DENT 3005: Introduction to Pharmacology¹

Cardiovascular systems

Dr Thuy Linh Truong thuy.truong@uwa.edu.au

Acknowledgement of country²

The University of Western Australia acknowledges that its campus is situated on Noongar land, and that Noongar people remain the spiritual and cultural custodians of their land, and continue to practise their values, languages, beliefs and knowledge.

Artist: Dr Richard Barry Walley OAM

Learning Outcomes³

Learning objectives

Understand the classes and mechanisms of major classes of cardiovascular drugs
Recognise oral and dental side effects of cardiovascular drugs
Management of emergencies related to cardiovascular conditions in the dental setting
Understand drugs interactions with dental medications
Applied knowledge to clinical scenarios

Hypertension⁴

Definition
- The force of the blood pushing against the artery walls is consistently too high $\to$ heart works harder
- Grade 1, 2, 3
Two types
- Primary HTN
- Secondary HTN
Complications: many
Treatment rationale
- Reduce premature cardiovascular morbidity & mortality & microvascular disease affecting the brain, kidney & retina

Grade	Systolic/diastolic mmHg
1	140-159/90-99
2	160-179/100-109
3	$> 180/ > 110 mmHg$

Complications
Heart attack, stroke
Aneurysm
Heart failure
Microvascular damage : eye, brain
Metabolic syndrome

Normal regulation of BP⁵

Blood Vessels

BLOOD FLOW FROM HEART
BLOOD FLOW TO HEART

To Cells

Oxygen
Nutrients

From Cells

Waste
Carbon dioxide

Vessel Types

ARTICLES
Arteriole
Capillaries
Venule
VEIN

Heart and lungs blood flow

Pulmonary Arteries
Blood to the lungs
Lungs
Blood from the lungs
Right ventricle
Blood from the body
Blood to the body
Heart

Normal regulation of BP⁵

Factors determining BP
- CO = SV x HR
- Systemic vascular resistance
- Blood volume & viscosity
- Elasticity
Nervous systems
- Receptors in aortic arch & common carotid artery
- Relay information to vasomotor center
- Alpha adrenergic receptors
Humoral systems
- Endocrine-renal interactions
- Endothelial vasoactive substances

Renin-angiotensin system⁶

graph TD
    subgraph Left Side: Angiotensinogen Conversion and Effects
        A[Angiotensinogen] -->|Renin| B(Angiotensin I)
        B -->|ACE| C(Angiotensin II)
        C --> D[AT1 receptor]

        D --> E[Kidney]
        D --> F[Adrenal gland]
        D --> G[Heart]
        D --> H[Vessels]
        D --> I[Brain]

        F --> F1[Aldosterone release]

        E[Kidney] --> E1[Sodium retention]
        E --> E2[Fibrosis]

        G[Heart] --> G1[Inotropy]
        G --> G2[Chronotropy]
        G --> G3[Hypertrophy]
        G --> G4[Fibrosis]

        H[Vessels] --> H1[Constriction]
        H --> H2[Hypertrophy]

        I[Brain] --> I1[Thirst]
        I --> I2[Salt appetite]
        I --> I3[Sympathetic activation]
        I --> I4[Vasopressin release]

        style A fill:#DAC163
        style B fill:#3DABD5
        style C fill:#E63539
        note over A: DRVYIHPFHL...
        note over B: DRVYIHPFHL
        note over C: DRVYIHPF
    end

    subgraph Right Side: Regulation and Pharmacological Intervention
        subgraph Triggers
            J[Renal perfusion pressure ↓] --> K(Renin release)
            L[Renal sympathetic nerve activity ↑] --> K
            M[Glomerular filtration ↓] --> K

            style K fill:#E63539
            style N fill:#3DABD5
        end

        N[Atrial natriuretic peptide] --> K

        K --> P[Angiotensinogen]
        note over P: **Protein produced by the liver**
        P --> Q[Angiotensin I]
        note over Q: Inactive precursor
        Q --> R[Angiotensin II]

        Q --> S[ACE]
        R --> S

        S --> T[ACE inhibitors]
        T --> U[Decreases vasoconstriction]
        T --> V[Aldosterone secretion]
        T --> W[Sympathetic circulation]
        T --> X[Lowers blood pressure]
        style U fill:#8BC249
        style V fill:#8BC249
        style W fill:#8BC249
        style X fill:#8BC249

        R --> Y[AT₁ receptors]

        Y --> Z[Angiotensin II AT₁ subtype receptor antagonists]
        Z --> AA[Decreases vasoconstriction]
        Z --> AB[Aldosterone secretion and sodium retention]
        Z --> AC[Prevention of vascular growth and remodeling]
        Z --> AD[Lower blood pressure]
        style AA fill:#8BC249
        style AB fill:#8BC249
        style AC fill:#8BC249
        style AD fill:#8BC249

