THE UNIVERSITY OF
WESTERN
AUSTRALIA
DENT 3005:Introduction to
Pharmacology
**Cardiovascular systems**
Dr Thuy Linh Truong
thuy.truong@uwa.edu.au
# **DENT 3005: Introduction to Pharmacology**
## **Cardiovascular systems**
**Dr Thuy Linh Truong**
thuy.truong@uwa.edu.au
THE UNIVERSITY OF
**WESTERN**
AUSTRALIA
Acknowledgement
of country
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
![]()
A black and white aboriginal-style painting.
# **Acknowledgement of country**
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 Outcomes**
Learning objectives
1) Understand the classes and mechanisms of
major classes of cardiovascular drugs
2) Recognise oral and dental side effects of
cardiovascular drugs
3) Management of emergencies related to
cardiovascular conditions in the dental
setting
4) Understand drugs interactions with dental
medications
5) Applied knowledge to clinical scenarios
![]()
A set of outlined icons representing medical and cardiovascular themes, including hearts with ECG lines, heart with lightning bolt, heart being held by hands, anatomical heart, stethoscope, blood pressure cuff, doctor, monitor showing ECG, ultrasound equipment, and ambulance.
# **Learning Outcomes**
## **Learning objectives**
1. Understand the classes and mechanisms of major classes of cardiovascular drugs
2. Recognise oral and dental side effects of cardiovascular drugs
3. Management of emergencies related to cardiovascular conditions in the dental setting
4. Understand drugs interactions with dental medications
5. Applied knowledge to clinical scenarios
# Hypertension
* **Definition**
* The force of the blood pushing against the artery walls is consistently too high $\rightarrow$ 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 | $>180/>110\text{mmHg}$ |
| **Complications** |
| :---: |
| Heart attack, stroke |
| Aneurysm |
| Heart failure |
| Microvascular damage : eye, brain |
| Metabolic syndrome |
# **Hypertension**
- **Definition**
- The force of the blood pushing against the artery walls is consistently too high $\rightarrow$ 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 | $>180/>110\text{mmHg}$ |
| **Complications** |
| :---: |
| Heart attack, stroke |
| Aneurysm |
| Heart failure |
| Microvascular damage : eye, brain |
| Metabolic syndrome |
**Normal regulation of BP**
**BLOOD VESSELS**
**BLOOD FLOW FROM HEART**
**BLOOD FLOW TO HEART**
**TO CELLS**
Oxygen
Nutrients
**FROM CELLS**
Waste
Carbon dioxide
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 BP**
## **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 BP**
* **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
# **Normal regulation of BP**
- **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 system
```mermaid
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
```
<img src='A diagram showing the overall structure and components of the Renin-Angiotensin System (RAS) and its effects on various organs and its regulation by pharmacological agents.'> </img>
# **Renin-angiotensin system**
```mermaid
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 inhibitor**
* **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 inhibitor**
- **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 Inhibitors**
* 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
# **ACE Inhibitors**
## **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
**Sartans**
* **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 |
# **Sartans**
- **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 |
<img alt="The image shows a diagram of a nephron and the sites of action of different classes of diuretics. Starting with the glomerulus, the initial filtration rate is 120 ml/min. The proximal convoluted tubule is shown to reabsorb Na+ (60%), Cl- (45%), HCO3-, H2O, K+, Ca2+, and Mg2+. Carbonic anhydrase inhibitors (1) and osmotic diuretics (2) are shown acting at this segment. The thin descending loop reabsorbs H2O. The thick ascending loop reabsorbs Na+ (25%) and Cl-. Loop diuretics (3) act here. The distal convoluted tubule reabsorbs Na+ (10%), Cl-, and Ca2+. Thiazides (4) act here. The collecting duct reabsorbs H2O (stimulated by ADH) and reabsorbs Na+ (5%) while secreting K+ and H+. K+-sparing diuretics (5) and Aldosterone antagonists (6) act here. The different parts of the nephron are labeled in relation to the cortex and medulla." />
