Nitrates and Erectile Dysfunction Medicines: Understanding a Dangerous Drug Interaction

Nitrates and Erectile Dysfunction and cardiovascular disease frequently share common vascular pathology. Endothelial dysfunction, atherosclerosis, and reduced arterial compliance mean that a substantial proportion of men with ischemic heart disease or chronic stable angina also experience erectile difficulties. Consequently, concurrent management of sexual dysfunction and cardiovascular health is a frequent clinical reality. However, combining oral treatments for erectile dysfunction with nitrate medications represents one of the most critical drug–drug interactions in clinical practice.

Phosphodiesterase type 5 (PDE5) inhibitors the primary oral pharmacotherapy for erectile dysfunction and organic nitrates both exert their therapeutic effects through vascular smooth muscle pathways. When co-administered, their complementary mechanisms result in synergistic vasodilation. This can precipitate a rapid, profound, and potentially refractory drop in systemic blood pressure, severely compromising coronary, cerebral, and vital organ perfusion.

Understanding this interaction is essential for healthcare providers and patients alike. This article provides a comprehensive, evidence-based review of the underlying nitric oxide–cyclic guanosine monophosphate (cGMP) pathway, the specific medications involved, evidence-based avoidance intervals, non-nitrate cardiovascular interactions, and emergency protocols for acute chest pain.

What Are Nitrates and Why Are They Prescribed?

Organic nitrates are vasodilators that have formed the cornerstone of anti-anginal pharmacotherapy for over a century. They are prescribed primarily to manage, prevent, and alleviate acute episodes of angina pectoris resulting from obstructive coronary artery disease, as well as selected presentations of acute coronary syndromes and decompensated heart failure.

How Nitrate Medicines Work

Nitrates act as prodrugs of nitric oxide (NO). Following oral, sublingual, or transdermal administration, organic nitrates are metabolized in vascular endothelial and smooth muscle cells—predominantly through enzymatic bioactivation involving mitochondrial aldehyde dehydrogenase (ALDH-2) or microsomal enzymes—to yield exogenous nitric oxide.

Free nitric oxide diffuses into vascular smooth muscle cells, activating soluble guanylyl cyclase (sGC). Activated sGC converts guanosine triphosphate (GTP) into intracellular cyclic guanosine monophosphate (cGMP). Elevated cGMP triggers protein kinase G (PKG), which inhibits calcium influx, stimulates potassium efflux, and reduces intracellular free calcium concentrations. This cascade results in vascular smooth muscle relaxation.

At therapeutic doses, nitrates exert their primary hemodynamic benefit through systemic venodilation (capacitance vessel relaxation), which decreases systemic venous return, left ventricular end-diastolic volume, and ventricular wall tension (cardiac preload). Reduced preload diminishes myocardial oxygen demand. At higher doses, nitrates also promote systemic arterial vasodilation and dilate epicardial coronary collateral vessels, enhancing subendocardial blood flow to ischemic myocardium.

Common Nitrate Medicines

Nitrates are formulated in various pharmacokinetic preparations depending on whether they are intended for immediate symptom relief or chronic maintenance prophylaxis:

• Glyceryl trinitrate (GTN) / Nitroglycerin: Available as rapid-acting sublingual tablets, sublingual lingual sprays, intravenous infusions, and slow-release transdermal patches. Sublingual formulations are typically utilized for immediate relief or situational prophylaxis of acute exertional angina.
• Isosorbide mononitrate (ISMN): A long-acting nitrate available as immediate-release or modified-release oral formulations for chronic maintenance therapy of angina pectoris.
• Isosorbide dinitrate (ISDN): Used both orally for prophylaxis and sublingually for acute angina, requiring hepatic conversion to active mononitrates.
• Amyl nitrite: A volatile liquid historically used medically for angina and cyanide poisoning, but frequently encountered recreationally (commonly referred to as “poppers”). Inhalation delivers rapid, massive systemic surges of nitric oxide, posing acute hypotensive risks when combined with vasodilators.

Where Does Nicorandil Fit?

Nicorandil is an anti-anginal agent with dual mechanisms of action: it acts as a potassium-channel opener ( channel agonist) and incorporates an organic nitrate-like moiety capable of donating nitric oxide. Because its nitrate functional group stimulates soluble guanylyl cyclase to generate cGMP, nicorandil is strictly contraindicated with PDE5 inhibitors, presenting the identical catastrophic hypotensive risks seen with conventional organic nitrates.