        R --> AE[Vascular growth:]
        AE --> AE1[1. Hyperplasia]
        AE --> AE2[2. Hypertrophy]

        R --> AF[Vasoconstriction:]
        AF --> AF1[1. Direct]
        AF --> AF2[2. Via increased noradrenaline release from sympathetic nerves]

        R --> AG[Salt retention:]
        AG --> AG1[1. Aldosterone secretion]
        AG --> AG2[2. Tubular Na⁺ reabsorption]

        note for S: Primarily occurs in the lungs
        note for Y: Binding to AT1 receptors lead to: Vascular growth, vasoconstriction, salt retention
    end

ACE inhibitor⁷

MOA: block conversion of angiotensin I to II, Inhibit breakdown of bradykinin
Dental implications
- Many ☺

Generic name	Brand Name
Captopril	Zedace, Capoten
Enalapril	Renitec, Auspril
Fosinopril	Monopril, Fosipril
Lisinopril	Zestril, Zinopril
Perindopril	Coversyl, Prexum
Quinapril	Acupril, Qpril
Ramipril	Tritace, Tryzan
Trandolapril	Gopten, Tranalph

ACE Inhibitors⁸

Dental Relevance

Hypotension Risk: monitor BP during GA/sedation & postural changes
Angioedema: swelling (lips, face, tongue) – refer to GP if suspected
Orthostatic Hypotension: sit patient up slowly before standing
Neutropenia: delay procedures if signs of infection – request WBC count

Oral Side Effects

Dysgeusia: advise avoiding bitter foods & metal utensils
Burning Mouth Syndrome: avoid irritants; suggest cold fluids, sugar-free gum
Dry Mouth: monitor for caries/infections; manage early
Oral Lichenoid Reactions: minimise trauma; adjust prostheses

Drug Interactions

Quinapril + Tetracyclines: dose 2 hrs apart
Prolonged NSAIDs: ↓ ACE efficacy, ↑ renal risk → prefer paracetamol

Sartans⁹

MOA
- Competitively block binding of angiotensin II to type 1 angiotensin receptors
Dental implications
- Hypotension but mainly implicated in GA
- NSAIDs: may increase risk for hyperkalemia & reduce renal function

Generic name	Brand Name
Candesartan	Adesan, Atacand
Irbesartan	Avapro, Karvea
Losartan	Cozavan, Cozaar
Olmesartan	Olmetec
Telmisartan	Micardis
Valsartan	Diovan

$↓$ AV Conduction Velocity: Slows electrical signal transmission through AV node; useful in supraventricular tachycardia
$↓$ SA Node Pacemaker Rate: Reduces heart rate (negative chronotropy); helps manage atrial fibrillation
$↓$ Myocardial Contractility: Decreases calcium entry during depolarization; lowers force and rate of cardiac contractions

Smooth muscle cells | Heart¹⁰

graph LR
    subgraph Smooth muscle cells
        A[Vasodilation of mainly arteriolar smooth muscle] --> B(Ca²⁺)
        B --> C[CCB]
        C --> D{Calcium Channel Blocker action}
        D --> E[Activation of myosin light chain kinase]
        E --> F[Phosphorylation of light chain myosin]
        F --> G[Actin-myosin cross-bridging]
        G --> H[Vasoconstriction]
    end
    subgraph Heart
        I[myocardial contractility] --> J[Ca²⁺ entry]
        K[AV conduction velocity]
        L[SA node pace maker rate]
        M[Frequency of CC opening in response to depolarization] --> N(Ca²⁺)
        N --> O[CCB]
        O --> P{Calcium Channel Blocker action}
        P --> Q[Stimulation of Ca²⁺ release from internal store]
        Q --> R(Ca²⁺)
        R --> S[Heart constriction]
    end

Calcium Channel Blockers (CCBs)¹¹

Mechanism of Action
- Block L-type calcium channels in heart & blood vessels
- ↓ Calcium entry → ↓ muscle contraction → Vasodilation
- ↓ Heart rate (negative chronotropy), ↓ contractility (negative inotropy), ↓ AV conduction
Key Uses
- Hypertension: ↓ Vascular resistance (esp. dihydropyridines – e.g., amlodipine)
- Angina: ↑ Coronary blood flow & ↓ cardiac oxygen demand
- Arrhythmias: Stabilize heart rhythm (non-dihydropyridines – e.g., verapamil, diltiazem)
Types of CCBs
- Dihydropyridines: Amlodipine, Nifedipine – act on blood vessels
- Non-dihydropyridines: Verapamil, Diltiazem – act on heart & rhythm
Clinical Highlights
- ↓ Blood Pressure via smooth muscle relaxation
- Relief of Chest Pain via improved perfusion
- Rhythm Control in AF, SVT via slowed conduction