- $\downarrow$ **AV Conduction Velocity:** Slows electrical signal transmission through AV node; useful in supraventricular tachycardia
- $\downarrow$ **SA Node Pacemaker Rate:** Reduces heart rate (negative chronotropy); helps manage atrial fibrillation
- $\downarrow$ **Myocardial Contractility:** Decreases calcium entry during depolarization; lowers force and rate of cardiac contractions
## **Smooth muscle cells | Heart**
```mermaid
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
```
# **Thiazide & related diuretics**
* **MOA:** inhibit reabsorption of Na & Cl
* **Dental implications**
* NSAIDs: may reduce renal function
| **Generic name** | **Brand Name** |
| :--- | :--- |
| Hydrochlorothiazide | Dithiazide |
| Chlorthalidone | Hygroton |
| Indapamide | Natrilix |
# **Potassium sparring diuretics**
* **MOA:** inhibit reabsorption of Na in the distal tubule
* **Dental implications**
* NSAIDs: may increase risk for hyperkalemia & reduce renal function
* Dry mouth
| **Generic name** | **Brand Name** |
| :--- | :--- |
| Amiloride | Kaluril |
| Triamterene | Only available w/ hydrochlorothiazide |
# Calcium channel blockers (CCBs)
**Calcium Channel Blockers**
(CCBs) inhibit $\text{Ca}^{2+}$ influx in arteriolar
smooth muscle
**Calcium** is essential for muscle
contraction via MLCK activation
**Blocking** $\text{Ca}^{2+}$ **channels** prevents
smooth muscle contraction
Results in **vasodilation**, reduced
peripheral resistance, and **lowered**
**blood pressure**
<img > </img>
$\downarrow$ **AV Conduction Velocity:** Slows
electrical signal transmission
through AV node; useful in
supraventricular tachycardia
$\downarrow$ **SA Node Pacemaker Rate:**
Reduces heart rate (negative
chronotropy); helps manage atrial
fibrillation
$\downarrow$ **Myocardial Contractility:**
Decreases calcium entry during
depolarization; lowers force and rate
of cardiac contractions
## Smooth muscle cells | Heart
```mermaid
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)**
* 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)**
- **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)**
Ca - Calcium
SMC - Smooth muscle cell
LV - Left ventricle
HR - Heart rate
ICS - Impulse conduction system
```mermaid
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 blockers (CCBs)**
Ca - Calcium
SMC - Smooth muscle cell
LV - Left ventricle
HR - Heart rate
ICS - Impulse conduction system
```mermaid
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 Blockers
* **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 $\rightarrow$ QT prolongation
* LA technique: always aspirate
<table><thead><tr><th>Generic name</th><th>Brand Name</th></tr></thead><tbody><tr><td>Amlodipine</td><td>Nordip, Norvasc</td></tr><tr><td>Clevidipine</td><td>Cleviprex inj</td></tr><tr><td>Felodipine</td><td>Felodur</td></tr><tr><td>Lercanidipine</td><td>Zanidip, Lercan</td></tr><tr><td>Nifedipine</td><td>Adalat, Adefin</td></tr><tr><td>Nimodipine</td><td>Nimotop</td></tr><tr><td>Diltiazem*</td><td>Cardizem</td></tr><tr><td>Verapamil *</td><td>Cordilox, Veracaps</td></tr></tbody></table>
# **Calcium Channel Blockers**
- **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 $\rightarrow$ QT prolongation
- LA technique: always aspirate
<table><thead><tr><th>Generic name</th><th>Brand Name</th></tr></thead><tbody><tr><td>Amlodipine</td><td>Nordip, Norvasc</td></tr><tr><td>Clevidipine</td><td>Cleviprex inj</td></tr><tr><td>Felodipine</td><td>Felodur</td></tr><tr><td>Lercanidipine</td><td>Zanidip, Lercan</td></tr><tr><td>Nifedipine</td><td>Adalat, Adefin</td></tr><tr><td>Nimodipine</td><td>Nimotop</td></tr><tr><td>Diltiazem*</td><td>Cardizem</td></tr><tr><td>Verapamil *</td><td>Cordilox, Veracaps</td></tr></tbody></table>
Beta blockers
```mermaid
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 blockers**
