GPS: CV Physiology (Wondisford) - 11/1/16 Flashcards
What are the major changes that occur during the transition from fetal to adult circulation?
Before birth:
- Oxygenated blood travels from placenta via umbilical vein (single)
- Deoxygenated blood returns to placenta via umbilical arteries (paired)
At birth:
- 3 bypass channels close (ductus venosus, foramen ovale, ductus arteriosis)
- Removal of placenta
Cardiac Muscle:
Involuntary / voluntary?
Striated / smooth?
Uninuclear cells / Multinuclear cells?
How are cells connected?
- Involuntary
- Striated tissue containing:
- Uninuclear cells
Cells are connected end to end by intercalated discs
- Gap junctions (ion channels to propagate depolarization signal)
- Desmosomes (“spot welds”)
- Tight junctions
Myocardial/Ventricular Action Potential:
Main difference between cardiac myocyte and skeletal muscle AP
Steps in myocyte contraction
Main difference:
- cardiac myocyte AP has a plateau: due to Ca2+ influx and K+ efflux
- cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from SR (Ca2+-induced Ca2+ release)
- cardiac myocytes are electrically coupled to each other by gap junctions
Steps:
- Phase 0 = rapid upstroke, INa
- Phase 1 = initial repolarization
- Phase 2 = plateau, ICa + IK
- Phase 3 = rapid repolarization, IK
- Phase 4 = resting potential, IK
Frank-Starling Curve
What does it measure?
How can you inc. contractility?
How can you dec. contractility?
Force of contraction (stroke volume) is proportional to ventricular EDV (preload)
Inc. contractility:
- Catecholeamines
- Positive inotropes (e.g. digoxin)
Dec. contractility:
- Beta-blockers (acutely)
- Loss of myocardium (MI)
- Non-dihydropyridine Ca2+ channel blockers
- Dilated cardiomyopathy
Cardiac output = ?
SV = ?
CO = SV * HR
SV = EDV - ESV (all filled up - vol. after contraction)
Factors that affect SV (3)
- Inc. in preload inc. EDV and SV
- Inc. in afterload on the heart inc. ESV → dec. SV
- Inc. inotropy (contractility) dec. ESV → inc. SV
Fick Principle
Another way to calculate CO =
rate of O2 consumption / (arterial O2 content - venous O2 content)
(ml/min)/(ml/L) = L/min
Mean Arterial Pressure (MAP) =
CO * TPR
2/3 diastolic pressure + 1/3 systolic pressure
Pulse Pressure =
What is pulse pressure proportional/inversely proportional to?
In what conditions do you see inc. pulse pressure (4)?
In what conditions do you see dec. pulse pressure (4)
Systolic pressure - diastolic pressure
PP is proportional to SV and inversely proportional to arterial compliance
Conditions with inc. pulse pressure:
- Hyperthyroidism
- Aortic regurg
- Aortic stiffening (isolated systolic apnea) → inc. sympathetic tone ** not b/c diastolic goes down like in 1 & 2 but b/c systolic goes up
- Exercise (transient)
Conditions with dec. pulse pressure:
- Aortic stenosis
- Cardiogenic shock
- Cardiac tamponade
- Advanced HF
HR + contractility controlled by autonomic nervous system (PSNS + SNS).
