The Heart and

Circulatory System
and The Kidney 1

Asst. Prof. Dr. Izzuddin Ahmad

Nadzirin
Dept. of Biomedical Science
Kulliyyah of Allied Health Sciences
Cardiac Output (CO)
•CO is the product of heart rate (HR) & stroke
volume (SV)
•SV is the amount of blood ejected from the
ventricles with each beat – average is
approximately 70 mls
•SV is affected by preload, contractility & after load
 Preload

•the stretch of the ventricle at the end of diastole

•the amount of stretch decides the amount of blood ejected
•volume administration is used to increase preload
•ventricular myocardium responds by contracting more
forcefully
•care must be taken not to overstretch the myocardium
Contractility

• the force of the myocardial contraction for a given preload

• the ability of the ventricles to increase stroke volume
• affected by electrolytes Na+, K+, Mg2+, Ca2+, pH, +ve & -ve
inotropes  preload & after load
• affected by oxygenation, areas of damage & disease &
ischaemic
After load

•the resistance of the arteries against ejection

•increasing after load reduces stroke volume
•increases cardiac workload
•a reduction in after load will reduce preload with dilated
vessels
Reasons for using
cardiac medications
•Angina – chest pain caused by reduced blood flow to the heart
muscles.
•Hypertension – common condition in which the long-term force of
the blood against your artery walls is high enough that it may
eventually cause health problems, such as heart disease.
•Arrhythmias – problem with the rate or rhythm of your heartbeat.
•Cardiac failure – condition that develops when your heart doesn't
pump enough blood for your body's needs.
•Fluid retention leading to cardiac conditions
•Hyper volume increases the work of the heart
Goals for treatment
•To reduce the work load of the myocardium to protect it
•To reduce systemic vascular resistance, hence potentially reducing
afterload
•To maintain sinus rhythm as arrhythmias can increase work on the
myocardium and increase the risk of angina and embolism
•Once the myocardium is diseased or damaged some sort of cardiac
failure could be predicted. To lessen the chances of having cardiac
failure affect the patient systemically i.e. kidney failure from
hypotension
Medication Groups
 Beta blockers
 Calcium channel blockers
 Nitrates
 ACE inhibitors
 Angiotensin II receptor blockers (ARB)
 Diuretics
 Digoxin
Medication Groups
BETA BLOCKERS
• action on β1 adrenoreceptors in the sinus node, conducting
system and contracting myocytes.
• block β1 adrenoreceptors  adrenaline/noradrenaline cannot
bind  sympathetic effects blocked.
• if conduction is blocked then HR is decreased leading to a fall in BP
• caution in asthma and COPD because they can also block β2-
receptor in lungs which causes bronchoconstriction.
• used for relief from angina, hypertension, arrhythmia
• side effects: Fatigue, shortness of breath on exertion, bradycardia,
postural disorders/dizziness, palpitation, headache, 1st degree heart
block (rare)
• E.g.: Propanolol, labetolol, metoprolol, (betaloc), sotalol, celiprolol,
atenolol, carvedilol
Medication Groups
CALCIUM CHANNEL BLOCKERS
• action on Ca2+ transfer in cell function affecting muscle
contraction
• if blocked, contraction slows & reduces
• Two groups:
• Dihydropyridines - Amlodipine/ Nicardipine/ Nifedipine/
Felodipine acts on blood vessels
• Non- Dihydropyridines – Verapamil/ Diltiazem acts on the
heart muscle
• used for relief from angina, hypertension, arrythmia,
coronary spasm.
• side effects: GI discomfort, oedema, arrhythmia, headache,
fatigue, rash, dizziness, heart block (rare).
Mechanism of contraction of the cardiac myocyte
by L-type voltage
Medication Groups
NITRATES
• action has direct effect on veins
• dilates veins so less blood is returning to the heart, therefore, the
heart does not have to pump so hard and fast (systole)
• resting phase is longer hence allowing more blood and O2 to the
myocardium (diastole)
• used for relief from angina, HT & cardiac failure
• side effects: Hypotension, vascular headache/initially dizziness,
flushing, syncope
• E.g.: Isosorbide mono-nitrate, (duride) isosorbide di-nitrate,
(coronex) glyceryl tri-nitrate (nitrolingual)
Nitrite ions are converted to nitric oxide which in turns activates guanylate cyclase and
increases the cells’ cyclic guanosine monophosphate (cGMP).
1) Elevated cGMP ultimately leads to dephosphorylation of the myosin light chain, resulting in
vascular smooth muscle relaxation.
2) Elevated cGMP activates SERCA pump that in turns reuptakes Ca 2+ into SR. This decreases
Ca2+ in the cytosol and causes relaxation.
 Medication Groups
ACE INHIBITORS
[Angiotensin Converting Enzyme]

• action affects both the heart and kidneys

• kidneys detect changes in BP, releasing renin when BP is low
• renin stimulates angiotension I leading to the development of
angiotension II leading to vasoconstriction
• vasoconstriction affects kidney function, hence lowered diuresis,
conserving fluids
• ACE inhibitors block the cycle
• dilation lowers preload, lowers afterload & increases diuresis
• used for relief from HT & cardiac failure
• Side effects: hypotension, rash, cough
• E.g.: Lisinopril, captopril, cilazopril, enalapril, quinapril, accupril
Medication Groups
ARB
[Angiotensin II receptor blockers]

• blocks angiotensin II action

• blocking causes dilatation of blood vessels  lowers BP
• generally prescribed for those that cannot tolerate ACE inhibitors.
• used for relief from HT & congestive heart failure
• Side effects: dizziness, diarrhoea, confusion, vomiting, cough (rare).
• E.g.: Losartan, telmisartan, eprosartan, Olmesartan, irbesartan.
 Medication Groups
•DIURETICS
• action is directly on the kidney
• Thiazides work by inhibiting the re-absorption of Na & Cl in the distal
convoluted tubule
• Loop diuretics inhibit Na & Cl absorption in the ascending loop of Henle
• K+ sparing diuretics act on the collecting tubule
• used for relief from HT & cardiac failure
• E.g.:
◦ Bendrofluazide – long term diuretic therapy and work by inhibiting the re-absorption of
Na & Cl in the distal convoluted tubule thereby, increasing diuresis. Maximal effect is 2
hours after oral dose, with their effect lasting 12 – 36 hours
◦ Furosemide, Bumetanide - Loop diuretics inhibit Na & Cl absorption in the ascending loop
of Henley and are effective at low rates of glomerular filtration.
◦ Aldactone, Amiloride - K+ sparing diuretics act on the collecting tubule, partially inhibiting
reabsorption of Na therefore, limiting exertion of potassium
• Side effects: electrolyte/fluid imbalance – require monitoring, GI upset, dizziness, vertigo
Medication Groups
•DIGOXIN

• action is to inhibit Na+/K+ exchange across the cell membrane

• this augments the Ca2+ influx leading to delayed, stronger contraction
• caution: low K+ enhances digoxin action and increased K+ decreases
digoxin effects
• belongs to the glycoside family
• side effects: bradycardia, toxicity, nausea, vomiting, heart block can
(rare).
Medication Groups cont’d

•SUMMARY

• usually cardiac medications work in combination

• withholding 1 medication may interrupt the ‘combination
action’
• symptomatic patients must be assessed by medical staff to
address the cause
• if apex < 60bpm or BP low & patient is asymptomatic,
continue medications, report to medical staff
THANK YOU