```mermaid
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 blockers
* **β1 receptor blockade (cardio-selective effects)**
* $\downarrow$ Heart rate $\rightarrow$ Negative chronotropic effect
* $\downarrow$ Contractility $\rightarrow$ Negative inotropic effect
* $\downarrow$ Cardiac output
* $\downarrow$ Renin release $\rightarrow$ Suppresses RAAS, lowers BP
* *Examples: Metoprolol, Atenolol*
* **β2 receptor blockade (non-cardio-selective effects)**
* $\uparrow$ Peripheral vasoconstriction
* $\uparrow$ Bronchoconstriction $\rightarrow$ *Caution in asthma/COPD*
* *Example: Propranolol (blocks both β1 & β2)*
* **Mixed alpha & beta blockade**
* *Labetalol, Carvedilol*
* Block $\beta1$, $\beta2$, and $\alpha1$ 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 blockers**
- **β1 receptor blockade (cardio-selective effects)**
- $\downarrow$ Heart rate $\rightarrow$ Negative chronotropic effect
- $\downarrow$ Contractility $\rightarrow$ Negative inotropic effect
- $\downarrow$ Cardiac output
- $\downarrow$ Renin release $\rightarrow$ Suppresses RAAS, lowers BP
- *Examples: Metoprolol, Atenolol*
- **β2 receptor blockade (non-cardio-selective effects)**
- $\uparrow$ Peripheral vasoconstriction
- $\uparrow$ Bronchoconstriction $\rightarrow$ *Caution in asthma/COPD*
- *Example: Propranolol (blocks both β1 & β2)*
- **Mixed alpha & beta blockade**
- *Labetalol, Carvedilol*
- Block $\beta1$, $\beta2$, and $\alpha1$ 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 blockers**
* **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 $\le$ 5 days
* Adrenaline (LA): use caution with non-selective $\beta$-blockers $\rightarrow$ risk of $\uparrow$ BP & reflex bradycardia
* **Surgical considerations**
* Monitor vitals during sedation or general anaesthesia
* Be aware of cardiac risks (bradyarrhythmia, hypotension)
# **Beta blockers**
- **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 $\le$ 5 days
- Adrenaline (LA): use caution with non-selective $\beta$-blockers $\rightarrow$ risk of $\uparrow$ BP & reflex bradycardia
- **Surgical considerations**
- Monitor vitals during sedation or general anaesthesia
- Be aware of cardiac risks (bradyarrhythmia, hypotension)
**Selective alpha blockers**
* **MOA**: block alpha$_1$ receptors $\rightarrow$ 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 |
# **Selective alpha blockers**
- **MOA**: block alpha$_1$ receptors $\rightarrow$ 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
implications
- **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
# **Hypertension: Dental implications**
- **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
**Hypertension
Dental
implications**
Management of Syncope in Dental practice
| 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 |
## **Management of Syncope in Dental practice**
| Scenario | Actions |
|---|---|
| If patient feels faint | - Stop dental treatment <br> - Lay patient flat (tilt chair or lie down) <br> - Raise legs <br> - Check heart rate <br> - Talk to assess consciousness |
| If patient loses consciousness | - Stop dental treatment <br> - Raise legs, lower head (horizontal position) <br> - Check BP and heart rate <br> - Allow slow recovery under supervision |
| If no recovery of consciousness | - Call 000 <br> - Start basic life support (refer to BLS chart) <br> - Place patient on side <br> - Continue until help arrives or patient wakes up |
**Arrythmia**
* **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
# **Arrythmia**
- **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
**Class I**
**Sodium-channel blocker**
Ia (moderate): quinidine,
procainamide
Ib (weak): lidocaine, mexiletine
Ic (strong): flecainide,
propafenone
**Class IV**
**Calcium-channel blocker**
Verapamil
Diltiazem
**Class III**
**Potassium-channel**
**blocker**
Amiodarone
Sotalol
**Class II**
**Beta-blocker**
Propranolol
Metoprolol
K⁺/Cl⁻ (out)
Ca²⁺ (in)
K⁺ (out)
Na⁺ (in)
K⁺ (rectifier)
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
## **Antiarrhythmic Drug Classification**
| Class | Type | Examples |
