Cardiovascular Sequence, October 2000

CH. 1 Physiology
Vascular flow: (mL/min); constant throughout system (equal flow in arteries, capillaries, veins); F=P/R
Cardiac output: CO = MAP/TPR, MAP=mean arterial pressure, TPR=total peripheral resistance (excludes lungs & heart)
CO= (Paortic – Pvenous)/TPR; Pvenous =0 in healthy people; Pvenous >0 in people w/ CHF (congestive heart failure)
CO= HR x SV; HR=heart rate, SV=stroke volume
Compliance: C=V/P; V=volume, P=pressure; Cvein >> Cartery; can add/remove volume from vein w/o much pressure change;
small change in venous pressure reflects large change in volume
Cardiac pumping: effective when 1) synchronized (not arrhythmic), 2) valves open fully (not stenotic), 3) valves don’t leak
(not regurgitant), 4) forceful (not failing), 5) heart must fill (not dry)

Contraction: isometric = fixed length; isotonic = constant load

Afterloaded contraction: 1st isometric (add weight to resting muscle), 2nd isotonic contraction (contract muscle)
Norepinephrine: incr. contractility of isometric contraction; incr. shortening (& SV) of afterloaded contraction
Pressure-volume cycle & muscle length-tension cycle: see figure; 1) passive filling (stretch), AV valves close; 2) muscle
tension increases, aortic valve opens; 3) muscle shortens, aortic valve closes;
4) isometric relaxation, AV valves open
Preload: resting length (resid. vol.=LV EDV); more shortening & more stroke volume (w/ constant contractility & afterload)
Starling’s law: greater resting length (due to greater preload)  greater shortening
EDVV = end-diastolic ventricular volume (just before contraction)
Afterload: stenotic valve or atherosclerosis; load against which heart must contract to open aortic valve (=MAP);
less shortening and less stroke volume (when contractility & preload constant); more power used
Contractility: NE incr. peak isometric tension; more shortening and more stroke volume (when preload & afterload constant)
Cardiac output: HR (heart rate) x SV (stroke volume)
HR: decr. by parasymp. nn. (negative chronotropic); incr. by symp. nn. (positive chronotropic)
SV: incr. by contractility (symp. nn., positive inotropic); decr. by afterload (MAP); incr. by preload (filling pressure)
Normally: CO=4.9 L/min; HR= 70 beats/min; SV= 0.07 L/beat
Inotropic: alters stroke volume (eg. + sympathetic, + epinephrine, + dopamine)
Chronotropic: alters heart rate (eg. + sympathetic, – parasympathetic) by changing slope of pacemaker potential
Pacemaker potential: faster by symp. stim. (decr. K+ perm.); slower by parasymp. stim. (incr. K+ perm. hyperpolarized);
Fluids:  CVP   RV preload   MAP   HR (baroreceptor relex); extent of HR lowering indicates how badly patient
needed fluids; (fluids also  PCWP)
Bleeding:  PCWP

Left Heart: see notes; no valves on LA inflow  no isovolumic contraction  no rise in LA pressure ( if leaky mitral valve)
1. Atrial contraction: increases ventricular volume to peak (130 mL)
a wave in atrial pressure
2. AV valve closes: 1st heart sound (LUB); just as LV begins to contract
3. Isovolumic contraction: steep rise in LV press; const. LV volume when all valves closed; metabolically costly; isometric
4. Aortic valve opens: just as LV press. > aortic press.
c wave in atrial pressure – blood drums against AV valve as ventricles contract
5. Ejection: most blood leaves at beginning of ejection; peak systolic LV/aortic press. (~125)
6. Aortic valve closes: just as LV press. < aortic press.; 2nd heart sound (DUB)
7. Isovolumic relaxation: steep drop in LV press; const. LV volume when all valves closed
dichrotic notch: elastic recoil of aortic valve
8. AV valve opens: just as LV press. < LA press.
v wave in atrial pressure = passive filling of atria
9. Ventricular filling: rapid inflow (LA  LV); ventricle compliant – large volume change w/ little pressure change

