body and aortic body in aortic arch) - local hypoxia
central (medulla)


Describe the central and peripheral regulation of BP and HR for hypertension and hypotension

1) Hypertension
High pressure baroreceptors and chemoreceptors activated --> travel on IX and X--> medulla --> interneurons in medulla inhibit SNS preganglionic fibers and activate PSNS fibers --> PSNS fibers exit brainstem --> innervate heart via left and right vagal tracts --> TPR reduced, HR lowered, SNS activity blocked, urine excretion increased
2) Low pressure baroreceptors and chemoreceptors activated --> travel on IX and X --> medulla --> interneurons inhibit PSNS and activate SNS fibers --> SNS fibers exit brainstem --> innervate heart via upper thoracic spinal cord --> increased venous return tot he heart, increased HR (via beta1), vasoconstriction (via alpha1)


Explain how chronic hypertension can cause left ventricular hypertrophy

1) chronic systolic wall stress - concentric left ventricular hypertrophy where sarcomeres layer on
-pressure overload eg hypertension + aortic stenosis (pathologic), or isometric strength training (physiologic)
2) chronic diastolic wall stress - eccentric LVH where sarcomeres add in series
-volume overload eg aortic regurgitation (pathologic) or isotonic running (physiologic)


Explain the difference between pathologic and physiologic left ventricular hypertrophy (LVH)

What are the EKG symptoms of LVH?

1) Pathologic
renal-angiotensin-aldosterone system (RAAS) directly affect ventricular myocardium and VSM in favorable and unfavorable ways --> induction of cell signaling pathways and cascades that does not happen in physiologic
if activity is abnormally high --> pathogenic effects in cardiovascular tissue eg interstitial fibrosis, endothelial cell dysfunction (compensation --> decompensation)
associated with heart failure and increased mortality
2) Physiologic
highly trained professional athletes
doesnt involve unfavorable model that involves RAAS
LVH usually reversible

3) Left axis deviation
Deep S wave in V1
Increased R in left lateral leads (I, aVL, V5, V6)


Explain how the RAAS system leads to increased BP

RAAS - renal angiotensin aldosterone system
Renin: synthesis of angiotensin II (increased fluid volume inhibits renin release)
Angiotensin (AII): vasoconstrictor, stimulates secretion of aldosterone hormone from the adrenal cortex, blocks high pressure baroreceptor input, stimulates release of norepi from postganglionic SNS fibers --> vasoconstriction --> higher BP
Aldosterone: vasoconstrictor, promotes Na+ reabsorption --> water retention --> higher BP
*RAAS receptors on myocardium vascular endothelium


What drugs are prescribed to address hypertension?

What is the general order of diagnosis?

1) Cardiac function:
beta blockers - metoprolol, atenolol
Ca2+ channel antagonists - verapamil
2) Renal function
diuretics - HCTZ
ACE inhibitors (inhibit angiotensin) - enalapril
renin inhibitors
ARB - angiotension II receptor blockers - losartan
aldosterone antagonist - eplerenone
3) ANS function
alpha2 agonists (alpha2 antagonizes alpha1)
4) Vascular smooth muscle
Ca2+ channel antagonists - amlodipine
alpha1 antagonists - prazosin

generally start with HCTZ diuretic or ACE inhibitor or ARB
then add Ca2+ blocker
last should be aldosterone antagonist


What is chronic stable angina?
Explain the pathophysiology of the symptoms: tachycardia, SOB, diaphoresis, chest pressure/tightness
What are the EKG abnormalities?
How do you treat chronic stable angina?

1) angina - severe and constricting pain
chronic stable angina - narrowing of 1+ coronary vessels

2) when cardiac demand is increased (eg exercise): 02 demand > 02 supply (hypoxia) --> impaired LV function --> increased LV diastolic pressure and wall tension:
--> increased pulmonary pressure --> shortness of breath
--> increased myocardial 02 consumption --> increased heart rate + contractility

hypoxia --> pain and anxiety --> increased SNS --> sweating (diaphoresis)

hypoxia --> lactate --> acidosis --> insult to sarcolemma --> Adenosine dumped from myocardium --> Adenosine activates nociceptors in afferent pain fibers

3) EKG: horizontal/downsloping ST depression
inverted/flattened T waves
*ECG anomalies resolve once symptoms disappear

4) vasodilator eg N0, beta blockers, Ca2+ channel blockers
dilation --> Reduces pressure --> reduces 02 demand


What is the role of veins? What are the two key properties that allow for reaction to arterial BP?