|---|---|---|
| **Class I** | **Sodium-channel blocker** | Ia (moderate): quinidine, procainamide <br> Ib (weak): lidocaine, mexiletine <br> 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 Phases**
* **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
# **Cardiac action potential: Key Phases**
- **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)
* 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 |
# **Antiarrhythmic drugs (Vaughan Williams classification)**
- 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 |
**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
## **Specific Antiarrhythmics**
### **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**
**implications**
* **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
# **Arrythmia: Dental implications**
- 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
$$\textbf{Heart Failure}$$
* $\textbf{Systolic HF}$
* Responds to conventional tx
* $\textbf{Diastolic HF}$
* No drug tx shown to improve survival
* $\textbf{Common cause is coronary heard disease}$
* Asoc w/ hx of myocardial infarction & HTN
* $\textbf{Prognosis for chronic HF is poor: 60-70\% mortality within 5yrs}$
* $\textbf{Impairment of pumping ability}$
* RHS: accumulation of blood in venous circulation $\rightarrow$ organ congestion & peripheral oedema
* LHS: accumulation of blood in pulmonary circulation $\rightarrow$ pulmonary congestion & fluid in lungs
# **Heart Failure**
- **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 $\rightarrow$ organ congestion & peripheral oedema
- **LHS:** accumulation of blood in pulmonary circulation $\rightarrow$ pulmonary congestion & fluid in lungs
**Heart Failure**
* **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
# **Heart Failure**
- **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 HF**
- 1) Start ACE inhibitor
- Start low, increase slow
- If cough/angioedema: switch to sartan
- 2) When stable, add beta blocker
- Start low, increase slow
- 3) If still symptomatic
- + aldosterone antagonist
- 4) If still symptomatic
- + digoxin or ivabradine
- 5) Fluid overload
- + loop diuretic
- 6) Acute pulmonary oedema
- Nitrates & diuretics
- 7) If acute severe HF
- + vasodilators, parenteral inotropes
# **Drugs for systolic HF**
1. **Start ACE inhibitor**
- Start low, increase slow
- If cough/angioedema: switch to sartan
2. **When stable, add beta blocker**
- Start low, increase slow
3. **If still symptomatic**
- + aldosterone antagonist
4. **If still symptomatic**
- + digoxin or ivabradine
5. **Fluid overload**
- + loop diuretic
6. **Acute pulmonary oedema**
- Nitrates & diuretics
7. **If acute severe HF**
- + vasodilators, parenteral inotropes
**Aldosterone antagonists**
* **MOA:** antagonize aldosterone $\rightarrow$ 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 |
# **Aldosterone antagonists**
- **MOA:** antagonize aldosterone $\rightarrow$ 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 |
A diagrammatic representation of the nephron and its related structures:
Glomerulus
Proximal
convoluted
tubule
Acids Bases
Lumen
$120 \text{ml} \text{min}^{-1}$
Cortex
Medulla
HCO$_3^-$
(reabsorption)
$\text{Na}^+ (60\%)$
$\text{Cl}^- (45\%)$
$\text{H}_2\text{O}$
$\text{K}^+$
$\text{Ca}^{2+}$
$\text{Mg}^{2+}$
$\text{Cl}^-$
$\text{Na}^+$
$(25\%)$
$\text{H}_2\text{O}$
$\text{H}_2\text{O}$
Thin
descending
loop
Loop of
Henle
Thin
ascending
loop
Distal
convoluted
tubule
$\text{Na}^+$
$(10\%)$
$\text{Cl}^- \text{PTH sensitive (ADH)}$
$\text{Ca}^{2+}$
$\text{K}^+\text{H}^+$
$\text{Na}^+ (5\%)$
Thick
ascending
loop
(ADH)
$\text{H}_2\text{O}$
$\text{H}_2\text{O}$
$\text{Na}^+$
Collecting
Ducts
(1) Carbonic anhydrase inhibitors
(2) Osmotic diuretics
(3) Loop diuretics
(4) Thiazides
(5) K$^+\text{ sparing}$
(6) Aldosterone antagonists
## **Nephron Diagram Key**
- **Glomerulus:** Filtration rate $120 \text{ml} \text{min}^{-1}$
- **Proximal convoluted tubule:** Reabsorption of HCO$_3^-$, $\text{Na}^+ (60\%)$, $\text{Cl}^- (45\%)$, $\text{H}_2\text{O}$, $\text{K}^+$, $\text{Ca}^{2+}$, $\text{Mg}^{2+}$. Secretion of Acids, Bases.