Ejection fraction: percentage change in volume

Ventricular systole: AV valve closes (LUB)  AV valve opens
Arterial systole: Aortic valve open  aortic valve closes (DUB)
RA pressure: mean= 3; central venous pressure = CVP  RV preload
RV pressure: syst= 24; diast= 4
Pulmonary pressure (PAP): syst= 24, diast= 9, mean= 15
Pulmonary capillary wedge pressure (PCWP): mean= 10; approx. LA pressure (can’t measure w/ catheter)  LV preload
LV pressure: syst= 130, diast= 9
Aortic pressure: syst= 125, diast= 70, mean= 90; aka systemic arterial pressure  LV afterload
CH. 4 Electrocardiogram: Rate, Rhythm, Axis, Calibration, Intervals; RA = right arm; LA = left arm; LL = left leg
Positive wave toward positive pole = positive deflection
Einthoven’s triangle: 3 leads (I – RA to LA; II – RA to LL; III – LA to LL); bipolar = I, II, III
Ischemia = inadequate blood flow; infarct = tissue death due to ischemia  deviant mean electrical axis
Segment: no electrical activity between waves; Intervals: include wave & segment
P wave: due to atrial depolarization
QRS interval: due to ventricular depolarization; Q = 1st neg; R = 1st pos; S = 1st neg after pos
T wave: ventricular repolarization, but in opposite direction (last to depolarize is first to repolarize)
Normal interval values: PR = 0.12 – 0.20 sec; QRS  0.10 sec; corrected QT  0.44 sec; see Lilly table 4.2
Augmented voltage (right, left, foot): yields 6 frontal plane leads; unipolar = aVR, aVL, aVF
Planar axis: -30 (aVL); 0 (I); 60 (II); 90 (aVF); 120 (III); -150 (aVR)
Precordial leads: exploring (roving) lead to look at horizontal plane; V1 – V6
HR calc: HR = (25 mm/s (paper speed) x 60 s/min) / mm/beat = 1500 / boxes between beats
Bundle branch block: QRS step; infarct in septum; Purkinje fibers slower on one side than other; depol. out of phase
Deviations: LV hypertrophy  left axis deviation (> –30); RV hypertrophy  right axis deviation (> +90)
Transmural MI: entire wall damaged; resting state is partially depolarized  baseline shifted down  ST segment elevation
Non-transmural MI: sub-endocardium damaged; resting state is partially depolarized  baseline shifted up  ST segment
depression (also seen w/ angina)
Pathologic Q wave: indicates LV is dead  dominated by RV & septum, away from aVL
Localization of MI:
Site EKG leads Coronary aa.
SA, AV RCA
Inferior II, III, aVF RCA
Septal (His) V1, V2 LAD
Anterior V3, V4 LAD
Lateral I, aVL LCx
Apical V5, V6 any of 3

Vasoconstriction: decr. radius  incr. tissue R  decr. tissue blood flow

globally: decr. radius  incr. TPR  incr. MAP or decr. CO
Vasodilation: incr. radius  decr. tissue R  incr. tissue blood flow
Vascular smooth muscle control mechanisms
VSM tone: intrinsic contractile state
Autoregulation: constant flow; steady-state after sustained pressure increase
Metabolic control: constant pressure; active hyperemia (incr. metabolism) or reactive hyperemia (after releasing a clamp);
many metabolic factors
Neural control:
Sympathetic vasocontrictor: -adrenergic
Parasympathetic vasodilator: acetylcholine released; in brain, heart, genitalia
Sympathetic cholinergic: acetylcholine, vasodilators
Humoral response: -adrenergic vasodilators (low epin.); epin/norepinephrine systemic vasoconstrictors
Venoconstriction: moves blood to central venous pool (CVP) from peripheral venous pool (PVP)
Venous return: equal to cardiac output; movement of blood from PVP to CVP
Swan Ganz catheter: balloon tip inflated when enters vena cava, measures pressure; wedges in pulmonary capillaries  PCWP
Thermodilution cardiac output: deflate balloon, inject 5-10 cc cold saline into RA  measure temp change in Swan cath
if large cooling change  low CO; if small cooling change  high CO; if saline warms up, overestimates CO

CH. 11-12 Cardiac Arrhythmias

Bradyarrhythmias
Bundle Branch Block (BBB): RBBB ; LBBB ;Fascicular block
AV Block: First degree: Second degree: Type I: Type II: Third degree: Escape rhythms: Physiologic AV block:
Sinus bradycardia: SA block: Type I: Type II: Sinus arrest: Sick sinus syndrome (tachycardia-bradycardia):