1) Role: blood storage, venous return
on the capacitance side (arteries are resistance, capillaries are exchange)
2) highly distensible --> lowers resistance
very compliant --> blood can be accommodated when arterial blood pressure rises
low blood pressure but high flow velocity


What are the myocardial 02 requirements, in order of demand?

1) ventricular wall stress ie systolic ventricular pressure
2) heart rate
3) contractility ie inotropy


What are key vasodilators?
What are key vasoconstrictors?

1) CO2
lactic acid
2) angiotensin II
stretch (Activates plasma membrane ion channels)
Ca2+ (Activates PKC which inhibits SERCA)


What are two general mechanisms underlying cardiac ischemia?

1) fixed vessel narrowing - through formation of artherosclerotic plaques
2) abnormal vascular tone - damage to vascular endothelium --> no local vasodilators produced --> alpha alpha mediated vasoconstriction


What is the function of splanchnic circulation in regards to overall circulation?

Splanchnic - in the gut, contains 20% of blood volume and lots of alpha1 receptors
highly compliant - can accommodate or release large blood volume
low threshold - with small amount of SNS tone, will vasoconstrict and increase right atrial venous return --> increase cardiac output


What is vasomotion? What sets the rate of vasomotion in a capillary bed?

1) Vasomotion - spontaneous rhythmic contraction of small resistance vessels
2) Set by 02 usage
more 02 usage --> vascular smooth muscle decreases vasomotion --> relaxes --> increases rate of flow in capillary beds --> increases 02 delivery to active tissue


What is the renal (kidneys) involvement in maintaining MAP?

when there is decreased TPR or Pa --> MAP decreases --> kidneys decrease urine output --> this maintains or increases circulatory volume --> mean circulatory filling volume increases (Pmcf) --> arterial pressure increases --> MAP increases


What are the borders of the heart?

Upper right: behind 3rd costal cartilage, 0.5 inches away from sternum
Lower right: behind 6th costal cartilage, 0.5 inches away from sternum
Upper left: behind 2nd costal cartilage, 0.5 inches away from sternum
Lower left: behind 5th intercostal space, 3.5 inches away from sternum


What is the relationship between venous pressure RAP and cardiac output CO?

How does edema form if there is a problem with RAP-CO relationship? What hormones are involved

RAP dependent on CO - as CO increases, RAP decreases
therefore if RAP increases --> CO increases through higher inotropy --> RAP lowered --> CO activity decreases (shut off bc no longer needed)

if that doesnt happen (eg decreased CO, heart failure): increased RAP --> decreased venous return --> increased Pcap (back pressure) --> increased filtration from capillaries into lung tissues --> increased interstitial fluid build up too much for lymphatic system to get rid of + increased jugular venous pressure --> Edema
increased RAP --> increased venous hydrostatic pressure (can reduce by moving legs for example)
increased RAP --> increase plasma levels of ANP --> Decrease plasma levels of RAAS

*increase in intravascular volume can be alleviated by vasopressin, angiotensin, aldosterone (promote Na+ reabsorption)


What are the different signs and symptoms for right vs left heart failure?

Right heart failure: increased RAP --> decreased CO --> decreased MAP --> fluid overload due to increased venous pressure --> edema in lower extremities

Left heart failure: decreased CO --> Increased pulmonary venous pressure --> pulmonary edema
nocturia, shortness of breath


How is the pressure/volume relationship affected by:
1) diastolic heart failure
2) systolic heart failure

1) diastolic heart failure - ventricular stiffness --> doesnt distend as much --> impaired filling during diastole
effect: decreased EDV, ESV is the same (as is ejection fraction), but pressure increases --> increased stroke work to maintain cardiac output

2) Systolic heart failure - impaired contractility --> can't eject blood as efficiently --> ineffective systole --> ineffective CO
effect: increased ESV (and therefore decreased ejection fraction) --> heart cannot generate systolic pressures to overcome afterload


Where is the superior mediastinum and what are its component layers?

What is the vagus nerve course in the superior mediastinum?

1) Superior mediastinum - region in thoracic cavity above the plane at the level of tracheal bifurcation (T4)

From anterior to posterior:
Glandular layer - thymus
Venous layer - distal part of SVC branching into R/L brachiocephalic veins (which form from internal jugular and subclavian veins)
Aortic layer - distal ascending aorta, aortic arch (branches are brachiocephalic trunk, left common carotid, and left subclavian), and descending aorta most posteriorly
Tracheal layer - since trachea birfurcates at T4, it is ONLY in the superior mediastinum
Digestive layer - esophagus

2) left vagus - enters with L common carotid, passes anterior to aortic arch and recurrent branch ducks under ligamentum arteriosum, vagus goes to anterior surface esophagus
right vagus - recurrent branch loops under R subclavian artery, vagus goes to posterior surface of esophagus; right vagus passes between arch of azygos and esophagus


Where is the posterior mediastinum and what are its components?