How Erectile Dysfunction Medicines Work

Understanding PDE5 Inhibitors

Phosphodiesterase type 5 (PDE5) inhibitors are the first-line oral medical therapy for erectile dysfunction. During sexual arousal, parasympathetic non-adrenergic, non-cholinergic (NANC) postganglionic neurons and cavernous vascular endothelial cells release endogenous nitric oxide into the corpus cavernosum. This endogenous NO stimulates sGC to produce intracellular cGMP, causing smooth muscle relaxation within the trabecular cavernosal tissue and helicine arterioles. This relaxation permits blood engorgement, venous compression against the tunica albuginea, and penile erection.

Under normal physiological conditions, cGMP is continually degraded and inactivated into 5′-GMP by the cyclic nucleotide-degrading enzyme phosphodiesterase type 5 (PDE5). PDE5 inhibitors act as competitive, selective inhibitors of this enzyme, preventing cGMP hydrolysis and allowing cGMP to accumulate.

Common PDE5 Inhibitor Medicines

Four principal selective PDE5 inhibitors are approved across international markets, including by the Australian Therapeutic Goods Administration (TGA) and the US Food and Drug Administration (FDA):

Generic Name	Recognised Brand Name(s)	Primary Formulations	Selectivity Highlights
Sildenafil	Viagra, Revatio (PAH)	Oral tablets, oral solution	Highly selective for PDE5; minor cross-inhibition of PDE6 (retinal).
Tadalafil	Cialis, Adcirca (PAH)	On-demand tablets, once-daily low-dose tablets	High PDE5 selectivity; longer duration of action; minor cross-inhibition of PDE11 (skeletal muscle).
Vardenafil	Levitra, Staxyn (ODT)	Film-coated tablets, orally disintegrating tablets	Potent PDE5 inhibition; minor cross-inhibition of PDE6.
Avanafil	Spedra, Stendra	Rapid-absorption oral tablets	High selectivity for PDE5 over other PDE isozymes; rapid onset.

Why These Medicines Affect Systemic Blood Vessels

Although PDE5 is concentrated within the corpus cavernosum, it is also expressed throughout systemic vascular smooth muscle, platelets, visceral smooth muscle, and the pulmonary arterial bed. Consequently, therapeutic doses of PDE5 inhibitors produce minor, self-limiting systemic vasodilation in healthy individuals, generally manifesting as modest transient reductions in resting systolic and diastolic blood pressure (typically by 5–10 mmHg systolic and 3–6 mmHg diastolic). Under isolated administration, autonomic counter-regulatory mechanisms easily compensate for these modest drops.

Why Should Nitrates and ED Medicines Never Be Combined?

The combination of organic nitrates and PDE5 inhibitors creates an unmitigated, synergistic pharmacodynamic amplification of vascular smooth muscle relaxation. Rather than a simple additive effect, the interaction compromises normal autonomic blood-pressure regulation.

The Nitric Oxide–cGMP Pathway Explained

Vascular smooth muscle tone is governed by the dynamic equilibrium between cGMP synthesis and cGMP breakdown:

• Step 1: Unrestrained Production. Nitrates deliver an exogenous flood of nitric oxide throughout the entire systemic circulation, bypassing physiological feedback loops and driving continuous, high-volume cGMP synthesis via sGC.
• Step 2: Complete Clearance Blockade. Simultaneously, the PDE5 inhibitor blocks the primary physiological degradation pathway responsible for clearing cGMP from vascular smooth muscle cells.

Pathophysiological Consequences

When synthetic output surges while breakdown mechanisms are pharmacologically shut down, intracellular cGMP levels climb exponentially. The systemic vascular consequences include:

1. Massive Systemic Vasodilation: Splanchnic, cutaneous, and peripheral arterial beds dilate simultaneously.
2. Venous Pooling and Preload Collapse: Unchecked venodilation sequesters blood in capacitance veins, severely reducing cardiac venous return, stroke volume, and cardiac output.
3. Severe Hypotension: Mean arterial pressure drops precipitously, often failing to sustain end-organ capillary bed perfusion.
4. Impaired Coronary Autoregulation: The fall in systemic diastolic pressure reduces coronary perfusion pressure. In patients with preexisting coronary stenosis, this hypoperfusion can trigger acute myocardial ischemia, malignant ventricular arrhythmias, or fatal myocardial infarction.