- **Thin descending loop of Henle:** Reabsorption of $\text{H}_2\text{O}$.
- **Thick ascending loop of Henle:** Reabsorption of $\text{Cl}^-$, $\text{Na}^+ (25\%)$.
- **Distal convoluted tubule:** Reabsorption of $\text{Na}^+ (10\%)$, $\text{Cl}^-$, $\text{Ca}^{2+}$ (PTH sensitive).
- **Collecting Ducts:** Reabsorption of $\text{H}_2\text{O}$ (ADH sensitive), $\text{Na}^+ (5\%)$. Secretion of $\text{K}^+$, $\text{H}^+$.
### **Sites of Diuretic Action**
1. **Carbonic anhydrase inhibitors** (Proximal tubule)
2. **Osmotic diuretics** (Proximal tubule)
3. **Loop diuretics** (Thick ascending loop)
4. **Thiazides** (Distal convoluted tubule)
5. **K$^+$-sparing diuretics** (Collecting duct)
6. **Aldosterone antagonists** (Collecting duct)
**Sympathomimetics**
* 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** |
# **Sympathomimetics**
- **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**
**implications**
- 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
# **Heart Failure: Dental implications**
- 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 implications**
* **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
## **Drugs for HF: Dental implications**
- **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
**Heart Failure Dental implications**
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
## **Management of cardiac arrest in dental practice**
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 Whammy
1. ACE inhibitor dilates the efferent arteriole, and reduces GFR
2. Diuretics reduce plasma volume and GFR
3. NSAIDs constrict blood flow into the glomerulus via the afferent arteriole and reduce GFR
# **Tripple Whammy**
1. **ACE inhibitor** dilates the efferent arteriole, and reduces GFR
2. **Diuretics** reduce plasma volume and GFR
3. **NSAIDs** constrict blood flow into the glomerulus via the afferent arteriole and reduce GFR
**Angina**
* 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
# **Angina**
- 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
**Nitrates**
* MOA: provide exogenous source of nitric oxide
→ vasodilatory effect
**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 |
| :--- | :--- |
| **Glyceryl trinitrate** | **Nitrolingual** |
| **Isosorbide dinitrate** | **Isordil** |
| **Isosorbide mononitrate** | **Duride, Imdur** |
| Generic name | Brand Name |
| :--- | :--- |
| **Ivabradine** | **Coralan** |
| **Nicorandil** | **Ikorel** |
| **Perhexiline** | **Pexig** |
# **Nitrates**
- **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 implications**
- 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
# **Angina: Dental implications**
- **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
**Angina**
**Dental**
**implications**
Management of angina or ACS in the dental setting
<table>
<thead>
<tr>
<th>Scenario</th>
<th>Actions</th>
</tr>
</thead>
<tbody>
<tr>
<td>If chest pain occurs in a patient with a history of angina:</td>
<td>- Stop dental treatment <br> - Measure blood pressure, heart rate, and pulse oximetry <br> - Assess consciousness by talking to the patient <br> - Ask the patient to sit down (due to risk of hypotension) <br> - Administer glyceryl trinitrate: <br> • Spray: 400 micrograms sublingually, repeat every 5 min if needed, up to 3 doses (if tolerated) <br> OR <br> • Tablet: 300–600 micrograms sublingually, repeat every 5 min if needed, up to 3 doses (if tolerated)</td>
</tr>
<tr>
<td>If pain persists for more than 10 minutes (after 2 doses):</td>
<td>- Administer third dose <br> - Manage as for severe/new chest pain</td>
</tr>
<tr>
<td>If the patient recovers:</td>
<td>- Do not proceed with dental treatment <br> - Refer for medical evaluation even if patient appears well</td>
</tr>
<tr>
<td>If chest pain is severe or new:</td>
<td>- Call **000** <br> - If patient has angina history, give glyceryl trinitrate as above <br> - For **all patients**, give: aspirin (not detailed in image but implied standard protocol)</td>
</tr>
</tbody>
</table>
## **Management of angina or ACS in the dental setting**
<table>
<thead>
<tr>
<th>Scenario</th>
<th>Actions</th>
</tr>
</thead>
<tbody>
<tr>
<td>If chest pain occurs in a patient with a history of angina:</td>