Tachyarrhythmias
Supraventricular tachycardia (SVT): Paroxysmal (PSVT): AV junctional re-entrant tachycardia: AV nodal re-entry:
Orthodromic AV re-entrant: Accessory pathway w/ ventricular pe-excitation (Wolff-Parkinson-White): Sinus tachycardia:
Premature atrial complaex (PAC): Atrial tachycardia: Atrial flutter: Atrial fibrillation: Premature ventricular complex (PVC):
Ventricular tachycardia (VT): Torsades de Pointes (TDP): Ventricular flutter: Ventricular fibrillation:
CH. 5 Atherosclerosis: majority of plaques have no Sx and no consequences
CAD Risk Factors: age, male, high LDL cholesterol (>130), low HDL cholesterol (<35), hypertension, smoking,
diabetes, family Hx
Arterial wall: intima (endothelium); media (smooth m.); adventitia (fibroblasts, vessels)
Fatty streak: foam cells (lipid-filled macrophages) accum. in intima
Endothelial cells: usu. non-thrombogenic (prostacyclin)
Smooth muscle cells: produce ECM
Fibrous plaque: expansion of intima; central necrotic core = necrotic debris, cholesterol crystals, inflammatory cells;
Plaque erosion: endothelium focally disrupted, collagen exposed; slow indolent growth (0-1% growth index)
Plaque rupture: rupture of fibrous cap is main event leading to thrombosis (release of tissue factor)  occlusion
Consequences: plaque rupture, intraplaque hemorrhage (plaque volume  abruptly), arterial stenosis (70% = exertional angina),
distal embolization (infarct, stroke), aneurysm (usu. abdom. aorta)
Similar lesions: re-stenosis (after stent or ballon cath), bypass graft arteriosclerosis (surgical trauma), intimal thickening (often
in prosthetic grafts, dialysis), heart transplant arteriosclerosis (rejection by T cells, macs; smooth m  ECM)

CH. 6 Ischemic Heart Disease: Chronic Coronary Syndrome (Angina)

Myocardial O2 supply: vascular tone (external compression, intrinsic regulation), perfusion pressure (approx. diastolic BP;
 BP due to hypotension or aortic regurg), collaterals, diastole duration ( flow to LAD, RCA; compromised by HR)
Myocardial O2 demand: wall tension ( LV pressure,  radius,  thickness), contractility, HR, preload, afterload
CAD: coronary artery disease = atherosclerosis
Vasoconstricters: -adrenergic sympathetics, endothelin-1
Vasodilators: -adrenergic sympathetics, prostacyclin, EDRF-NO, low O2, low ATP (adenosine)
External compression: during systole; also local Venturi effect
Angina: stable; unstable; variant; silent ischemia
Pathogenesis: due to vessel narrowing, endothelial dysfunction, & non-coronary factors in addition to CAD
Vessel stenosis: resting coronary flow OK up to 70% occlusion; maximum coronary flow OK up to 40% occlusion
Endothelial dysfunction: insufficient EDRF-NO release in response to stress  vasoconstriction
Non-coronary factors:  O2 supply (anemia, hypoxia,  pressure),  O2 demand (aortic stenosis, severe HCM, thyrotoxicosis)
Diagnosis
EKG stress test: severe CAD if 1) Sx/EKG occur in 1st 3-6 min or persist >5 min, 2) ST depression > 2mm, 3) systolic BP falls
during exercise, 4) sustained VT occurs, or 5) cannot exercise beyond 2-3 min.
Myocardial perfusion scintigraphy: tracer injected at peak exercise, image heart; compare to normal  cold spot = stenotic
Echocardiogram: ultrasound at rest & then peak; ischemia =  systolic wall thickening (dyskinetic) & motion (hypokinetic)
Coronary angiography: gold standard; inject dye into coronary aa.; most reliable anatomical data
Treatment: prevent atherosclerosis progression, prevent conversion of stable to unstable, relieve Sx, prolong life
Percutaneous coronary intervention (PCI): balloon angioplasty or stent; relieves angina caused by >50-60% stenosis; however,
does not prevent acute MI in stable angina pts (b/c 30% occluded aa. more likely to thrombose to MI)
CABG: bypass graft; relieves angina; preferred left internal mammary a. to LAD; prolongs life in pts w/ 1) left main stenosis,
2) 3 vessel disease, 3) 2 vessel w/ proximal LAD disease
Prognosis: predicted by age, LV dysfunction, extent of CAD (# vessels)
Acute Coronary Syndromes (ACS)
Pathogenesis: plaque rupture  platelet aggregation  clotting cascade  downstream ischemia/infarction (MI)

Advanced Cardiac Life Support (ACLS): ultimate goal = return patient to prearrest level of neurologic function
defibrillation class I: most frequent initial rhythm in witnessed sudden cardiac arrest is VF  bext Tx is defibrillation
probability of successful defib diminished 7-10% each minute; epinephrine 1mg IV every 3-5 min. for V-fib,
pulseless VT, asystole, or PEA (pulseless electrical activity); (epi not for bradycardia?)

