Acute Deterioration of Cardiovascular Conditions

Definition / Overview

• Acute deterioration of cardiovascular conditions encompasses a spectrum of time-critical presentations that a GP must recognise, stabilise, and escalate promptly.
• In the primary care setting, these presentations may arrive without warning: a patient attending for a routine review suddenly becomes diaphoretic, or a new patient walks in with crushing chest pain.
• The GP's role is to perform rapid clinical assessment, initiate first-line management, and coordinate emergency transfer while avoiding delays that worsen outcomes.

Key presentations covered in this note:

• Acute coronary syndrome (ACS): unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI)
• Acute decompensated heart failure (ADHF)
• Hypertensive emergency and urgency
• Haemodynamically significant arrhythmias
• Cardiac arrest

Pathophysiology

Acute Coronary Syndrome

• ACS results from rupture or erosion of an atherosclerotic coronary plaque, triggering platelet aggregation and thrombus formation.
• Complete occlusion causes STEMI; partial occlusion or transient complete occlusion causes NSTEMI or UA.
• The degree of myocardial injury correlates with the duration and severity of ischaemia: irreversible necrosis begins within 20-40 minutes of complete occlusion.

Acute Decompensated Heart Failure

• ADHF occurs when cardiac output falls or filling pressures rise acutely, precipitated by fluid overload, arrhythmia, infection, medication non-adherence, or uncontrolled hypertension.
• Pulmonary oedema results from elevated left ventricular end-diastolic pressure transmitted to the pulmonary venous circulation.

Hypertensive Emergency

• Defined as severe hypertension (typically systolic ≥180 mmHg or diastolic ≥120 mmHg) with acute target organ damage (brain, heart, kidneys, retina).
• Hypertensive urgency is similarly severe elevation without target organ damage.
• Rapid end-organ ischaemia results from failure of cerebrovascular autoregulation and direct vascular injury.

Arrhythmias

• Haemodynamic compromise arises when heart rate is excessively fast (reduced diastolic filling time) or slow (inadequate cardiac output), or when loss of atrial kick reduces ventricular filling.
• Severity depends on the underlying rhythm, rate, and degree of pre-existing ventricular dysfunction.

Clinical Features and Diagnosis

Acute Coronary Syndrome

Classic features:

• Central chest pain; pressure, tightness, or heaviness
• Radiation to jaw, left arm, or interscapular region
• Diaphoresis, nausea, vomiting
• Duration >20 minutes not relieved by GTN

Atypical features (more common in women, older adults, diabetic patients):

• Epigastric discomfort or indigestion-like pain
• Dyspnoea as the dominant or sole symptom
• Fatigue, syncope, or unexplained deterioration

Red flags requiring immediate action:

• Pain at rest or crescendo pattern
• Haemodynamic instability (hypotension, shock)
• Pulmonary oedema concurrent with chest pain
• New ECG changes

ECG interpretation in the GP clinic:

• STEMI: ST elevation ≥1 mm in two contiguous limb leads or ≥2 mm in precordial leads; new left bundle branch block (LBBB) is a STEMI equivalent
• NSTEMI/UA: ST depression, T-wave inversion, or transient ST elevation; troponin differentiates NSTEMI (elevated) from UA (normal)
• A normal ECG does not exclude ACS

Acute Decompensated Heart Failure

• Acute dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
• Bilateral fine crackles on auscultation; wheeze (cardiac asthma)
• Raised JVP, peripheral oedema, S3 gallop
• Oxygen saturation $\text{SpO}_2 < 94\%$ at rest
• Precipitants: arrhythmia, infection, dietary sodium excess, missed diuretic doses, NSAID use

Hypertensive Emergency

• Blood pressure ≥180/120 mmHg plus any of:
  • New neurological deficit, severe headache, visual disturbance (hypertensive encephalopathy, stroke)
  • Chest pain (aortic dissection, ACS)
  • Acute pulmonary oedema
  • Haematuria, acute kidney injury
  • Hypertensive retinopathy (papilloedema, flame haemorrhages on fundoscopy)

Haemodynamically Significant Arrhythmias

Investigation and Monitoring

In the GP setting, investigations serve to confirm the diagnosis and guide escalation; do not delay transfer for investigations if the patient is unstable.