Calcium channel blockers (CCBs)¹²

Ca - Calcium SMC - Smooth muscle cell LV - Left ventricle HR - Heart rate ICS - Impulse conduction system

flowchart TD
    A[Calcium Channel Blockers] --> B(Intracellular Ca²⁺ Influx Inhibition)
    B --> C(Vascular SMC Contraction Inhibition)
    B --> D(LV Contraction and HR↓)
    B --> E(ICS excitement↓)
    E --> F[Arrythmia Treatment]
    C --> G(Peripheral Vessel Dilatation)
    C --> H(Coronary Artery Dilatation)
    D --> I(O₂ Consumption In Myocardium↓)
    G --> J(Peripheral Vascular Resistance↓)
    J --> K(Blood Pressure↓)
    J --> L(Afterload↓)
    K --> M[Hypertension Treatment]
    L --> N(O₂ Consumption In Myocardium↓)
    H --> O(Coronary Blood Flow↑)
    O --> P(O₂ Supply in Myocardium↑)
    P --> Q[Angina Treatment]
    N --> Q
    I --> Q
    subgraph ICS excitement↓
        E((Sinus node automaticity↓, atrioventricular node excitation conduction↓))
    end

Calcium Channel Blockers¹³

MOA:
- Block inward current of Ca into cells
- Reduce vascular resistance
Dental implications
- Gingival hyperplasia , taste disturbance, exfoliative dermatitis, angioedema
- Except for clevidipine, CCBs & CYP3A4 inH
- Diltiazem, Verapamil: +erythromycin $\to$ QT prolongation
- LA technique: always aspirate

Generic name	Brand Name
Amlodipine	Nordip, Norvasc
Clevidipine	Cleviprex inj
Felodipine	Felodur
Lercanidipine	Zanidip, Lercan
Nifedipine	Adalat, Adefin
Nimodipine	Nimotop
Diltiazem*	Cardizem
Verapamil *	Cordilox, Veracaps

Beta blockers¹⁴

graph TD
    A[Beta blocker] -->|Block the effects of adrenaline (epinephrine) and noradrenaline (norepinephrine) on β-adrenergic receptors. Part of the sympathetic nervous system| B(β1 (Cardiac))
    A --> C(β2 (Peripheral and respiratory))
    B --> D[Heart rate]
    B --> E[Contractility]
    B --> F[Cardiac output]
    B --> G[Inhibition of renin release]
    C --> H[Peripheral vasoconstriction]
    C --> I[Bronchoconstriction]
    
    subgraph Location and Action
        style B fill:#e0965d
        style C fill:#f0d162
        B -- "Found primarily in the heart and kidneys"
        C -- "Found primarily in smooth muscles of blood vessels, lungs (bronchi), liver"
    end
    
    subgraph Clinical Notes
        style B fill:#e0965d
        style C fill:#f0d162
        I -- "Non-selective beta blockers like **Propranolol** can block both β1 and β2 receptors. While effective for hypertension and anxiety, can cause side effects like **bronchoconstriction**, making it less suitable for patients with asthma / COPD"
    end

Beta blockers¹⁴

β1 receptor blockade (cardio-selective effects)
- $↓$ Heart rate $\to$ Negative chronotropic effect
- $↓$ Contractility $\to$ Negative inotropic effect
- $↓$ Cardiac output
- $↓$ Renin release $\to$ Suppresses RAAS, lowers BP
- Examples: Metoprolol, Atenolol
β2 receptor blockade (non-cardio-selective effects)
- $↑$ Peripheral vasoconstriction
- $↑$ Bronchoconstriction $\to$ Caution in asthma/COPD
- Example: Propranolol (blocks both β1 & β2)
Mixed alpha & beta blockade
- Labetalol, Carvedilol
- Block $β 1$ , $β 2$ , and $α 1$ receptors
- Enhanced BP lowering via vasodilation

Generic name	Brand Name
Cardio-selective
Beta 1 blockers
Atenolol	Noten, Tenormin
Bisoprolol	Bispro, Bicor
Metoprolol	Betaloc
Nebivolol	Nebilet
Nonselective
Beta1&2 blockers
Propranolol	Deralin
Nonselective
Beta1&2 blockers
& alpha1 blocker
Carvedilol	Dilatren
Labetalol	Presolol, Trandate
Injection
Esmolol	Brebviloc inj
Antiarrhythmic
Sotalol	Sotacor, Cardol