Posterior mediastinum - between fibrous pericardium and vertebral column

descending aorta- moves posterior to esophagus
thoracic duct - moves to left of midline at T6
azygos vein - to the right of the esophagus
hemiazygos vein - to left of esophagus
vagus nerves - make esophageal plexus on anterior surface of esophagus
sympathetic trunks - not really in the mediastinum bc its behind the pleural cavities


Where are the anterior and middle mediastinum and what are their components?

Anterior - between pericardium and sternum, contains inferior portion of thymus

Middle - fibrous pericardium and everything within it (heat, proximal SVC, proximal ascending aorta)
*phrenic nerve sits on lateral surface of fibrous pericardium and crosses in front of hilus of the lung


What is the function and mechanism of:
1) lisinopril (the "-prils")
2) losartan (the

1) ACE inhibitors - inhibit angiotensin II
lead to vasoconstriction, release block on high pressure baroreceptor activity, limit release of aldosterone --> used for hypertension treatment

2) Angiotensin Receptor Blockers - inhibit specific angiotensin AT1 receptor
lead to vasoconstriction, release block on high pressure baroreceptor activity, limit release of aldosterone --> used for hypertension treatment


What is the function and mechanism of:

atropine - cholinergic-muscarinic antagonist
inhibits PSNS synapse of ACh at CM receptors
antiparasympathetic: dilates pupil, increases heart rate, leads to constipation, decreases saliva


What is the function and mechanism of:
metoprolol (the "-olols")

Beta blockers - negative inotrope; inhibits type Beta1 SNS receptors, prevents epi and norepi from synapsing
decrease heart rate (at SA node) and contractility --> Decrease ejection fraction, stroke volume, pulse pressure

use in heart failure/impaired cardiac function when digoxin is prescribed --> heart rate control which lowers myocardial 02 demand/consumption
used in treatment of arrythmias eg long QT syndrome, tachycardia
can also use for HTN mgmt


What is the function and mechanism of:
verapamil, diltiazem

1) Amlodipine - Type L Ca2+ channel blocker in vascular smooth muscle; antihypertensive
vasodilator --> reduces TPR (afterload) against which the heart works --> reduces blood pressure --> reduces myocardial 02 demand
treats high blood pressure and angina (chest pain caused by reduced blood flow to the heart)
side effect is peripheral edema (dilation leads to increased filtration in capillaries)

2) Verapamil, diltiazem, cardizem- Type L Ca2+ channel blocker in cardiac muscle
affects depolarization --> negative inotrope
delays AV nodal conduction (blocks reentry)
treats high blood pressure, angina, arrythmia eg ventricular rate control in AFib


What is the function and mechanism of:

Epi and Norepi- binds to alpha1 receptors in increase vasoconstriction and BP
binds to beta1 receptors to increase contractility and heart rate --> increase cardiac output
part of SNS tone


What is the function and mechanism of:

1) Furosemide - loop diuretic
blocks Na, K, Cl reabsorption in kidneys --> inhibits water reabsorption --> urination
treats edema due to heart failure, hypertension
very potent diuretic

2) HCTZ- thiazide diuretic
blocks Na reabsorption by the kidneys --> inhibits water absorption --> urination
*Acts on different part of kidney


What is the function and mechanism of:
albuterol, sameterol

Beta2 adrenoceptor agonists
short and long acting, respectively
promotes bronchiolar smooth muscle vasodilation/relaxation
treats asthma, SOB, coughing, wheezing


What is the function and mechanism of:

Fluticasone - inhaled glucocorticoid receptor agonist
anti-inflammatory - treats asthma attacks


What are the layers of the heart?

Endocardium - simple squamous epithelium; contains conduction system of Purkinje fibers
Myocardium - muscle cells
Epicardium - outer most layer- contains coronary blood vessels and fat


What is ANP and BNP? What is their purpose

ANP granules stored in atrium - decreases blood volume and BP, antagonist to renin so promotes excretion of salt and water by kidneys

BNP produced by ventricular myocytes (not stored in granules) - decreases blood volume and pressure
*used as diagnostic sign of congestive heart failure (released to deal with edema)


Describe the 3 different types of capillaries and where they are found:
1) continuous
2) fenestrated
3) sinusoidal

1) continuous - tight junctions, pericyte stem cells present, function as pinocytic vesicles for transport, continuous basal lamina, found in muscle brain (constitute blood brain barrier) thymus bone lung

