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Cardiovascular Anatomy, Physiology and Pharmacology
BS913
Lecture 9: Drugs used in the treatment of cardiac diseases, effects, adverse reactions,
…
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Martini, Figure 20.12
Revision Physiology …
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Martini; Figure 20–12
The Conducting System
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Action Potentials in Skeletal and Cardiac Muscle
Martini; Figure 20–15
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Cardiodynamics
- Cardiac output
- End-diastolic volume
- End-systolic volume
- Stroke volume
- Heart rate
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SUMMARY: Factors Affecting Heart Rate and Stroke Volume
Martini; Figure 20–24
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Dynamics of Blood Circulation
Interrelationships between
- Flow
- Pressure
- Resistance
- Control mechanisms that regulate blood pressure and blood flow
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Heart SNS PSNS
• inotropy + -• chronotropy + -
Vessels
• Pulm./coronary constrict dilate• most others constrict no effect
ANS effects on heart and vessels
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How is Heart Rate Regulated?• Intrinsic pacemaker rate = 100 bpm• Autonomic Influences– SNS------> B1 receptor-------> Increased
HR– PSNS-> Muscarinic (Ach)--> Decreased
HR
• Stretch Reflex (Bainbridge): Increased filling------> Increased HR
• Drugs
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- Anything that increases Ca++ availability in the heart muscle cell will increase Contractility.
- Anything that decreases Ca++ availability in the heart muscle cell will decrease Contractility.
What Factors Affect Contractility?
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Cardiac conditions
- Hypertension
- Ischemic heart disease, Angina
- Heart failure; poor left ventricular function
- Arrhythmias
- Hyperlipidaemia
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Common drugs administered to cardiac patients
- Nitrates
- ß-blockers
- ACE inhibitors
- Digoxin
- Diuretics
- Anti-arrhythmics
- Ca-ch. blockers
- Aspirin
- Warfarin
- Statins
- others
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Cardiac medication: ß-blockers
- Body releases noradrenaline (sympathetic nervous system)
- Response to increased activity, danger, positive and negative stress:- increases HR and BP- bronchodilation
- ß-Blockers block effect of released noradrenaline
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Cardiac medication: ß-blockers
- used for: - hypertension- angina- post MI- heart failure- arrhythmias- migraine
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Cardiac medication: ß-blockers
- Effects and side effects:- bradycardia- hypotension- dizziness - tiredness, fatigue- cold fingers / toes- sleep disturbances- airway constriction- impotence
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Cardiac medication: ß-blockers
- Should not be stopped suddenly
- can cause rapid rise in BP and HR
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Cardiac medication: alpha-blockers
- Alpha receptors in blood vessels respond to release of noradrenaline vasoconstriction
- Alpha blockers block this effect
- Used for hypertension (usually combined with thiazid diuretics or ß-blockers)
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Cardiac medication: alpha-blockers - Effects / side effects:
- rapid drop in BP after initial dose- postural hypotension- headache- palpitations
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Cardiac medication: nitrates
- Act as vasodilator
- Coronary arteries: blood flow to heart muscle increased
- Great veins: reduces preload
- Great arteries: reduces afterload
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Cardiac medication: nitrates
- Used for:
- Angina
- Heart failure
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Cardiac medication: nitrates
- Effects and side effects:
- Facial flushing
- Headache
- dizziness
- Nausea
- Postural hypotension particularly after exercise
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Cardiac medication: potassium channel activators
- Dilate the large coronary arteries and smaller resistance vessels
- Increase coronary blood flow
- Additional vasodilatory effect on systemic blood vessels
- Reduces pre- and afterload
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Cardiac medication: potassium channel activators
- Used for: angina
- Effects and side effects:- Dizziness- Headache- Hypotension- Vasodilation- vomiting
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Cardiac medication: Ca channel blockers
- Intracellular Ca is essential for contraction
- Ca channel blockers prevent influx of Ca into specific cells leading to inhibition of contraction
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Cardiac medication: Ca channel blockers
- Effects of Ca channel blockers
- Dilate arteries in systemic circulation: reduced afterload
- Dilate great veins: reduced preload
- Relax coronary arteries
- Diltiazem / Verapamil: reduce contractility reduce oxygen demand of heart
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Cardiac medication: Ca channel blockers
- Used for:
- Type 1:verapamil
- Acts mainly on conducting pathway; slows heart
- angina, hypertension, and arrhythmias
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Cardiac medication: Ca channel blockers
- Used for:
- Type 2: Nifedipin etc.