Beta blockers¹⁴

Dental implications
- Orthostatic hypotension: sit patient up slowly post-treatment
- Xerostomia (rare): increases caries and infection risk
- Dysgeusia: altered/bitter taste; avoid metallic utensils
- Oral lichenoid reactions: white lacy lesions; may require referral
- Rare blood dyscrasia: delay treatment if infection symptoms present
Drug interactions
- NSAIDs: may reduce antihypertensive effect — limit use to $\leq$ 5 days
- Adrenaline (LA): use caution with non-selective $β$ -blockers $\to$ risk of $↑$ BP & reflex bradycardia
Surgical considerations
- Monitor vitals during sedation or general anaesthesia
- Be aware of cardiac risks (bradyarrhythmia, hypotension)

Selective alpha blockers¹⁵

MOA: block alpha $_{1}$ receptors $\to$ reduce vasoconstrictions
Dental implications
- Orthostatic hypotension

Generic name	Brand Name
Prazosin	Minipress
Terazosin	Hytrin

Other antihypertensives

MOA: predominantly arteriola vasodilators
Dental implications
- Dry mouth: clonidine, methyldopa, moxonidine

Generic name	Brand Name
Clonidine	Catapres
Diazoxide	Diazoxide
Hydralazine	Alphapress
Methyldopa	Hydopa
Minoxidil	Loniten
Moxonidine	Physiotens
Sodium Nitroprusside	Sodium Nitroprusside

Hypertension: Dental implications¹⁶

Patient factors
- Other comorbidities
- Short appointments
- LA delivery technique
- Monitor patient & BP
Medication factors
- Orthostatic hypotension
- Xerostomia
- Gingival hyperplasia: CCBs
- Gingival bleeding: vasodilators
- Lichenoid drug rxn
- Angioedema: ACE InHs

Management of Syncope in Dental practice¹⁷

Scenario	Actions
If patient feels faint	- Stop dental treatment - Lay patient flat (tilt chair or lie down) - Raise legs - Check heart rate - Talk to assess consciousness
If patient loses consciousness	- Stop dental treatment - Raise legs, lower head (horizontal position) - Check BP and heart rate - Allow slow recovery under supervision
If no recovery of consciousness	- Call 000 - Start basic life support (refer to BLS chart) - Place patient on side - Continue until help arrives or patient wakes up

Arrythmia¹⁸

Abnormal beating of the heart
- Too quick, too slow, irregularly
Symptoms
- Chest pain, dizziness, sweating, SOB, anxiety
Rationale of drug therapy
- Prevent sudden cardiac arrest
- Restore sinus rhythm & hemodynamic stability
- Control sx relief
- Control ventricular rate in AF
Complications
- Stroke, HF, cardiac arrest, sudden death

Antiarrhythmic Drug Classification¹⁹

Class	Type	Examples
Class I	Sodium-channel blocker	Ia (moderate): quinidine, procainamide Ib (weak): lidocaine, mexiletine Ic (strong): flecainide, propafenone
Class II	Beta-blocker	Propranolol, Metoprolol
Class III	Potassium-channel blocker	Amiodarone, Sotalol
Class IV	Calcium-channel blocker	Verapamil, Diltiazem

Action Potential Phases

K⁺/Cl⁻ (out)
Ca²⁺ (in)
K⁺ (out)
Na⁺ (in)
K⁺ (rectifier)
Phases: 1, 2, 3, 0, 4, 4
Atrial repolarisation
ventricular repolarisation
Atrial depolarisation
Ventricular depolarisation

Barton, A.K., McGowan, M., Smyth, A., Wright, G.A. and Gardner, R.S. (2020), Classification and choice of antiarrhythmic therapies. Prescriber, 31: 11-17. https://doi.org/10.1002/psb.1828

Cardiac action potential: Key Phases²⁰

Phase 0: Depolarization
- Rapid sodium (Na⁺) influx
- Triggers action potential (electrical signal)
Phase 1: Initial Repolarization
- Sodium channels close
- Brief potassium (K⁺) efflux
- Slight drop in membrane potential
Phase 2: Plateau
- Calcium (Ca²⁺) enters via L-type channels
- Potassium continues to exit
- Maintains a steady voltage; supports muscle contraction
Phase 3: Repolarization
- Calcium channels close
- Potassium efflux continues
- Cell returns to negative resting potential
Phase 4: Resting State
- Stable resting potential maintained by Na⁺/K⁺ pump
- Cell is ready for the next beat

Antiarrhythmic drugs (Vaughan Williams classification)²¹

Used to treat abnormal heart rhythms
Vaughan Williams classification

Table 1: Simplified Vaughan Williams classification of antiarrhythmic drugs

Class	Action	Examples
I	Interfere with depolarisation	disopyramide quinidine mexiletine flecainide
II	Beta blockade	beta blockers other than sotalol
III	Prolong repolarisation	amiodarone sotalol
IV	Calcium channel blockade	verapamil