Because the underlying interaction is absolute and synergistic, nitrates in any form must never be co-administered with PDE5 inhibitors.

Which Erectile Dysfunction Medicines Interact With Nitrates?

The absolute contraindication applies across all approved PDE5 inhibitors, irrespective of structural differences or administration schedules.

Sildenafil and Nitrates

Early hemodynamics trials demonstrated that co-administering sildenafil with sublingual nitroglycerin produces marked, unpredictable blood-pressure reductions that persist significantly longer than those observed with nitrates alone. A sublingual dose of nitroglycerin taken within 24 hours of sildenafil can drop mean arterial pressure by 30 to 50 mmHg or more, provoking symptomatic hypotension and ischemic complications.

Tadalafil and Nitrates

Tadalafil is distinct from other agents in its class due to its prolonged elimination half-life ( hours). Hemodynamic studies confirmed that co-administration of sublingual nitroglycerin with tadalafil results in significant, clinically dangerous blood-pressure reductions for up to 48 hours post-dose. The interaction risk remains elevated even with low-dose daily tadalafil regimens (2.5 mg or 5 mg) prescribed for erectile dysfunction or benign prostatic hyperplasia (BPH).

Vardenafil and Nitrates

Vardenafil exhibits pharmacokinetic timing similar to sildenafil. In placebo-controlled trials, combining vardenafil with sublingual or transdermal nitrates provoked significant drops in upright systolic and diastolic blood pressure. The absolute contraindication applies equally to standard film-coated tablets and orally disintegrating formulations.

Avanafil and Nitrates

Avanafil is characterized by rapid oral absorption and relatively short systemic elimination. Nevertheless, co-administration with nitroglycerin produces substantial synergistic blood pressure drops. Avanafil carries the same class-wide contraindication prohibiting co-prescription with all organic nitrates or nitric oxide donors.

How Long Must Patients Wait Before Nitrates Can Be Safely Considered?

Determining the minimum safe interval between administering a PDE5 inhibitor and subsequently receiving a nitrate is a critical protocol in cardiovascular emergency medicine.

Crucial Medical Caveat:

The clearance intervals below are clinical reference windows for emergency medical personnel managing life-threatening acute ischemia. They are not guidelines for patients to self-administer nitrates or self-medicate for chest pain. Patients taking a PDE5 inhibitor who develop chest pain must never self-administer GTN spray or tablets, but must instead seek emergency medical assistance immediately.

Pharmacokinetic Comparison and Safe Clinical Intervals

Active Substance	Typical Tmax (Peak Concentration)	Elimination Half-Life (t1/2)	Absolute Minimum Nitrate Avoidance Interval	Clinical Source / Regulatory Standard
Sildenafil	30–120 minutes	3–5 hours	At least 24 hours	TGA Product Information; Princeton IV (2024); AHA/ACC (2023)
Vardenafil	30–120 minutes	4–5 hours	At least 24 hours	TGA Product Information; Princeton IV (2024); AHA/ACC (2023)
Tadalafil	120 minutes (2 hours)	hours	At least 48 hours	TGA Product Information; Princeton IV (2024); AHA/ACC (2023)
Avanafil	30–45 minutes	3–5 hours	24 hours (Consensus) /  hours (Critical US Label Exception)	Princeton IV (2024); US FDA Labeling / TGA PI

Explaining Tadalafil’s Extended Window

Tadalafil’s chemical structure confers high lipophilicity, slow hepatic metabolism (primarily by CYP3A4), and an extended elimination half-life of 17.5 hours in healthy adults (and longer in older patients or those with renal impairment). Approximately five half-lives are required to eliminate a drug from the body. Consequently, clinically significant concentrations of tadalafil circulate up to 48 hours or more after a single dose. Administering a nitrate inside this 48-hour window risks critical vasodilation.