CH. 7 Acute Myocardial Infarct

CH. 8 Valvular Heart Disease

CH. 9 Heart Failure

CH. 10 Cardiomyopathies
Basic Radiology
Imaging: ionizing radiation = CXR, fluoroscopy, nuclear imaging, CT, angiography; no ionizing radiation = MRI, echo (no
contrast needed either); radiation  malignancies, contrast  damages heart
Normal heart contours
Frontal: left margin = LV, right margin = RA; upper left = aorta & pulmonary trunk; upper right = SVC
Lateral: posterior upper margin = LA, posterior lower margin = LV, anterior margin = RV
Right atrial pattern: RA expands lateral right; tricuspid valve atresia
Right ventricular pattern: RV expands up & out, displaces LV & forms left border; RV contacts chest wall & sternum; RVH
due to pulmonary HTN, tetralogy of Fallot
Left atrial pattern: upper heart dilates, 4th bulge on left; mitral valve stenosis
Left ventricular pattern: LV goes down & lateral left; lower posterior margin bulges; aortic valve insufficiency, LVH
Normal pulmonary blood flow pattern: more flow in lung bases than apices (gravity); normal vessel diameters: base = 4-6 mm,
mid-lung = 2-3 mm, upper lung = 1-2 mm
Increased flow pattern: all vessels dilate; due to shunt, incr. volume (renal failure), incr. CO (pregnancy, hyperthyroid)
Decreased flow pattern: all vessels small; due to low flow (oligemia): dehydration, embolic obstruction, tetralogy of Fallot
Precapillary obstruction: central aa. dilate; due to pulmonary hypertension
Postcapillary obstruction: redistribution of flow from bases to upper lung; high capillary bed pressure; due to mitral
stenosis (LA bulge), aortic stenosis; aka cephalization
Lung water: pulmonary edema = capillary hydrostatic pressure > osmotic pressure
Interstitial pulmonary edema: thickened septal lines (Kerley B lines); lobules normally 8-15 mm; blurred vessel margins =
perivascular or peribronchial cuffing
Alveolar pulmonary edema: butterfly pattern opacity

Heart Failure
Left HF: systolic dysfxn due to impaired contractility (MI, TIA, chronic volume overload (mitral regurg, aortic regurg),
DCM), incr. afterload (aortic stenosis, HTN); diastolic dysfxn due to impaired LV relaxation (LVH, HCM, RCM,
TIA), obstructed LV filling (mitral stenosis, pericardial restriction or tamponade)
Right HF; due to left HF, pulmonary emboli
Classification of cardiac failure: NYHA
Class Physical activity 2 yr mortality on ACE-I
I ASx 10%
II slight limitations 20%
III marked limitations 30-40%
IV Sx at rest 40-50%

Aging
Changes: myocardial stiffness (decr. myocyte number, incr. myocyte size, same heart size), vascular stiffness (incr. thickness
of intima/media, etc.), diminished heart function (contraction speed), decr. parasympathetic response, decr. HR
response to exercise (CO dependent on SV), impaired diastolic filling, incr. sympathetic activity (more NE), decr.
sympathetic receptor sensitivity, decr. baroreceptor sensitivity, incr. BP variability, decr. LV function w/ exercise
Unchanged: resting HR & systolic function, epinephrine levels
Epidemiology: CVD most common cause of death in elderly; heart failure is geriatric syndrome (seen after age 60); most
common HTN is isolated systolic HTN (more women); first MI rate exponential incr. w/ age
CV risk assessment: PP > SBP > DBP; pulse pressure indicates reduced vascular compliance

Women
Syndrome X: chest pain + abnl stress EKG + normal coronary aa.; may respond to hormone supplements
Proven benefit: aspirin, -blockers, ACE-I, statins
Unproven benefit: hormone replacement therapy (HRT), anti-oxidant vitamins
MI: women age 50-70 have increased mortality after MI
Stroke: more prevalent in men, but women more likely to die of CVA
Oral contraceptives: MI :usu. low risk, but high risk when older (>35), smokers, uncontrolled HTN; CVA: 3x risk; VTE:
3-4x risk; VTE w/ factor V Leiden: 30x risk
Estrogen: mixed results; incr. benefit when combined w/ statins
Guidelines: statins, >30 min physical activity daily, target BMI < 25
Pregnancy: acute MI occurs in 3rd trimester, women > 33 y.o., multigravid pts; ACE-I & warfarin contraindicated
Peripartum cardiomyopathy: dilated CM; usu. 3rd trimester, Dx’ed post-partum; discourage subsequent pregnancies
Maternal mortality: assoc. w/ primary pulmonary HTN, cyanotic congenital heart disease; pts should avoid pregnancy
Blacks & Hypertension
Expanded plasma volume: causes  renin; BUT, majority of blacks are NOT volume expanded (don’t need diuretics)
Blacks w/ HTN have more end-stage renal disease: related to BP & baseline renal fxn (not genetic ‘black kidney’)
CV protection: by ALL drug classes; 5 mmHg decr. in MAP causes 42% decr. in CVA