- Acts mainly on smooth muscle fibres in arterial walls
- Angina and hypertension
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Cardiac medication: Ca channel blockers
- Used for:
- Type 3: Diltiazem
- Combines action of type 1 and 2
- Angina and hypertension
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Cardiac medication: Ca channel blockers
- Side effects:
- Facial flushing
- palpitations
- headache
- Ankle swelling
- Constipation (verapamil)
- Heart failure
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Cardiac medication: ACE inhibitors
- Inhibits synthesis of angiotensin II, a very strong vasoconstrictor which also causes fluid retention
- Main effects are:
- Reduction of BP- Prevention of vasoconstriction, reducing
afterload and increasing cardiac output
- Reduction of fluid retention
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Renin – Angiotensin system
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Renin-Angiotensin-Aldosterone
Angiotensinogen AI AII AIII
Renin ACE
vasoconstrictionaldosteronesecretion
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Cardiac medication: ACE inhibitors
- Used for:- hypertension- heart failure- post MI
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Cardiac medication: ACE inhibitors
- Side effects
- dry, annoying cough
- Low blood pressure (start withlow dose and gradually increase)
- Skin rash; metallic taste
- Reduced kidney function in kidney patients
- Very rarely: angio-oedema
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Cardiac medication: Angiotensin II receptor antagonists
- Block angiotensin II receptors
- Used for - hypertension
- Used as alternative to ACE inhibitors if they are not well tolerated
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Cardiac medication: Angiotensin II receptor antagonists
- Side effects:
- Fatigue
- Hypotension and dizziness
- rash
- Taste disturbance
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Cardiac medication: Diuretics
- Increase urine output by removing salt and water from circulation
- Reduction in circulating fluids
- Reduction in cardiac workload and BP
- Three groups: - loop diuretics - thiazide diuretics - potassium-sparing
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Cardiac medication: Diuretics
- Loop diuretics: e.g Furosemid
- Used for: acute severe heart failure
- Very quick acting; large volumes of urine to be passed within one h
- Reduces effectively dyspnoe and ankle swelling
- Also used for hypertension
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Cardiac medication: Diuretics
- Side effects- Loss of potassium which causes
- tiredness- muscle weakness, cramps- loss of appetite- ventricular arrhythmias
- Can cause diabetes and gout
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Cardiac medication: Diuretics
- Thiazide diuretics
- Prevent sodium absorption in kidneys which is then lost in urine
- Reduce initially by loosing volume of blood, thus reducing BP
- Used for - mild heart failure - hypertension
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Cardiac medication: Diuretics
- Side effects:
- Low potassium
- diabetes, gout
- Can increase lipids
- Impotence in high doses
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Cardiac medication: Diuretics
- Potassium sparing: e.g. Amiloride, Triamterene
- Minimise loss of potassium
- Usually administered together with other more powerful diuretics
- Used for: - treating oedema in heart failure and cirrhosis
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Cardiac medication: Diuretics
- Side effects:
- gastro-intestinal disturbances
- Dry mouth
- rashes
- Orthostatic hypotension
- hyperkalaemia
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Cardiac medication: Antiarrhythmics
- Affect the conduction system of the heart
- ß-blockers
- Ca channel blockers
- Digoxin
- Amiodarone
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Cardiac medication: Digoxin
- Reduces conductivity of the heart
- Increases myocardial contraction
- Controls HR by preventing rapid rates
- Used for: - supraventricular tachycardias - (heart failure)
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Cardiac medication: Digoxin
- Side effects (excessive dosage):
- nausea, vomiting
- Loss of appetite
- Fatigue
- Slow pulse
- Ventricular arrhythmias
- Disturbance of vision
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Cardiac medication: Amiodarone
- Increases refractory period
- Used for
- Atrial fibrillation
- Atrial flutter
- Often used with digoxin
- Other (ventricular) arrhythmias
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Cardiac medication: Amiodarone
- Side effects:
- photo-sensitivity
- Metallic taste
- nightmares
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Case 1: Philip
- Male, 30 yr, non-smoker, runner
- Was sent to a doctor
- Blood pressure was taken
- BP was 200 / 110 mm Hg
- Hypertension
- builder
- Nearly fell off the ladder because he felt dizzy and unwell
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Case 1: Blood pressure
- Blood pressure: force of blood against walls of arteries
- Measured non-invasively with sphygmomanometer
- Measured by listening for Korotkoff sounds produced by turbulent flow in arteries as pressure released from blood pressure cuff
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Blood pressure
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Classification of Hypertension
Category
Normal <130 <85 Recheck in 2 years
High Normal 130-139 85-89 Recheck in 1 year
Hypertension
Stage 1 (mild) 140-159 90-99 Confirm within 2 mo
Stage 2 (mod) 160-179 100-109 Eval or refer 1 mo
Stage 3 (severe) 180-209 110-119 Eval or refer 1 week
Stage 4 (very sev) >210 >120 Eval or refer immediately
SBP DBPRecommended
Followup
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Case 1: Hypertension …
- Serious condition - causes the heart to work harder - contributes to atherosclerosis
- Increases risk of - heart diseases - congestive heart failure - kidney disease - blindness - stroke
- “silent killer” because it has no warning symptoms
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Differential Diagnosis of Hypertension
• Primary Hypertension (95%)• Primary Hypertension (95%)
• Secondary Hypertension, e.g. caused by – Contraceptive use– Renal disease– Renal artery stenosis– Cushing’s syndrome– Pregnancy induced hypertension
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Risk factors for Hypertension
- Increases risk of (primary) hypertension- smoking - age (women > 65 yr, men > 55 yr) - obesity- diabetes - lack of physical activity- chronic alcohol consumption- family history- sex (men and postmenopausal women)
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Treatment of hypertension
- Lifestyle changes- quitting smoking- weight loss- reduction of stress- dietary changes (less salt)- regular aerobic exercise
- Case “Phil”: normal weight, non-smoker, regular exercise training
- If not sufficient drug therapy required
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Treatment of hypertension
- What kind of drugs would you choose?