PSNS
- via vagus nerve (cholinergic M2 receptors on SA and AV node) → REDUCE HR
SNS
- (adrenergic B1 receptors on SA and AV node, cardiac myocyte) → INC. HR + CONTRACTILITY
Contractility (and SV) increase with:
Contractility (and SV) decrease with:
Contractility (and SV) increase with:
-
Catecholamines (B1 receptor)
- Phosphorylation of Ca2+ channels cause Ca2+ channels to remain open longer
- Phosphorylation of proteins in SR enhances release of Ca2+
- Phosphorylation of myosin inc. myosin ATPase → inc. speed of cross-bridge cycling
- Phosphorylation of Ca2+ pumps in SR inc. speed of calcium re-uptake, and relaxation
- inc. intracellular Ca2+
- dec. extracellular Na+ (dec. activity of Na+/Ca2+ exchanger)
- NCX removes calcium from cells (1 Ca2+ out for every 3 Na+ in) so if you dec. Na+ amt or if NCX works poorly, calcium accumulates in myocyte
- digitalis
- (blocks Na+/K+ pump by competing with K+ for binding to Na+/K+ ATPase → inc. intracellular Na+ → dec. Na+/Ca2+ exchanger activity … no Na+ to come in for Ca2+ to go out → inc. intracellular Ca2+
- hypokalemia increases risk of drug toxicity
Contractility (and SV) decrease with:
- Beta-blockade
- Heart failure
- Acidosis
- Hypoxia
- Ca2+ channel blockers
Effect of SV on CO
Inc. SV with:
- Inc. contractility (e.g. anxiety, exercise)
- Inc. preload (e.g. early pregnancy)
- Dec. afterload
Effect of Preload and Afterload on Cardiac Output
Preload: approximated by ventricular EDV; depends on venous tone and circulating blood volume
- vEnodilators (e.g. nitroglycerin) dec. prEload
- causes veins in leg to dilate –> all blood gets pooled down there –> result: dec. in preload
Afterload: afterload approximated by MAP
- vAsodilators (e.g. hydrAlAzine) dec. Afterload (Arterial)
- inc. afterload → inc. pressure → inc. wall tension per Laplace’s law
- LV compensates for inc. afterload by thickening (hypertrophy) in order to dec. wall tension
- Inc. MAP → LV hypertrophy
ACE inhibitors and ARBs _____ (inc/dec) both preload and afterload
decrease
Laplace’s Law
Describes factors that affect wall tension
Wall tension = (Pressure x Radius)/2 * Thickness
MyoCARDial oxygen consumption (MVO2) = directly related to wall tension and inc. by inc.
- contractility,
- afterload,
- heart rate, and
- ventricular diameter
Types of cardiac hypertrophy
-
Concentric → Pressure Overload (sarcomeres added in parallel)
- Inc. LV wall stress (T) → LV wall thickens (h) → LV chamber radius decreases to attempt to reduce wall stress
-
Eccentric → Volume Overload (sarcomeres added primarily in series)
- Inc. BV (i.e. mitral regurg) → inc. chamber radius → inc. wall thickness can reduce tension
Cardiac hypertrophy can be physiologic or pathologic.
Physiologic:
- reversible
- pregnancy/endurance training → eccentric (cell predominately grows in length)
- Isometric exercise training (weight-lifting) → concentric
Pathologic:
- irreversible
- chronic HTN
- aortic stenosis
BP, CO, Resistance, and Ohm’s Law
MAP = CO * TPR
- MAP = 2/3 diastolic pressure + 1/3 systolic pressure
V = IR
During early stages of exercise, CO maintined by inc. HR and SV.
During late stages of exercise?
CO maintained by increased HR only (SV plateaus)
SV taps out - only so much that the heart can pump
Very high HRs compromise diastolic filling → actually reduce SV (e.g. ventricular tachycardia)
Swan-Ganz Catheter
pulmonary artery catheter measures left atrial pressure (pulmonary capillary wedge pressure)
In mitral stenosis, PCWP > LV end diastolic pressure
Viscosity depends most on _______.
Viscosity is increased in _______ and _______.
Hematocrit
Viscosity is increased in polycythemia (abnormally inc. hemoglobin amount in blood) and hyperproteinemic states.
Circulatory Resistance
Total resistance in series = sum of individual resistances
Total resistance in parallel < lowest individual resistance
(liver gets largest share of systemic CO)
Autoregulation
- Organ (6)
- Factors determining autoregulation
- Why is the pulmonary vasculature unique?
how blood flow to an organ remains constant over a wide range of perfusion pressures or metabolic needs
Capillary fluid exchange
Starling forces determine fluid movement through capillary membranes
Filtration happening on arteriolar side
Reabsorption happening on venous side
What is edema?
Common causes (4)
All cause pitting edema unless edema is long-standing or highly inflammatory.
Excess fluid outflow into interstitium
Cardiac Function Curves
As RAP increases, venous return decreases to a point (X-axis) called mean systemic pressure (arrow).