Generic name	Brand Name
Adenosine	Adenocor inj
Amiodarone	Aratac, Cordarone
Atropine	Atropine inj
Digoxin	Lanoxin, Sigmaxin
Disopyramide	Rythmodan
Esmolol	Brevibloc inj
Flecainide	Flecatab, Tambocor
Isoprenaline	Isuprel inj
Lignocaine	Lignocaine inj
Sotalol	Cardol, Sotacor
Verapamil	Cordilox, Veracaps

Specific Antiarrhythmics²²

Amiodarone

MOA: prolong refractory period in all cardiac tissue
Dental implications: taste disturbance, skin pigmentation

Disopyramide

MOA: prolong refractory period of myocardial tissue
Dental implications: dry mouth

Isoprenaline

MOA: beta agonist
Dental implications: dry mouth

Arrythmia: Dental implications²³

Well-controlled arrhythmias do not contraindicate routine dental care
Stress reduction and proper anaesthesia technique are central to safe treatment
Amiodarone may reduce the effectiveness of certain opioids and cause oral pigmentation
Calcium channel blockers can lead to gingival overgrowth, requiring careful monitoring and, occasionally, surgical management

Heart Failure²⁴

Systolic HF
- Responds to conventional tx
Diastolic HF
- No drug tx shown to improve survival
Common cause is coronary heard disease
- Asoc w/ hx of myocardial infarction & HTN
Prognosis for chronic HF is poor: 60-70% mortality within 5yrs
Impairment of pumping ability
- RHS: accumulation of blood in venous circulation $\to$ organ congestion & peripheral oedema
- LHS: accumulation of blood in pulmonary circulation $\to$ pulmonary congestion & fluid in lungs

Heart Failure²⁴

Rationale for drug therapy
- Provide sx relief & improve exercise tolerance
- Prevent hospitalization & deterioration in left ventricular function
- Reduce mortality
Identify cause & treat
- Eg, coronary artery disease, HTN, valvular heard disease
Identify & treat precipitants
- Eg. Acute myocardial ischemia, arrythmia, anemia, iron deficiency etc.
Drug tx for systolic HF
- Table next slide

Drugs for systolic HF²⁵

Start ACE inhibitor
- Start low, increase slow
- If cough/angioedema: switch to sartan
When stable, add beta blocker
- Start low, increase slow
If still symptomatic
- - aldosterone antagonist
If still symptomatic
- - digoxin or ivabradine
Fluid overload
- - loop diuretic
Acute pulmonary oedema
- Nitrates & diuretics
If acute severe HF
- - vasodilators, parenteral inotropes

Aldosterone antagonists²⁶

MOA: antagonize aldosterone $\to$ inhibit Na absorption in distal tubule
Dental implications
- Orthostatic hypotension & drug interaction w/ NSAIDS

Generic name	Brand Name
Eplerenone	Inspra
Spironolactone	Aldactone, Spiractin

Loop diuretics

MOA: inhibit reabsorption of Na & Cl in ascending limb of loop of Henle
Dental implications
- Orthostatic hypotension & drug interaction w/ NSAIDS

Generic name	Brand Name
Bumetanide	Burinex
Ethacrynic acid	Edecrin
Frusemide	Lasix, Urex

Nephron Diagram Key²⁷

Glomerulus: Filtration rate $120 ml min^{- 1}$
Proximal convoluted tubule: Reabsorption of HCO $_{3}^{-}$ , $Na^{+} (60%)$ , $Cl^{-} (45%)$ , $H_{2} O$ , $K^{+}$ , $Ca^{2 +}$ , $Mg^{2 +}$ . Secretion of Acids, Bases.
Thin descending loop of Henle: Reabsorption of $H_{2} O$ .
Thick ascending loop of Henle: Reabsorption of $Cl^{-}$ , $Na^{+} (25%)$ .
Distal convoluted tubule: Reabsorption of $Na^{+} (10%)$ , $Cl^{-}$ , $Ca^{2 +}$ (PTH sensitive).
Collecting Ducts: Reabsorption of $H_{2} O$ (ADH sensitive), $Na^{+} (5%)$ . Secretion of $K^{+}$ , $H^{+}$ .