Congenital Heart Defects

Normal development: cardiac myocytes  straight tube  loops to right  inlet/outlet to midline  divides in half (septate)
by endomyocardial cushion
Arrested development: double-inlet LV, double-outlet RV, AV septal defect, truncus arteriosus, ASD, VSD
Abnormal development: transposition of great vessels, tetralogy of Fallot, aortic arch abnormalities
Neural crest migration: patterns aortic arches; maturation of myocardial cushions in outflow tract & AV canal
Conotruncus division: undivided = truncus arteriosus; anterior deviation = tetralogy of Fallot; posterior deviation = aortic
stenosis & VSD; under-rotation = transposition of great vessels
Fetal circulation: provide most oxygenated blood to brain & myocardium; 3 fetal shunts (also placenta); RV has 2/3 flow,
LV has 1/3 flow; highest O2 saturation is 70% (IVC); highest pO2 is 35 torr
Ductus venosus: umbilical v. bypasses hepatic v. to IVC (50% flow to each)
Patent foramen ovale: oxygenated blood from IVC to RA through flap valve to LA (bypass lungs); baby cries  lungs fill with
air   PVR   pulmonary flow   flow to LA   LAP closes foramen ovale
Patent ductus arteriosus: blood from RV to pulmonary a. to aorta (bypass lungs) due to high pulmonary resistance; less flow
through ductus arteriosus when umbilical cord cut  incr. systemic resistance  more flow from RV to lungs;
constricts due to pO2 or indomethacin (also aspirin, NSAIDs), dilates due to prostaglandin E (PGE2)

Patient with Palpitations

Palpitations = awareness of one’s heartbeat; skipped beats, fluttering, pounding, racing
Holter monitor: EKG records all beats in 24 hour period
Event monitor: patient-initiated EKG record; worn days-weeks; memory loop; transmitted by phone
Intracardiac E-P study: electrode catheters directly in heart; can differentiate bet. AV nodal vs. His-Purkinje 2:1 2 AV block;
can induce & terminate tachycardias
SVT treatment: 1) drugs, 2) radiofrequency catheter ablation
PVC (premature ventricular complexes): clinically significant only in presence of heart disease; no study has proven that PVC
suppression saves lives; Tx: if LVEF > 0.40, -blocker; if LVEF < 0.40 & non-sustained VT, test for inducible VT

Patient with Syncope

Syncope = sudden temporary loss of consciousness w/ spontaneous & rapid mental recovery (may be followed by seizure)
Seizures: aura, lasts minutes, post-ictal confusion, CNS origin
Hypovolemia/shock: orthostatic BP  reflex tachycardia
Neurocardiogenic: hypotension precedes bradycardia; consciousness returns once supine; mis-interpreted signal  overactive
parasympathetic response
Long QT syndrome (LQTS): QT prolonged w/ slow HR; “ion channelopathy” of dysfunctional K-channels; predisposes to
torsade de pointes, esp. women; QTc = QT/RR (sec), QTc > 0.45 men, > 0.46 women; avoid QT-prolonging drugs
w/ congenital LQTS: quinidine, procainamide, disopyramide, sotalol, amiodarone, dofetilide, macrolides, terfenadine

Nutrition: see handout & phi chis

Salt required for CHF pts is 5-6 g NaCl, which is 2 - 2.4 gm Na.
1 liter of 0.9% normal saline contains 9 gms of NaCl
Increased triglycerides respond to a diet moderately reduced in fat but primarily reduced in white flowers, and simple sugars.
3500 calories up or down is the energy in calories or burned to increase or decrease 1 lb.
Micronutrient supplements (vit E and beta carotene for example) are not as important as dietary sources because they have only
a portion of the important tocopherols and carotenoids for examples.
Saturated fat increases LDL-C by down regulating LDL receptor activity or clearance
anorexia nervosa is associated with sudden death.
Obesity is associated with hypertension, low HDL-C, high triglycerides, diabetes, and hypertension. Also in some sleep apnea
which can be associated with pulmonary hypertension and cor pulmonale.
*Treatment for Increased Triglycerides levels
*Saturated fats downreg. LDL clearance
*prescribed salt intake in grams.
Women
What are major risk factors for CVD for Women vs. Men? What are gender differences in risk?
Know AHA/ACC guidelines for prevention
Know what illnesses are contraindications to pregnancy, and what major classes of CV complications of pregnancy are.