Understanding the Avanafil Interval Discrepancy

Avanafil presents a minor point of divergence between international clinical consensus guidelines and drug labeling:

• The US FDA Prescribing Information states that if nitrate therapy becomes medically unavoidable for a life-threatening acute cardiac event, at least 12 hours must elapse after the last dose of avanafil, and administration must occur only in a fully equipped healthcare setting under continuous invasive hemodynamic monitoring.
• The Princeton IV Consensus (2024) and European Guidelines advise a conservative 24-hour interval for avanafil, aligning it with sildenafil and vardenafil. This conservative recommendation accounts for inter-patient pharmacokinetic variability, delayed gastric emptying, and renal or hepatic variations that may extend drug clearance.

In practical emergency medicine, the 24-hour interval remains the safest standard worldwide.

What Are the Potential Risks of Combining Nitrates and ED Medicines?

The clinical presentation of this interaction ranges from distressing autonomic instability to fatal cardiovascular collapse.

• Profound, Refractory Hypotension: Mean arterial pressures can fall well below 60 mmHg. Such drops are often resistant to standard postural restoration (Trendelenburg position) and modest intravenous fluid boluses.
• Syncope and Unconsciousness: Inadequate cerebral blood flow triggers lightheadedness, vertigo, presyncope, or abrupt loss of consciousness. Secondary physical injuries, such as concussions or fractures from falling, are common.
• Coronary Hypoperfusion and Myocardial Infarction: Because coronary arteries fill primarily during ventricular diastole, a major drop in systemic diastolic pressure reduces perfusion across stenotic coronary vessels. The resulting imbalance between myocardial oxygen supply and demand can transform stable angina into an acute myocardial infarction.
• Reflex Tachycardia and Arrhythmias: The autonomic nervous system responds to low pressure with sympathetic baroreceptor activation, driving sinus tachycardia. In a myocardium already compromised by ischemia, rapid heart rates amplify oxygen demand and can trigger malignant ventricular arrhythmias.

What Should You Do If Chest Pain Occurs After Taking an ED Medicine?

Erectile activity corresponds to modest physical exertion (roughly 3 to 5 METs, equivalent to walking briskly or climbing two flights of stairs). In patients with underlying coronary artery disease, this physical effort can unmask myocardial ischemia and cause chest discomfort.

Recognising Symptoms of Acute Cardiac Ischemia

Patients and partners must recognize warning signs that require emergency intervention:

• Central chest tightness, heavy pressure, squeezing, or aching.
• Pain radiating down the left arm, neck, jaw, back, or epigastrium.
• Associated sudden breathlessness, diaphoresis (cold sweats), nausea, or lightheadedness.

Why Self-Administering GTN Can Be Dangerous

Many individuals with chronic stable angina keep sublingual GTN spray or tablets on hand for immediate use. If you have taken any PDE5 inhibitor in the past 24 to 48 hours, you must NEVER take GTN spray or tablets. Self-administering nitrates after an ED medicine risks precipitating the exact cardiovascular collapse described above, transforming a manageable ischemic episode into life-threatening cardiogenic shock.

Actions for Patients and Emergency Clinicians

1. Stop all physical activity and sit or rest in a comfortable, semi-reclining position.
2. Call emergency services immediately (Dial 000 in Australia, 911 in North America, or 112 in Europe/UK).
3. Disclose your medication history completely and clearly: Tell the emergency operator and paramedics:
   • The exact name of the ED medication taken (e.g., sildenafil, tadalafil, vardenafil, avanafil).
   • The dose taken.
   • The exact time of ingestion.
4. Do not conceal ED medicine use out of embarrassment. Emergency physicians have protocols to manage acute chest pain without nitrates. They can utilize non-nitrate anti-anginal drugs (such as beta-blockers, calcium channel blockers, or opioids) and prioritize urgent diagnostic coronary angiography.
5. If a patient inadvertently takes both medicines and collapses: Position them flat with their legs elevated (if conscious and breathing normally), call emergency services immediately, and prepare to initiate cardiopulmonary resuscitation (CPR) if the individual becomes pulseless or stops breathing. Paramedics treat this toxicity with rapid intravenous crystalloid infusions, alpha-adrenergic vasopressors (such as phenylephrine or noradrenaline), and continuous telemetry.

Other Medicines That May Interact With PDE5 Inhibitors

While nitrates represent an absolute contraindication, several other pharmacological classes interact with PDE5 inhibitors and require careful clinical review.