Sites of Diuretic Action

Carbonic anhydrase inhibitors (Proximal tubule)
Osmotic diuretics (Proximal tubule)
Loop diuretics (Thick ascending loop)
Thiazides (Distal convoluted tubule)
K $^{+}$ -sparing diuretics (Collecting duct)
Aldosterone antagonists (Collecting duct)

Sympathomimetics²⁸

MOA: mimic agonistic action of adrenaline & noradrenaline on ɑ &/or β-adrenoceptors
Pt need to be stabilized, tx in restricted setting under close monitoring

Generic name	Brand Name
Adrenaline	Adrenaline inj
Dobutamine	Dobutrex inj
Dopamine	Dopamine inj
Isoprenaline	Isuprel inj
Noradrenaline	Levophed inj

Other drugs for HF – digoxin

MOA: Inhibition of Na+/K+-ATPase pump in cardiac myocytes
Dental implications
- Low narrow therapeutic window! Monitor toxicity signs & defer tx
- Macrolide ABs: inH metabolism of digoxin

Generic name	Brand Name
Digoxin	Lanoxin, Sigmaxin
Milrinone	Primacor inj

Heart Failure: Dental implications²⁹

Unstable patients: defer treatment and refer
Short, stress-free appointments: minimize cardiovascular strain
Patient positioning: keep head above heart to reduce pulmonary congestion
Avoid sedation in-clinic: refer to hospital for GA or conscious sedation
Stress management: effective LA, calm communication, possible mild sedation (with cardiologist’s input)
Comprehensive medical history: identify class of HF, medications, comorbidities
Monitor vitals: BP and HR before and during treatment
Infective endocarditis risk: check need for antibiotic prophylaxis with cardiologist
Patient education: emphasize oral hygiene, diet, and lifestyle changes
Emergency readiness: oxygen, nitro-glycerine, trained staff, clear protocols

Drugs for HF: Dental implications³⁰

Medication factors
- Drug interactions: macrolide Abs, NSAIDs
- Safe delivery of LAs
- Orthostatic hypotension
Monitor sign of digoxin drug toxicity
- GI effects: nausea, vomiting
- Visual disturbances
- Cardiac arrythmia

Management of cardiac arrest in dental practice³¹

Figure 13.48 Management of cardiac arrest in dental practice

If cardiac arrest occurs:

Stop dental treatment.
Call 000.
Start basic life support, including CPR (for ‘Basic life support flow chart’, see Figure 13.43). Use an automated external defibrillator if available.
Maintain treatment until the patient regains consciousness or assistance arrives.

CPR = cardiopulmonary resuscitation

Tripple Whammy³²

ACE inhibitor dilates the efferent arteriole, and reduces GFR
Diuretics reduce plasma volume and GFR
NSAIDs constrict blood flow into the glomerulus via the afferent arteriole and reduce GFR

Angina³³

Type of chest pain or discomfort
Common symptom of coronary artery disease (CAD)
Typically caused by the narrowing or blockage of the coronary arteries
Rationale for drug therapy
- Provide symptom relief
- Reduce risk of death or MI
Drug choice
- Beta blockers, CCBs, long-acting nitrates, other groups of drugs

Nitrates³⁴

MOA: provide exogenous source of nitric oxide → vasodilatory effect

Generic name	Brand Name
Glyceryl trinitrate	Nitrolingual
Isosorbide dinitrate	Isordil
Isosorbide mononitrate	Duride, Imdur

Other anti-anginal drugs

Ivabradine
- MOA: Inh a current regulating the interval btw depolarization of the SA node
Nicorandil
- MOA: produces venous & arterial dilation & improve myocardial oxygen balance and decrease angina
Perhexiline
- MOA: unclear, but having anti-ischaemic effects

Generic name	Brand Name
Ivabradine	Coralan
Nicorandil	Ikorel
Perhexiline	Pexig

Angina: Dental implications³⁵

Angina attacks
- Know first aid for angina & acute coronary syndrome
Ensure pt have their meds on hand
- Not all clinic will have nitroglycerin
Caution: adrenaline-soaked retraction cord
CCBs: gingival hyperplasia
- OH education
- Surgical removal: will come back
- Referral to medical GP

Management of angina or ACS in the dental setting³⁶

Scenario	Actions
If chest pain occurs in a patient with a history of angina:	- Stop dental treatment - Measure blood pressure, heart rate, and pulse oximetry - Assess consciousness by talking to the patient - Ask the patient to sit down (due to risk of hypotension) - Administer glyceryl trinitrate: • Spray: 400 micrograms sublingually, repeat every 5 min if needed, up to 3 doses (if tolerated) OR • Tablet: 300–600 micrograms sublingually, repeat every 5 min if needed, up to 3 doses (if tolerated)
If pain persists for more than 10 minutes (after 2 doses):	- Administer third dose - Manage as for severe/new chest pain
If the patient recovers:	- Do not proceed with dental treatment - Refer for medical evaluation even if patient appears well
If chest pain is severe or new:	- Call 000 - If patient has angina history, give glyceryl trinitrate as above - For all patients, give: aspirin (not detailed in image but implied standard protocol)