Immediately available in most GP clinics:

• 12-lead ECG: first-line for any chest pain, dyspnoea, or palpitations
• Pulse oximetry: $\text{SpO}_2$
• Blood pressure (both arms if aortic dissection suspected)
• Point-of-care (POC) glucose to exclude hypoglycaemia mimicking cardiovascular deterioration

In-clinic or via urgent pathology (may not change immediate management):

• POC troponin (where available): aids NSTEMI diagnosis but a single negative result at presentation does not exclude ACS
• Electrolytes (hypokalaemia or hyperkalaemia exacerbate arrhythmias): $K^+ < 3.0\,\text{mmol/L}$ or >6.0 mmol/L are critical
• BNP/NT-proBNP (not routinely available POC): elevated in heart failure
• Full blood count: anaemia as a precipitant for decompensation

Ongoing monitoring during stabilisation:

• Continuous cardiac monitoring if available (AED in monitoring mode)
• Repeat blood pressure and heart rate every 5 minutes if unstable
• Serial ECGs if evolving STEMI is suspected

Management

General Principles for Any Acute Cardiovascular Deterioration

1. Call triple zero (000) immediately for suspected STEMI, ADHF with $\text{SpO}_2 < 90\%$, haemodynamically unstable arrhythmia, or hypertensive emergency with neurological signs.
2. Position the patient: semi-recumbent for dyspnoea/heart failure; supine with legs elevated for haemodynamic compromise (except pulmonary oedema).
3. Establish IV access.
4. Apply supplemental oxygen only if $\text{SpO}_2 < 94\%$: routine oxygen in normoxic ACS patients is not beneficial and may be harmful.
5. Attach cardiac monitor/AED; obtain 12-lead ECG.
6. Obtain IV access; take bloods if this does not delay transfer.
7. Provide a clear written handover to paramedics and pre-notify the receiving hospital.

Acute Coronary Syndrome Management

STEMI

Time is myocardium: the primary goal is rapid reperfusion.

1. Administer aspirin 300 mg orally (chewed), unless absolute contraindication.
2. Administer GTN 400 mcg sublingually every 5 minutes up to three doses, provided systolic BP >90 mmHg and no right ventricular infarction suspected (inferior STEMI with right-sided leads showing ST elevation in V4R).
3. Administer a second antiplatelet agent per local protocol (ticagrelor 180 mg orally is preferred over clopidogrel where available, unless contraindicated by planned CABG).
4. Analgesia: morphine 2.5-5 mg IV titrated, though note emerging evidence suggests morphine may slow antiplatelet absorption; use clinical judgement.
5. Arrange immediate transfer to a percutaneous coronary intervention (PCI)-capable centre: target door-to-balloon time <90 minutes from first medical contact.
6. If PCI is not available within 120 minutes: discuss facilitated fibrinolysis with the receiving cardiologist; tenecteplase weight-based dosing is the standard agent in Australia.

NSTEMI / Unstable Angina

1. Aspirin 300 mg orally (chewed).
2. GTN as for STEMI (observe BP contraindications above).
3. Second antiplatelet if not high bleeding risk, per hospital protocol.
4. Urgent transfer for inpatient risk stratification; NSTEMI requires hospital admission.
5. Anticoagulation is usually commenced in hospital (heparin, fondaparinux, or enoxaparin); do not routinely initiate in the GP setting unless directed by a specialist protocol.

Acute Decompensated Heart Failure

1. Sit the patient upright (legs dependent reduces preload).
2. Supplemental oxygen to maintain $\text{SpO}_2 \geq 94\%$.
3. GTN spray 400 mcg sublingually every 5-10 minutes if systolic BP >100 mmHg: venodilation reduces preload rapidly.
4. Frusemide (furosemide) 40-80 mg IV (or double the patient's usual oral dose if already on a diuretic): acts within 15-20 minutes.
5. If available and patient not hypoxic: high-flow oxygen via non-rebreather mask; consider CPAP in severe cases if CPAP equipment is available.
6. Identify and treat the precipitant: rate control for rapid AF, antibiotics for infective precipitant.
7. Urgent ambulance transfer for anyone with $\text{SpO}_2 < 90\%$ refractory to oxygen, systolic BP <90 mmHg, or altered consciousness.

Hypertensive Emergency vs Urgency

Hypertensive emergency:

• Immediate ambulance transfer.
• Do not reduce BP rapidly in the GP setting without IV agents and monitoring; an abrupt fall risks watershed ischaemia (especially in longstanding hypertension).
• Exception: sublingual GTN for acute pulmonary oedema component while awaiting transfer.