Absolute Contraindications

• Riociguat (Soluble Guanylyl Cyclase Stimulator): Prescribed for pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Riociguat directly stimulates sGC independently of nitric oxide and synergistically sensitizes sGC to endogenous NO. Combining riociguat with PDE5 inhibitors causes severe hypotension through the identical pathway as nitrates and is strictly contraindicated.
• Nicorandil: Because it acts partly as a nitric oxide donor, it shares the absolute contraindication associated with organic nitrates.

Interactions Requiring Caution and Dosage Adjustments

• Alpha-1 Adrenoceptor Antagonists: Prescribed for lower urinary tract symptoms secondary to benign prostatic hyperplasia (e.g., tamsulosin, alfuzosin, silodosin) or hypertension (e.g., prazosin, doxazosin). Both alpha-blockers and PDE5 inhibitors are peripheral vasodilators. When used simultaneously, they can cause additive orthostatic hypotension, dizziness, and falls.
  • Clinical Management: Patients should be hemodynamically stable on their alpha-blocker regimen before initiating a PDE5 inhibitor at the lowest available starting dose (e.g., sildenafil 25 mg or tadalafil 2.5–5 mg). Highly uroselective alpha-1a blockers like tamsulosin carry lower orthostatic risks than non-selective blockers like prazosin.
• Antihypertensive Combinations: In patients taking multiple antihypertensive medications (e.g., ACE inhibitors, ARBs, CCBs, thiazide diuretics), adding a PDE5 inhibitor generally produces minor incremental blood-pressure drops. While clinically manageable, careful titration and blood-pressure monitoring are advised.
• Strong CYP3A4 Inhibitors: Sildenafil, tadalafil, vardenafil, and avanafil are extensively cleared by hepatic cytochrome P450 3A4. Strong CYP3A4 inhibitors (including ketoconazole, itraconazole, clarithromycin, ritonavir, and cobicistat) dramatically impair their clearance, prolonging drug half-life and elevating systemic concentrations. Starting doses must be reduced, dosing intervals lengthened, and concurrent use approached with caution.
• Alcohol: Large amounts of alcohol (e.g.,  blood alcohol level, equivalent to 3–5 standard drinks) exhibit mild vasodilating properties. When combined with PDE5 inhibitors, alcohol can increase the frequency of orthostatic dizziness, headache, and reflex tachycardia.

Can People With Heart Disease Use Erectile Dysfunction Medicines?

Erectile dysfunction is an independent predictor of occult cardiovascular disease; penile arteries (1–2 mm diameter) typically manifest atherosclerotic narrowing and endothelial dysfunction years before larger coronary vessels (3–4 mm diameter) produce angina. Consequently, a diagnosis of ED offers an opportunity for comprehensive cardiovascular risk assessment.

Cardiovascular Assessment Before ED Treatment

Before prescribing any treatment for erectile dysfunction, clinicians perform a systematic risk stratification based on established frameworks, such as the Princeton IV Consensus Guidelines (2024) and the European Association of Urology (EAU) Guidelines (2025):

• Low-Risk Category: Patients with asymptomatic or mild stable angina, controlled hypertension, uncomplicated previous myocardial infarction ( weeks prior) with normal exercise tolerance, or mild valvular disease. These individuals can safely initiate PDE5 inhibitor therapy and engage in sexual activity without further invasive cardiac evaluation, provided they do not use nitrate medications.
• Intermediate-Risk Category: Patients with moderate stable angina, recent myocardial infarction ( weeks prior), left ventricular dysfunction, or multiple cardiovascular risk factors. These individuals require formal functional evaluation—such as an exercise treadmill stress test—to assess their ischemic threshold and functional reserve before starting ED treatment.
• High-Risk Category: Patients with unstable or refractory angina, severe decompensated heart failure (NYHA Class IV), recent high-risk arrhythmias, uncontrolled severe hypertension, severe aortic stenosis, or hypertrophic obstructive cardiomyopathy. In this group, sexual activity and PDE5 inhibitors are deferred until the cardiac condition is stabilized.

What Princeton IV Advises on Long-Term Nitrate Therapy

A frequent clinical dilemma arises when a patient with stable ischemic heart disease taking chronic daily oral nitrates (such as isosorbide mononitrate) requests therapy for erectile dysfunction.

