Applied cardiovascular physiology Flashcards
Principles of management of hyperkalaemia and actions (3)
1 membrane stabilization
- administer Ca+
- returns membrane excitability
2 promote cellular uptake of K+
- administer insulin
- stimulates Na/K ATPase
- blood glucose closely monitored
3 K+ excretion
- administer Resonium A
- promotes gut removal of K+ (in echnage for Na+)
SOB investigations for pt with history of MI, hypertension and diabetes + pitting edema, tachycardia, hypertension, low O2sat, hepatomegaly, ascites, raised JVP, hepatojugular reflex, displaced apex beat, S3 gallop, loud P2, bilateral basal crackles? (8)
1 ECG - cardiac failure
2 CXR - pulmonary congestion and cardiomegaly
3 Transthoracic echocardiography - structural abnormalities
4 BNP and N-terminal proBNP - differentiate cardiac vs non cardiac HF
5 EUC + GFR + LFT - baseline and guide pharmacotherapy
6 FBE - anaemia
7 blood glucose - co morbidities
8 TSH - exacerbate HF
Hyperkalaemia: What is normal range? What is considered elevated serum potassium levels at different severity levels?
Normal = 4-4.5mEq/l
Elevated = >5.5mEq/l
Mild: 5.5-6.5mEq/l = asymptomatic
Moderate/high: >6.5mEq/l = life threatening arrhythmias
List causes of hyperkalaemia (4)
1 pseudohyperK+ = haemolysis
2 increased intake
3 impaired excretion
4 other = cellular injury, DKA
Describe excitation-contraction coupling (6)
1 rapid depolarization triggers T tubules to release Ca+ from SR
2 Ca+ binds to troponin C
3 change in configuration of troponin/tropomyosin complex
4 contraction of myocyte
5 intracellular Ca+ rapidly removed from myocyte into SR or ECF
6 blocking of myosin interaction reducing tension = relaxation
Worker type cells vs pacemaker cells
Worker: large stable RMP + prolonged AP with plateau phase.
- atrial, ventricle and Purkinje cells –> Na+ channels –> rapid upstroke, brief refractory period
Pacemaker: smaller unstable RMP + spontaneously depolarise, generate intrinsic electrical activity of heart.
- slow upstroke and relatively long refractory period
Pathophysiology of heart failure
maladaptive haemodynamic compensation
e.g. myocyte modification –> decrease in CO –> neuroendocrine system response
How does a previous MI cause HF?
Pathological insult to myocardium reduces CO with neuroendocrine response (SNS and RAAS) = sodium and fluid retention, vasoconstriction, increased HR and contractility.
Leads to vicious cycle of maladaptive remodelling of LV function
Name 3 ion channels (ion and type) responsible for AP and outline role
Voltage gated Na+
- responsible for initial rapid depolarization
- open and close (at 20mV) quickly
Long type Ca+ slow
- responsible for muscle contraction (cardiac excitation contraction coupling)
- slow to open, for longer time
- balances initial low efflux of K+ = most responsible for plateau phase
Variable K+
- responsible for repolarization
- induced to open following rapid depolarization
Frank starling: SV vs EDV - in more specific terms?
Degree of muscle stretch (initial length of muscle fibers)
AND
force of contraction
Physiological result of hyperkalaemia in the heart cells (RMP)? What happens to ventricular depolarization? What if K+ levels are really high?
Elevated serum K+ = decreased K+ chemical gradient pushing K+ out of the cell = K+ stays in the cell = increased resting membrane potential (-75mV)
–> activates Na+ channels = less rapid influx of Na+ = slows AP conduction and ventricular depolarization
If K+ v high = all Na+ inactivated = asystole
Trans thoracic echo percentages - normal, mild, moderate, severe
Normal: 50-75%
Mild: 40-50%
Moderate: 30-40%
Severe: <30%
What is the threshold potential for pacemaker cells?
-40mV
RMP of cardiac cell? What ion is predominantly repsonsible?
-90mV
K+
Define heart failure
Heart failure is a complex clinical syndrome with typical signs and symptoms that generally occur on exertion, but can also occur at rest (particularly when recumbent). It is secondary to an abnormality of cardiac structure or function that impairs the hearts ability to fill with blood at normal pressure OR eject blood sufficient to fulfill the needs of the metabolising organs.
4 steps of valsalva maneuver and brief description of result
1 Breath out and hold = increased intrathoracic pressure = compresses heart and vessels
2 Increased thoracic pressure –> reduces venous return + compression of cardiac chambers = reduced preload = reduced CO = drop in aortic pressure = baroreceptor reflex = SNS –> vasoconstriction and tachycardia = recovery of BP
3 breathe normally = reduced intrathoracic pressure = reflex increase in HR
4 overshoot of BP above baseline = venous return increase into vasoconstricted circulation = increase BP –> baroreceptor reflex = decreased HR and vasodilation = normal BP