- Consider age and “lifestyle”
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Revision Alastair’s lecture
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Blood pressure regulation
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Case 1: Phil‘s treatment
- Diuretic
- Diuretic + ß-blocker
- BP decrease not sufficient
- BP decrease still not sufficient
- Diuretic + ß-blocker + ACE inhibitor
- BP decrease sufficient- Struggling with adverse effects
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Treatment of hypertension
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Treatment of hypertension
- Diuretics and ß-blockers are first-line drugs
- Mode of action in both cases unclear
- Several groups of drugs reduce BP by decreasing vasoconstrictor tone and hence peripheral resistance, e.g.
- ACE inhibitors
- Ca antagonists
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Thiazid diuretics - initially:
BP falls because of a decrease in- blood volume - venous return - cardiac output
- gradually: cardiac output returns to normal
- however, hypotensive effect remains because peripheral resistance has decreased
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Thiazid diuretics
- No direct effect on blood vessels
- Vasodilation seems to be associated with small but persistent reduction in body Na+
- Act on kidney inhibit NaCl reabsorption
- Excretion of Na+, Cl- and accompanying H2O is increased
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Thiazid diuretics
- however, also K+ excretion increased
- Safe drug, orally active
- Act within 1-2 hoursDuration of 12 hours
- Adverse effects are important because drug may be taken for life
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Thiazid diuretics: adverse effects
- Weakness
- Loss of libido, impotence
- Diarrhoea
- Tinnitus
- Metabolic side-effects:
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Thiazid diuretics: adverse effects
- Metabolic side-effects:
- hypokalaemia: can cause arrythmias
- hyperuricaemia: May precipitate gout
- lipids: Increase cholesterol levels, at least during the first 6 months of administration
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ß-adrenoreceptor antagonists
- initially:Produce a fall in BP by decrease in cardiac output
- gradually: Cardiac output returns to normal, but BP remains low
- Unknown mechanism “resets” peripheral vascular resistance at a lower level
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ß-blockers: adverse effects
- Cold hands
- Loss of libido, impotence
- Fatigue
- Serious side effects:- provocation of asthma- heart failure- conductance block
- Tend to raise trigycerides and decrease HDL-cholosterol
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ß-blockers: - Vary in lipid solubility and cardioselectivity
- All block ß1-receptors and are equally effective in reducing BP
- More lipid-soluble drugs: more rapidly absorbed, more first-pass hepatic metabolism, more rapidly eliminated
- Cardioselective ß-blockers may have sufficient ß2-activity to cause bronchospasm in patients with asthma
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Vasodilator drugs:
- ACE-inhibitors:- Inhibit synthesis of angiotensin II which is powerful vasoconstrictor
- Ca antagonists:- tone of vascular smooth muscle is determined by cytosolic Ca2+ concentration- prevent influx of Ca and as result inhibit contraction- dilate arteries reduce BP
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Case: Gerry
- 55 yr, sees his GP because of nose bleeding
- BP 180 / 100 mm Hg
- newly diagnosed with primary hypertension
- Lifestyle changes recommended and ß-blocker prescribed
- Second morning, very early he fell in the bathroom
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Case: Gerry
- Massive problems with orthostatic hypotension
- What would you recommend?
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Case: Paul
- healthy, successful modern pentathlete
- Took ß-blockers shortly before pistol shooting event
- Great results
- Change in follow-up of events: Now running event immediately after shooting and not the next day
- Great results in shooting but catastrophy in running
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Case: Paul
- Can you explain this?