Management of Severe/New Chest Pain (Continued)³⁷

Action	Details
Call Emergency Services	Call 000 immediately.
Administer Glyceryl Trinitrate	For patients with a history of angina, give glyceryl trinitrate as per protocol.
Give Aspirin	300 mg orally, chewed or dissolved before swallowing.
Monitor Vital Signs	Measure blood pressure, heart rate, and use pulse oximetry.
Oxygen Therapy	If $SaO_{2} < 90%$ , start supplemental oxygen. Titrate $SaO_{2}$ to 90–96% if possible.
Provide Reassurance	Calm and reassure the patient until help arrives.
If Unconscious	Start basic life support. Use an AED if available. Follow the Basic Life Support flow chart

Dyslipidemia³⁸

Abnormal levels of lipids in the bloodstream
Risk factor for cardiovascular (CV) diseases
Dysregulation in lipid levels $\to$ atherosclerosis and other CV complications
Rationale for drug therapy
- Reduce progression of atherosclerosis
- Improve survival
- reduce risk of MI & stroke in patients w/ CVD
- Prevent pancreatitis
Hypercholesterolemia
- Statins, bile acid binding resins, nicotinic acid, ezetimibe, fibrates
Hypertriglyceridemia
- Fibrates, nicotinic acid, fish oils

Atherosclerosis³⁹

Chronic disease
Buildup of plaques within the arterial walls
Leading to narrowing and hardening of the arteries $\to$ restrict blood flow.

Modifiable	Non-modifiable	Uncertain
Diabetes mellitus and impaired glucose tolerance	Age	Obesity
Dyslipidaemia	Male	Hypercoagulability
Cigarette	Family history of CVD	High carbohydrate intake
Raised serum C-reactive protein¹	Familial hypercholesterolaemia	Elevated serum triglyceride
Vitamin B6 deficiency	Increased levels of homocysteine²	Elevated serum uric acid
Hypothyroidism		Elevated serum fibrinogen
		Elevated serum lipoprotein
		Chronic systemic inflammation
		Hyperthyroidism
		Continuous pattern of short sleep duration
		Some bacterial infection

C-reactive protein ( $CRP$ ) is a protein made by the liver. Its level increases when there’s inflammation in the body.
Increased levels of homocysteine can damage the inside of arteries and raise the risk of blood clot formation

Statins⁴⁰

MOA: competitively inH HMG-CoA reductase enzyme → increase hepatic update of cholesterol
Drug interaction: other CYP3A4 inH
- Clarithromycin, erythromycin, azoles

Generic name	Brand Name
Atorvastatin	Lipitor
Fluvastatin	Vastin
Pravastatin	Pravachol
Rosuvastatin	Crestor
Simvastatin	Zocor

Bile acid binding resins

MOA: binds bile acid in intestinal lumen → prevent reabsorption → increase excretion in feces

Generic name	Brand Name
Cholestyramine	Questran lite
Colestipol	Colestid

Fibrates⁴¹

MOA: peroxisome proliferator-activated receptors (PPARs)

Generic name	Brand Name
Fenofibrate	Lipidil
Gemfibrozil	Lipigem

Other drugs for dyslipidemia

Ezetimibe
- MOA: reduce absorption of dietary & biliary cholesterol
Nicotinic acid
- MOA: unclear, possibly suppress fatty acid release

Generic name	Brand Name
Ezetimibe	Ezetrol
Nicotinic acid	Nicotinic acid

Dyslipidemia: Dental implications⁴²

Drug factors
- Interactions: Macrolide Abs, Itraconazole, ketoconazole, fluconazole antifungals
- Check individual drug monograph for CYP enzymes
- Myopathy
Patient factors
- Other comorbidities: HTN, diabetes…
Oral manifestations
- Increase calcification in pulp chambers