<td>- Stop dental treatment <br> - Measure blood pressure, heart rate, and pulse oximetry <br> - Assess consciousness by talking to the patient <br> - Ask the patient to sit down (due to risk of hypotension) <br> - Administer glyceryl trinitrate: <br> • Spray: 400 micrograms sublingually, repeat every 5 min if needed, up to 3 doses (if tolerated) <br> OR <br> • Tablet: 300–600 micrograms sublingually, repeat every 5 min if needed, up to 3 doses (if tolerated)</td>
</tr>
<tr>
<td>If pain persists for more than 10 minutes (after 2 doses):</td>
<td>- Administer third dose <br> - Manage as for severe/new chest pain</td>
</tr>
<tr>
<td>If the patient recovers:</td>
<td>- Do not proceed with dental treatment <br> - Refer for medical evaluation even if patient appears well</td>
</tr>
<tr>
<td>If chest pain is severe or new:</td>
<td>- Call **000** <br> - If patient has angina history, give glyceryl trinitrate as above <br> - For **all patients**, give: aspirin (not detailed in image but implied standard protocol)</td>
</tr>
</tbody>
</table>
**Angina**
**Dental implications**
| 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 $\text{SaO}_{2} < 90\%$, start supplemental oxygen. Titrate $\text{SaO}_{2}$ 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 |
## **Management of Severe/New Chest Pain (Continued)**
| 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 $\text{SaO}_{2} < 90\%$, start supplemental oxygen. Titrate $\text{SaO}_{2}$ 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 |
**Dyslipidemia**
* Abnormal levels of lipids in the bloodstream
* Risk factor for cardiovascular (CV) diseases
* Dysregulation in lipid levels $\rightarrow$ 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
# **Dyslipidemia**
- Abnormal levels of lipids in the bloodstream
- Risk factor for cardiovascular (CV) diseases
- Dysregulation in lipid levels $\rightarrow$ 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
**Atherosclerosis**
* Chronic disease
* Buildup of plaques within the arterial walls
* Leading to narrowing and hardening of the arteries $\rightarrow$ 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 |
1. C-reactive protein ($CRP$) is a protein made by the liver. Its level increases when there's inflammation in the body.
2. Increased levels of homocysteine can damage the inside of arteries and raise the risk of blood clot formation
## **Atherosclerosis**
- Chronic disease
- Buildup of plaques within the arterial walls
- Leading to narrowing and hardening of the arteries $\rightarrow$ 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 |
1. C-reactive protein ($CRP$) is a protein made by the liver. Its level increases when there's inflammation in the body.
2. Increased levels of homocysteine can damage the inside of arteries and raise the risk of blood clot formation
**Statins**
* 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 |
# **Statins**
- **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 |
**Fibrates**
* 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 |
# **Fibrates**
- **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 implications -->
**Dyslipidemia**
**Dental**
**implications**
* **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
# **Dyslipidemia: Dental implications**
- **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
**References**
* 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 $\underline{\text{Institute(Arrhythmia)}}$, $\underline{\text{Canberra Health Services (Holter Monitor)}}$, $\underline{\text{Heart}}$ $\underline{\text{Foundation (What is atrial fibrillation?)}}$, $\underline{\text{SA Health (Palpitations - Adult CPC)}}$, $\underline{\text{ANZCOR}}$ $\underline{\text{Guidelines (Guideline 11.9 - Managing Acute Dysrhythmias)}}$
* 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
$\text{}$
$\text{}$
$\text{}$
![]()
A woman blowing her nose surrounded by medicine bottles and capsules.
![]()
Three medicine bottles, one tipped over with capsules spilled out.
![]()
A woman blowing her nose surrounded by medicine bottles and capsules, similar to the first image.
# **References**
- 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 $\underline{\text{Institute(Arrhythmia)}}$, $\underline{\text{Canberra Health Services (Holter Monitor)}}$, $\underline{\text{Heart}}$ $\underline{\text{Foundation (What is atrial fibrillation?)}}$, $\underline{\text{SA Health (Palpitations - Adult CPC)}}$, $\underline{\text{ANZCOR}}$ $\underline{\text{Guidelines (Guideline 11.9 - Managing Acute Dysrhythmias)}}$
- 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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