- What does it tell you about pharmacokinetic and –dynamic of ß-blockers?
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Antihypertensive Therapy
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Ischemic Heart Disease
• Etiology:– Coronary Atherosclerosis
• Risks:• Clinical Syndromes:– angina pectoris– myocardial infarction– chronic ischemic heart disease– sudden cardiac death
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Angina pectoris
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Pathogenesis of Atherosclerosis
Lipid accumulates in vascular wall
Macrophages infiltrate the wall and oxidize the lipids
Cell injury and release of local growth factors(Angiotensin II)
Plaque formation on intimal wall
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Pathogenesis of Ischemia
Plaque Disruption or Breakdown
Tissue Thromboplastin Exposed
Platelet Aggregation and Clotting Cascade Activated
Thrombus Formation
Acute Ischemia
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Demand > Supply: Angina
Perfusion pressurefixed stenosisoxygen content
SUPPLY
DEMAND
afterloadcontractilitypreload heart rate
How to increase supply? How to decrease demand?
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StableAngina
Patho: Fixed stenosis Thrombus Thrombus>75% + lysis with occlusion
Pain: predictable unpredictable unpredictablerelieved by not relieved not relievedrest (3-5 min) rest rest (>15-30)
Serum Enz: not elevated not elevated elevated
UnstableAngina MI
Ischemic Syndromes
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• Indicative Leads show:
• Ischemia: ST elevation or depression
T-wave peaking, flattening, inversion
Bigger than normal Q-waves
ECG Changes with Ischemia
Q
ST elevation
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Decreased Myocardial Perfusion
Partially ischemic cells
Anaerobic metabolismand lack of ATP
No ATP
Ion leak across cell membrane
ST changes Dysrhythmias
Cell rupture and death
Q-wavesElevatedEnzymes
Totally ischemic cells
Sequela of Myocardial Infarction
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Decreased Stroke Volume
IMMEDIATE HOURS WEEKS
baroreceptoractivation
SNS
SV, CO SV, COSV, CO
RAS activity
fluid retained
preload
Increased LVwall tension
ventricularhypertrophy
Compensatory Response to Decreased Stroke Volume
Copyright © 2000 by W. B. Saunders Company. All rights reserved.
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Differential Diagnosis of Chest Pain
- Cardiac ischemia
- Chest wall trauma, costochondritis
- Pleural pain - pneumonias
- Pneumothorax
- Gastrointestinal (GERD)
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Treatment of Cardiac Ischemia
• Stable angina– SL nitroglycerin– Platelet inhibitor (e.g. Aspirin)– beta blocker– add long acting nitrate (remove at
night)– add calcium channel blocker (not
verapamil)
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Relief of Angina
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Treatment of Cardiac Ischemia
- Medication to - increase myocardial blood
supply- reduce the amount of work
the myocardium performs
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Treatment of Cardiac Ischemia
- Dilate coronary arteries- Slow heart rate- Reduce force of each contraction- Lower systolic BP
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Treatment of Cardiac Ischemia- Increase supply (coronary flow):
- Ca antagonists- nitrates- revascularization procedures
(bypass surgery, angioplasty ..)
- ß-blockers (extend diastole)
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Treatment of Cardiac Ischemia- Reduce demand:- decreased HR (ß-blockers)- reduced wall tension (nitrates,
Ca anatagonists, ß-blockers)
- reduced contractility (ß-blockers, Ca antagonists)
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Case: Michael
- Male
- 36 yr
- 65 stone
- Heart failure
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Case: Michael
- Symptoms
- fatigue
- oedema
- breathlessness
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Heart Failure
• Def: Inability to effectively PUMP the amount of blood delivered to the heart
• Etiologies: Many– MI– hypertension– Valve Disease– Congenital Defects– Cardiomyopathy
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Heart as a Two Pump System
rightheart
Leftheart
Tissues
arteriesveins
lungs
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Left Heart Failure
Backward Effects Forward Effects
Increased pressure behind the pump
Pulmonary congestion
Low Cardiac Output
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Right Heart Failure
Systemic VenousCongestion
Low Cardiac Output
Backward Effects Forward Effects
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Principles of Heart Failure Treatment
GOAL: Optimize Cardiac Output and Minimize Cardiac Workload
- Management of Preload
- Management of Afterload
- Management of Contractility
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Heart failure
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Heart Failure Treatment
Diuretics: reduce circulatory volumedecreases preload and oedema
Vasodilators: e.g. ACE inhibitors decrease pre- and afterload
Digoxin: increase cytosolic Caincrease force of contraction
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Drugs used to treat cardiac conditions: