Cardiovascular- physiology Flashcards
CO =
Fick principle:
Mean arterial pressure (MAP) =
MAP (at resting HR) =
stroke volume (SV) × heart rate (HR)
CO = rate of O2 consumption/ arterial O2 content − venous O2 content
CO × total peripheral resistance (TPR)
2 ⁄3 diastolic pressure + 1⁄3 systolic pressure
Pulse pressure =
SV =
systolic pressure – diastolic pressure. *Pulse pressure is proportional to SV, inversely proportional to arterial compliance.
end-diastolic volume (EDV) − end-systolic volume (ESV). *SV CAP: Stroke Volume affected by Contractility, Afterload, and Preload.
High pulse pressure in …
Low pulse pressure in …
hyperthyroidism, aortic regurgitation, aortic stiffening (isolated systolic hypertension in elderly), obstructive sleep apnea ( sympathetic tone), anemia, exercise
(transient).
aortic stenosis, cardiogenic
shock, cardiac tamponade, advanced heart
failure (HF).
Contractility
- High
- low
Catecholamine stimulation via β1 receptor, High intracellular Calcium, Lower extracellular sodium, digitals.
β1-blockade ( cAMP), HF with systolic dysfunction, Acidosis, Hypoxia/hypercapnia (Po2/ Pco2), Non-dihydropyridine Ca2+ channel blockers.
Preload
Afterload
Preload approximated by ventricular EDV; depends on venous tone and circulating blood volume.
Afterload approximated by MAP.
Increase afterload, increase pressure, increase wall tension percLaplace’s law.
Myocardial oxygen demand is increased by:
Increased Contractility
Increased Afterload (proportional to arterial pressure).
Increased heart Rate
Increased Diameter of ventricle (wall tension)
Ejection fraction
EF = SV/EDV = EDV − ESV/EDV
Left ventricular EF is an index of ventricular contractility.
Starling curve
Force of contraction is proportional to enddiastolic
length of cardiac muscle fiber (preload).
Resistance, pressure, flow
ΔP = Q × R
Volumetric flow rate (Q) = flow velocity (v) × cross-sectional area (A).
Resistance = Dividing pressure (ΔP)/ Flow (Q) =
8n (viscosity) x Length/ πr4
*Capillaries have highest total cross-sectional area and lowest flow velocity. Arterioles account for most of TPR. Veins provide most of blood storage capacity.
Compliance = ΔV/ΔP.
Cardiac and vascular function curves
- Inotropy
- Venous return
- Total periferal resistance
+ Catecholamines, digoxin ⊕, exercise
- HF with reduced EF, narcotic overdose, sympathetic inhibition ⊝.
+ Fluid infusion, sympathetic activity ⊕
- Acute hemorrhage, spinal anesthesia ⊝
+ Vasopressors ⊕
- Exercise, AV shunt ⊝
Phases—left ventricle:
Isovolumetric contraction—period between mitral valve closing and aortic valve opening; period of highest O2
consumption
Systolic ejection—period between aortic valve opening and closing
Isovolumetric relaxation—period between aortic valve closing and mitral valve opening
Rapid filling—period just after mitral valve opening
Reduced filling—period just before mitral valve closing
Heart sounds
S1—mitral and tricuspid valve closure. Loudest at mitral area.
S2—aortic and pulmonary valve closure. Loudest at left upper sternal border.
S3—in early diastole during rapid ventricular filling phase. Associated with increase filling pressures (eg, mitral regurgitation, HF) and more common in dilated ventricles (but can be normal in children, young adults, and pregnant women).
S4—in late diastole (“atrial kick”). Best heard at apex with patient in left lateral decubitus position. High atrial pressure. Associated with ventricular noncompliance (eg, hypertrophy). Left atrium must push against stiff LV wall. Consider abnormal, regardless of patient age.
Jugular venous pulse (JVP)
a wave—atrial contraction. Absent in atrial fibrillation (AF).
c wave—RV contraction (closed tricuspid valve bulging into atrium).
x descent—downward displacement of closed tricuspid valve during rapid ventricular ejection phase. Reduced or absent in tricuspid regurgitation and right HF because pressure gradients are reduced.
v wave—Increase right atrial pressure due to filling (“villing”) against closed tricuspid valve.
y descent—RA emptying into RV. Prominent in constrictive pericarditis, absent in cardiac tamponade
Normal splitting
Wide splitting
Fixed splitting
Paradoxical splitting
delayed closure of pulmonic valve with inspiration.
Seen in conditions that delay RV emptying (eg, pulmonic stenosis, right bundle branch block). Causes delayed pulmonic sound.
Heard in ASD
Heard in conditions that delay aortic valve closure (eg, aortic stenosis, left bundle branch block). P2 sound occurs before delayed A2 sound
Heart murmurs
Pag. 285
Auscultation of the heart (Where to listen: APT M)
- Aortic area:
- Pulmonic area
- Tricuspid area:
- Mitral area (apex):
- Left sternal border
Systolic murmur: Aortic stenosis, Flow murmur (eg, physiologic murmur), Aortic valve sclerosis.
Systolic ejection murmur: Pulmonic stenosis, Atrial septal defect, Flow murmur.
Holosystolic murmur: Tricuspid regurgitation, Ventricular septal defect,
Diastolic murmur: Tricuspid stenosis.
Holosystolic murmur: Mitral regurgitation
Systolic murmur: Mitral valve prolapse
Diastolic murmur: Mitral stenosis
Diastolic murmur: Aortic regurgitation, Pulmonic regurgitation
Systolic murmur: Hypertrophic cardiomyopathy
BEDSIDE MANEUVER (effect)
- Hand grip (increase afterload)
- Valsalva (phase II), standing up (decrease preload)
- Rapid squatting (Increase: venous return, preload, afterload)
Increase intensity of MR, AR, and VSD murmurs
Increase intensity of hypertrophic cardiomyopathy murmur.