The Princeton IV Consensus emphasizes that long-term nitrate therapy should be critically reassessed by a cardiologist. In many cases of stable coronary disease, daily nitrates are maintained by habit rather than clinical necessity. Modern evidence indicates that nitrates relieve symptoms but do not reduce mortality or prevent myocardial infarction in chronic coronary disease.

Under direct specialist supervision, patients taking prophylactic nitrates can often be safely transitioned to alternative, highly effective non-nitrate anti-anginal medications—such as:

• Cardioselective beta-blockers (e.g., bisoprolol, metoprolol).
• Non-dihydropyridine or dihydropyridine calcium channel blockers (e.g., amlodipine, diltiazem).
• Metabolic anti-anginal agents (e.g., ranolazine or ivabradine).

Once chronic nitrates have been safely tapered and fully cleared from the system under medical direction, the patient may then be considered for PDE5 inhibitor therapy.

Warning: Patients must never stop, taper, or adjust their prescribed nitrate therapy independently. Abrupt cessation of anti-anginal medications can trigger rebound angina, coronary vasospasm, or acute coronary events.

Conclusion

The interaction between organic nitrates and PDE5 inhibitors is one of the most clearly defined, pharmacologically predictable contraindications in clinical medicine. Co-administration causes unchecked, synergistic accumulation of intracellular cGMP, producing profound vasodilation, severe systemic hypotension, and life-threatening reductions in coronary and cerebral perfusion.

For patients and clinicians, safety depends on clear, transparent communication:

• Disclose all cardiovascular therapies, over-the-counter supplements, and erectile dysfunction medicines across all medical consultations.
• Never use rescue nitrates (such as sublingual GTN spray or tablets) if chest discomfort develops after taking an ED medication.
• If acute cardiac symptoms arise, immediately contact emergency services (000 in Australia) and disclose the exact medication and time taken so paramedics can manage the episode safely using alternative therapies.

References

1. Princeton Consensus (2024). Jackson, G., et al. “Cardiovascular Evaluation and Management of Erectile Dysfunction: The Princeton IV Consensus Recommendations.” Journal of Sexual Medicine, 2024. PubMed Search: Princeton Consensus Erectile Dysfunction
2. European Association of Urology (2025). Salonia, A., et al. “EAU Guidelines on Sexual and Reproductive Health.” EAU Guidelines Office, Arnhem, The Netherlands, 2025. European Association of Urology Guidelines
3. American Heart Association / American College of Cardiology (2023). Writing Committee Members. “2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease.” Circulation, 148(9), e9–e119. AHA/ACC Chronic Coronary Disease Guideline
4. Therapeutic Goods Administration (TGA) Australia (2023). Australian Public Assessment Reports & Product Information: Sildenafil Citrate, Tadalafil, Vardenafil, and Avanafil. Department of Health and Aged Care, Australian Government. TGA eBS Product Information Search
5. Kloner, R. A., et al. (2018). “Pharmacology and Drug Interactions of Phosphodiesterase Type 5 Inhibitors for Erectile Dysfunction.” Nature Reviews Urology, 15(11), 665–683. PubMed: 30185856
6. Healthdirect Australia (2024). “Medicines for Erectile Dysfunction: Mechanisms, Interactions and Safety.” Healthdirect Clinical Gateway. Healthdirect Erectile Dysfunction Medicines
7. National Institute for Health and Care Excellence (NICE) (2024). “British National Formulary (BNF): Phosphodiesterase Type-5 Inhibitors & Nitrates.” NICE Guidance. NICE BNF Interactions
8. Schwartz, B. G., & Kloner, R. A. (2023). “Cardiovascular Safety of Phosphodiesterase Type 5 Inhibitors: An Updated Review.” Cardiovascular Drugs and Therapy, 37(4), 789–802. PubMed: 35147823
9. Therapeutic Goods Administration (TGA) Safety Alert (2023). “Undeclared PDE5 Inhibitors in Adulterated Herbal Supplements: Safety Risks for Cardiovascular Patients.” Australian Government Safety Updates. TGA Safety Alerts

This article is intended solely for educational purposes and should not replace individual clinical evaluation, diagnosis, or treatment by a qualified medical professional. If you are experiencing chest pain or a medical emergency, call 000 (Australia) or your local emergency number immediately.