If RAP = -4, venous return tapers off b/c at this point, RA has collapsed. Venous return sort of stabilizes as RAP becomes more negative.
Curve:
Effect:
Examples:
Curve: Inotropy
Effect: Changes in contractility → altered CO for a given RAP (preload)
Examples:
- Digoxin (+ inotropy)
- Uncompensated HF, narcotic overdose (- inotropy)
Curve:
Effect:
Examples:
Curve: Venous return
Effect:
- Changes in circulating volume or venous tone → altered RAP for a given CO
- Mean systemic pressure (x-intercept) changes with volume/venous tone
Examples:
3. Fluid infusion, sympathetic activity (+ venous tone)
- this inc. systemic pressure b/c there is more pressure out in the periphery coming back to RA → shifts venous curve to the right → get more preload → more CO
4. Acute hemorrhage, spinal anesthesia (- venous tone)
Curve:
Effect:
Examples:
Curve: TPR
Effect: At a given mean systemic pressure (x-intercept) and RA pressure, changes in TPR → altered CO
Examples:
5. Vasopressors → insolated arteriolar constriction (+ TPR)
- CO and venous return curves both go down b/c when you constrict your blood vessels, you keep more blood on arteriolar side of circuit and less on venous side → still same amt of blood but it is harder to get that blood to the heart so you shift the slope of the line down → not decreasing the entire amount of blood
6. Exercise, AV shunt (- TPR)
Contraction is green.
Relaxation is red.
All PV loops must lie between the end-systolic PV relationship and the end-diastolic PV relationship
Cardiac cycle
- Isovolumetric contraction
- Systolic ejection
- Isovolumetric relaxation
- Diastolic Filling
- Isovolumetric contraction - period between mitral valve closure (B) and aortic valve opening (C); period of highest O2 consumption
- Systolic ejection - period between aortic valve opening (C) and closing (D)
- Isovolumetric relaxation - period between aortic valve closing (D) and mitral valve opening (A)
- Diastolic filling - period just after mitral valve opening (A) to mitral valve closing (B)
What do the following situations do to EDV and ESV?
A. Increased preload
B. Increased afterload
C. Increased contractility
A. Increased preload
- Inc. EDV
B. Increased afterload
- Inc. ESV
C. Increased contractility
- Dec. ESV
3 main types of systolic heart failure
What does systolic HF reduce?
diastolic heart failure
- MI, where myocardial mass is lost
- Alcoholism, which causes ventricular dilatation due to cardiomyopathy
- Pressure overload
Systolic HF reduces contractility and EF
- Weakened heart muscle can’t squeeze well
- Less blood pumped out of ventricles (low EF)
- Due to reduced contractility, SV first maintained by increased preload, resulting in increased end-diastolic pressure (EDP).
- Increased EDP transmitted to lungs
- Result: Dyspnea
Diastolic Heart Failure
- Stiff ventricle (concentric hypertrophy) inhibits ventricular filling (problem here is that you don’t have enough volume to begin with)
- EF is actually normal or elevated
Systolic HF:
Due to reduced contractility (solid line of ESPVR), stroke volume is at first maintained by increased preload, but end-diastolic pressure is increased as a result (arrow). This is transmitted to teh lungs resulting in dyspnea, etc.
Diastolic HF:
Due to concentric hypertrophy or other causes of a stiff LV, the EDPVR is shifted upward and to the left (solid line). This raises end-diastolic pressure (EDP), which also is transmitted to the lungs.
Heart Sounds:
S1
S2
S3
S4
S1: mitral and tricuspid valves close - loudest at mitral area
S2: aortic and pulmonic valves close - loudest at upper sternal border
S3: in early diastole during rapid ventricular filling phase
- associated w increased filling pressures (e.g. mitral regurg, HF)
- more common in dilated ventricles (but can be normal in children and young adults)
S4: in late diastole (“atrial kick”)
- best heard at apex with patient in left lateral decubitus position
- high atrial pressure
- associated with ventricular noncompliance (e.g. hypertrophy)
- LA must push against stiff LV wall
- consider abnormal, regardless of patient age