References⁴³

Ritter JM, Flower RJ, Henderson G, Loke YK, MacEwan D, Robinson E, editors. Rang & Dale’s pharmacology. 10th ed. Edinburgh: Elsevier; 2023
Australian Medicines Handbook Online [Internet]. Adelaide (AU): Australian Medicines Handbook Pty Ltd;2000. Cardiovascular; [updated 2025; cited 2025]. Available from: UWA Onesearch
Pharmaceutical Society of Australia. Australian Pharmaceutical Formulary and Handbook: A Guide to Best Practice. 25th ed. Canberra: Pharmaceutical Society of Australia; 2021
Ali K. Clinical dental pharmacology. 1st ed. Oxford: Wiley-Blackwell; 2023
Bullock S, Manias E. Fundamentals of pharmacology. 8th ed. Frenchs Forest, NSW: Pearson Australia; 2017
MIMS Australia. eMIMSelite: Consumer medicine information, specific clinical monograph [Internet]. Sydney: MIMS Australia; [updated 2025; cited 2025 Apr 17]. Available from: UWA Onesearch
Cardiovascular Expert Group. Therapeutic Guidelines Cardiovascular (Version 7). Therapeutic Guidelines Ltd;2023
Heart Foundation (What is an arrhythmia?), Victor Chang Cardiac Research $\underline{Institute(Arrhythmia)}$ , $\underline{Canberra Health Services (Holter Monitor)}$ , $\underline{Heart}$ $\underline{Foundation (What is atrial fibrillation?)}$ , $\underline{SA Health (Palpitations - Adult CPC)}$ , $\underline{ANZCOR}$ $\underline{Guidelines (Guideline 11.9 - Managing Acute Dysrhythmias)}$
Tahamtan S et al. The effect of statins on dental and oral health: a review of preclinical and clinical studies. Journal of Translational Medicine. 2020; 18(155)
Terence J et al. Amiodarone. Aust Prescr 2005;28:150-4

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L6 Cardivascular systems 2025_formatted_text

DENT 3005: Introduction to Pharmacology1

Cardiovascular systems

Acknowledgement of country2

Learning Outcomes3

Learning objectives

Hypertension4

Normal regulation of BP5

Blood Vessels

To Cells

From Cells

Vessel Types

Heart and lungs blood flow

Normal regulation of BP5

Renin-angiotensin system6

ACE inhibitor7

ACE Inhibitors8

Dental Relevance

Oral Side Effects

Drug Interactions

Sartans9

Smooth muscle cells | Heart10

Calcium Channel Blockers (CCBs)11

Calcium channel blockers (CCBs)12

Calcium Channel Blockers13

Beta blockers14

Beta blockers14

Beta blockers14

Selective alpha blockers15

Other antihypertensives

Hypertension: Dental implications16

Management of Syncope in Dental practice17

Arrythmia18

Antiarrhythmic Drug Classification19

Action Potential Phases

Cardiac action potential: Key Phases20

Antiarrhythmic drugs (Vaughan Williams classification)21

Specific Antiarrhythmics22

Amiodarone

Disopyramide

Isoprenaline

Arrythmia: Dental implications23

Heart Failure24

Heart Failure24

Drugs for systolic HF25

Aldosterone antagonists26

Loop diuretics

Nephron Diagram Key27

Sites of Diuretic Action

Sympathomimetics28

Other drugs for HF – digoxin

Heart Failure: Dental implications29

Drugs for HF: Dental implications30

Management of cardiac arrest in dental practice31

Tripple Whammy32

Angina33

Nitrates34

Other anti-anginal drugs

Angina: Dental implications35

Management of angina or ACS in the dental setting36

Management of Severe/New Chest Pain (Continued)37

Dyslipidemia38

Atherosclerosis39

Statins40

Bile acid binding resins

Fibrates41

Other drugs for dyslipidemia

Dyslipidemia: Dental implications42

References43

Footnotes

Graph View

Table of Contents

DENT 3005: Introduction to Pharmacology¹

Acknowledgement of country²

Learning Outcomes³

Hypertension⁴

Normal regulation of BP⁵

Normal regulation of BP⁵

Renin-angiotensin system⁶

ACE inhibitor⁷

ACE Inhibitors⁸

Sartans⁹

Smooth muscle cells | Heart¹⁰

Calcium Channel Blockers (CCBs)¹¹

Calcium channel blockers (CCBs)¹²

Calcium Channel Blockers¹³

Beta blockers¹⁴

Beta blockers¹⁴

Beta blockers¹⁴

Selective alpha blockers¹⁵

Hypertension: Dental implications¹⁶

Management of Syncope in Dental practice¹⁷

Arrythmia¹⁸

Antiarrhythmic Drug Classification¹⁹

Cardiac action potential: Key Phases²⁰

Antiarrhythmic drugs (Vaughan Williams classification)²¹

Specific Antiarrhythmics²²

Arrythmia: Dental implications²³

Heart Failure²⁴

Heart Failure²⁴

Drugs for systolic HF²⁵

Aldosterone antagonists²⁶

Nephron Diagram Key²⁷

Sympathomimetics²⁸

Heart Failure: Dental implications²⁹

Drugs for HF: Dental implications³⁰

Management of cardiac arrest in dental practice³¹

Tripple Whammy³²

Angina³³

Nitrates³⁴

Angina: Dental implications³⁵

Management of angina or ACS in the dental setting³⁶

Management of Severe/New Chest Pain (Continued)³⁷

Dyslipidemia³⁸

Atherosclerosis³⁹

Statins⁴⁰

Fibrates⁴¹

Dyslipidemia: Dental implications⁴²

References⁴³