2) fenestrated - many pores, continuous basal lamina, located in endocrine glands, kidneys, pancreas

3) sinusoidal - incomplete endothelial lining as well as basal lamina, blood cells pass through; found in liver spleen adrenal gland


histology: compare arteries and veins

Arteries: walls thick with respect to lumen, more elastic and smooth muscle tissue (Arranged in circular pattern; smaller arteries have more smooth and less elastic tissue), tunia have clear boundaries, no valves

Veins: walls thin with respect to lumen, more collagenous tissue, less elastic; thinner walls, tunica lack clear boundaries, often found with blood (no postmortem contraction)


histology: describe lymphatic vessels

no basement membrane, not found in CNS, no blood cells in lumen; found in CT of skin, respiratory, GI, UG tract


Describe the layers of blood vessels

1) Tunica intima - endothelium + basement membrane; all vessels have one

2) Tunica media - circularly arranged smooth muscle and elastic tissue to control distribution of blood pressure; much less in veins

3) Tunica adventitia - thin in arteries, thicker in veins; vaso vasorum and nervi vasorum


What are functions of endothelial cells

-selective permeability barrier
-metabolic properties
-contain cholinesterase and MAO (breaks up norepi)
-produce NO vasodilator
-can produce angiotensin II vasoconstrictor
-vWF coagulant if outer layer is damaged
-produce clot busters
-leukocyte adhesion and migration (recognize selectins on surface of ECs)
-formation of new blood vessels
-ECs in hypoxic tissue can secrete HIF-1


Describe the mechanism of artherosclerosis

fatty streaks in the tunica intima --> injury to endothelium --> forms artheromatous plaques in the intima (calcified fatty goo) --> invasion of monocytes from lumen and smooth muscle cells from tunica media -> more plaque --> occlusion or thrombus formation


What happens with arteriolar constriction? Dilation?

1) Arteriolar vasoconstriction --> increased TPR --> increased MAP --> Decreased vascular conductance/ blood flow --> decreased Pcap --> decreased capillary filtration (decreased lymph flow)--> increased reabsorption from ECF --> increased venous return --> increased CO --> increased blood pressure

2) Arteriolar dilation --> decreased TPR --> decreased MAP --> increased blood flow --> increased Pcap --> increased capillary filtration --> decreased venous return--> decreased blood pressure (can also lead to edema since lymphatic system cannot process all the increased filtration)
*increases capillary blood flow, venous hydrostatic pressure, filtration rate


What is the site of highest resistance in the cardiovascular system?

alpha1 receptors on arterioles of skin, splanchnic, renal
beta1 receptors on arterioles of skeletal muscles

*alpha1 and beta2 in vascular smooth muscle cause opposite effects, but beta2 is more sensitive to epi
so low epi --> dilation
high epi --> constriction

greatest increase in blood pressure and decrease in blood flow from arterioles to capillaries --> induces filtration of gas and nutrients from blood to cell

greatest decrease in pressure from arteries to arterioles (bc arterioles have highest resistance)


What happens when you go from a supine to standing position? How does body compensate?

What if there is high BP/autonomic failure?

When you stand up: gravity causes blood to pool in your leg veins --> decreases venous return to the heart --> decreases CO --> decreases MAP

to compensate: low pressure baroreceptors detect decrease in MAP --> activate medulla vasomotor center --> activate SNS and inhibit PSNS --> increase HR, contractility, TPR, MAP, and CO--> normotensive

if there is autonomic failure eg no low pressure baroreceptors --> orthostatic hypotension when standing up (low BP)

hypertension --> pressure diuresis --> volume loss through urine --> orthostatic hypotension


What is systolic blood pressure?
Diastolic blood pressure?
Pulse pressure? What is it proportional to

Systolic pressure (120 mm Hg) - highest pressure, right after rapid ventricular ejection, at start of reduced ventricular ejection (think of it as cardiac output)

Diastolic pressure (80 mm Hg) - lowest pressure, right before ventricular ejection during systole (think of it as vascular resistance)

Pulse pressure = systolic - diastolic pressure
it is directly proportional to stroke volume (EDV - ESV)
as stroke volume increases --> pulse pressure increases
*job of aorta is to reduce PP bc it is compliant


What is the coronary sulcus and what does it contain?
Anterior interventricular sulcus?
Posterior interventricular sulcus?

Coronary / atrioventricular sulcus separates atria and ventricles:
circumflex of LCA
coronary sinus
great cardiac vein

Anterior interventricular sulcus separates LV and RV on anterior surface:
great cardiac vein

Posterior interventricular sulcus separates LV and RV on posterior surface:
middle cardiac vein