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