Hypertensive urgency:

• Oral agent initiation or dose uptitration: amlodipine 5 mg orally, or captopril 12.5-25 mg orally.
• Recheck BP in 1-2 hours; aim for a controlled reduction over 24-48 hours.
• Ensure close GP follow-up within 48 hours.
• Review adherence, secondary causes, and medication regimen.

Arrhythmia Management

Cardiac Arrest (VF / Pulseless VT)

1. Call 000.
2. Begin CPR immediately: 30 compressions to 2 breaths; compression depth ≥5 cm, rate 100-120 per minute.
3. Attach AED as soon as available; follow prompts.
4. Adrenaline 1 mg IV every 3-5 minutes after the second shock (if IV access established and trained personnel present).
5. Continue until paramedics arrive; minimise interruptions to compressions.

Haemodynamically Unstable Tachyarrhythmia (conscious patient)

• Rapid AF, SVT, or VT with pulse and systolic BP <90 mmHg or altered conscious level.
• Arrange immediate transfer; consider synchronised DC cardioversion if the GP has the skills, equipment, and trained assistance.
• For stable SVT: vagal manoeuvres first (Valsalva, carotid sinus massage); if unsuccessful, adenosine 6 mg rapid IV push followed by 20 mL normal saline flush (repeat 12 mg if no response after 2 minutes), provided no pre-excitation (WPW) on ECG.

Symptomatic Bradycardia

• Atropine 600 mcg IV; repeat up to 1.8-3 mg total if needed.
• Transcutaneous pacing if atropine ineffective and equipment available.
• Urgent transfer for CHB or Mobitz type II block.

Complications and Special Considerations

Recognising Mechanical Complications of MI

• Acute mitral regurgitation (papillary muscle rupture): sudden pulmonary oedema, new pansystolic murmur, hypotension; surgical emergency.
• Ventricular septal defect post-MI: new harsh pansystolic murmur with haemodynamic collapse; requires urgent cardiac surgery.
• Free wall rupture: sudden electromechanical dissociation; near-universally fatal without immediate surgery.

Right Ventricular Infarction

• Complicates 30-50% of inferior STEMIs.
• Haemodynamic triad: hypotension, elevated JVP, clear lung fields.
• Avoid GTN, morphine, and diuretics (preload-dependent).
• Management: IV fluid challenge, early reperfusion.

Patients on Anticoagulation or Antiplatelet Therapy

• Existing anticoagulation (e.g. warfarin, DOAC) complicates fibrinolysis decisions; document current INR and last DOAC dose.
• Withhold further anticoagulants until specialist advice.

Diabetes and ACS

• Hyperglycaemia at presentation worsens ACS outcomes; blood glucose should be monitored but aggressive insulin correction in the acute phase is not routinely indicated in the GP setting.

Pregnancy and Cardiac Emergencies

• ACS in pregnancy is rare but increasing; management priorities are as per standard guidelines; fetal radiation exposure from cardiac investigations is not a reason to delay necessary imaging.
• Peripartum cardiomyopathy presents as ADHF in late pregnancy or up to 5 months postpartum; urgent obstetric and cardiology input required.

Long-term Care and Follow-up After Acute Cardiovascular Events

GP's role post-discharge is central to secondary prevention and rehabilitation.

• Medication reconciliation: confirm patient is established on aspirin, P2Y12 inhibitor (dual antiplatelet therapy for 12 months post-ACS unless bleeding risk), statin at high-intensity dose (atorvastatin 40-80 mg daily), ACE inhibitor or ARB, and beta-blocker.
• Cardiac rehabilitation: refer to a structured program; reduces mortality and rehospitalisation.
• Lipid targets post-ACS: LDL-C <1.8 mmol/L (or ≥50% reduction); review at 6 weeks post-discharge.
• Blood pressure target: <130/80 mmHg in most post-ACS patients.
• Driving restrictions: notify patient of State/Territory requirements (typically 2-4 weeks off driving after MI; longer for commercial licences or post-arrhythmia events).
• GP chronic condition management plan (GPCCMP; MBS item 965): appropriate for patients with heart failure or post-MI requiring coordinated multidisciplinary input (cardiologist, cardiac rehabilitation nurse, dietitian, pharmacist; MBS allied health by direct referral under the plan).
• Heart failure monitoring: weight diary, fluid restriction, medication titration; admission for >2 kg weight gain over 2 days.
• Psychosocial assessment: screen for depression post-MI (PHQ-9 or K10); depression is an independent risk factor for re-infarction and mortality.
• Absolute cardiovascular risk reassessment: formal calculation at each relevant review; target management to achieved risk reduction, not just individual risk factors.