Increase intensity of AS, MR, and VSD murmurs.
Myocardial action potential (Phases)
Phase 0 = rapid upstroke and depolarization—voltage-gated Na+ channels open.
Phase 1 = initial repolarization—inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open.
Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.
Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels.
Phase 4 = resting potential—high K+ permeability through K+ channels.
Pacemaker action potential (Phases)
Phase 0 = upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells. Results in a slow
conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.
Phases 1 and 2 are absent.
Phase 3 = repolarization—inactivation of the Ca2+ channels and increase activation of K+ channels, increase K+ efflux.
Phase 4 = slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current; Accounts for automaticity of SA and AV nodes.
*ACh/adenosine decrease the rate of diastolic depolarization and decrease HR
Electrocardiogram
- Conduction pathway:
- AV node—located in
- Pacemaker rates
- Speed of conduction
SA node atria AV node bundle of His right and left bundle branches Purkinje fibers ventricles; left bundle branch divides into left anterior and posterior fascicles.
posteroinferior part of interatrial septum. Blood supply usually from RCA. 100-msec delay allows time for
ventricular filling.
SA > AV > bundle of His/ Purkinje/ventricles
Purkinje > atria > ventricles > AV node.
Electrocardiogram
- P wave
- PR interval
- QRS complex
- QT interval
atrial depolarization. Atrial repolarization is masked by QRS complex.
time from start of atrial depolarization to start of ventricular depolarization (normally < 200 msec).
ventricular depolarization (normally < 120 msec).
ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization.
Electrocardiogram
- T wave
- J point
- ST segment
- U wave
ventricular repolarization. T-wave inversion may indicate ischemia or recent MI.
junction between end of QRS complex and start of ST segment
isoelectric, ventricles depolarized.
prominent in hypokalemia (think hyp“U”kalemia), bradycardia.
Torsades de pointes
Polymorphic ventricular tachycardia, Long QT interval
predisposes. Caused by drugs, Low K+, low Mg2+, congenital abnormalities.
Treatment includes magnesium sulfate
Drug-induced long QT
ABCDE AntiArrhythmics (class IA, III) AntiBiotics (eg, macrolides) Anti“C”ychotics (eg, haloperidol) AntiDepressants (eg, TCAs) AntiEmetics (eg, ondansetron)
Congenital long QT syndrome
Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness).
Jervell and Lange-Nielsen syndrome— autosomal recessive, sensorineural deafness.
Brugada syndrome
Autosomal dominant disorder most common in Asian males. ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3.
risk of ventricular tachyarrhythmias and SCD. Prevent
SCD with implantable cardioverter-defibrillator (ICD).
Wolff-Parkinson-White syndrome
Most common type of ventricular preexcitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent).
characteristic delta wave with widened QRS complex and shortened PR interval on ECG. May result in reentry circuit supraventricular tachycardia.
Atrial fibrillation
Chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes. Irregularly irregular heartbeat.
Most common risk factors include hypertension and coronary artery disease (CAD). Can lead to thromboembolic events, particularly stroke
Atrial flutter
A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves.
Definitive treatment is catheter ablation
Ventricular fibrillation
A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.
First-degree AV block
The PR interval is prolonged (> 200 msec). Benign and
asymptomatic. No treatment required.
Second degree Av block
- Mobitz type I (Wenckebach)
- Mobitz type II
Progressive lengthening of PR interval until a beat is “dropped”. usually asymptomatic.
Dropped beats that are not preceded by a change in the length of the PR interval (as in type I). May progress to 3rd-degree block. Often treated with pacemaker.
Third-degree (complete) AV block
The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically
associated.
Usually treated with pacemaker. Can be caused by Lyme disease
Atrial natriuretic peptide
Released from atrial myocytes in response to high blood volume and atrial pressure. Acts via cGMP.
Causes vasodilation and decrease Na+ reabsorption at the renal collecting tubule. Dilates afferent renal
arterioles and constricts efferent arterioles, promoting diuresis
B-type (brain) natriuretic peptide
Released from ventricular myocytes in response to tension. 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.
Chemoreceptors
- Peripheral
- Central
carotid and aortic bodies are stimulated by decrease Po2 (< 60 mm Hg), high Pco2, and decrease pH of blood.
are stimulated by changes in pH and Pco2 of brain
interstitial fluid, which in turn are influenced by arterial CO2. Do not directly respond to Po2.
Baroreceptors and chemoreceptors
Aortic arch transmits via vagus nerve to solitary nucleus of medulla.
Carotid sinus (dilated region at carotid bifurcation) transmits via glossopharyngeal nerve to solitary nucleus of medulla.
Pulmonary capillary wedge pressure (PCWP)
Is a good approximation of left atrial pressure. In mitral stenosis, PCWP > LV end diastolic pressure.
PCWP is measured with pulmonary artery catheter (Swan-Ganz catheter).
Autoregulation (factors determining)
- Heart
- Brain
- Kidneys
Local metabolites (vasodilatory): adenosine,NO, CO2, low O2.
Local metabolites (vasodilatory): CO2 (pH)
Myogenic and tubuloglomerular feedback
Autoregulation (factors determining)
- Lungs
- Skeletal muscle
- Skin
Hypoxia causes vasoconstriction
CHALK: CO2, H+, Adenosine, Lactate, K+ (during excercise). Sympathetic tone (at rest)
Sympathetic stimulation most important mechanism for temperature control.
