Overview

This lecture covers the overlap between anxiety/panic presentations and cardiac symptoms in ED and cardiology. It moves from how common non-cardiac chest pain (NCCP) and panic disorder are among chest-pain presentations, through how to distinguish (and where the distinction blurs between) panic attacks and acute cardiac events, into the bidirectional biological relationship between anxiety and cardiac disease (anxiety accelerating cardiac disease via the HPA axis, and cardiac disease raising anxiety risk), and finishes with communication strategies for reassuring NCCP patients.

Presentations in ED/cardiology

  • Of patients presenting with chest pain, a majority are non-cardiac rather than cardiac in origin.
  • Acute cardiac symptoms: crushing chest pain/chest tightness, palpitations (rapid, slow or irregular heartbeat), sweating, shortness of breath, tingling/numbness, nausea, faint/dizzy, vomiting.
  • Non-cardiac chest pain (NCCP) is an umbrella term for chest pain presentations without underlying heart issues, caused by: gastrointestinal issues, musculoskeletal issues, respiratory conditions, chest wall infections, or anxiety and panic disorders.
  • Panic attack patients often seek medical, not mental health, treatment.
  • 25-30% of all ED/cardiology presentations have panic disorder.

Anxiety vs panic attack

  • Anxiety: develops slowly, less intense but longer lasting; a general feeling of tension and restlessness; triggered by a perceived threat.
  • Panic attack: peaks within minutes, intense but short-lived; fear of losing control or dying; can start suddenly without a trigger.
  • Physical anxiety symptoms (e.g. in a stressful/exam situation) can include blurred vision, headache, echoing sounds, flushed cheeks, sweaty palms, short breath, dry mouth, heart pounding, nauseous stomach, shaky hands, stiff legs, sweaty feet.

Distinguishing panic attacks from acute cardiac events

Symptom overlap (Venn diagram):

  • Acute cardiac symptoms only: often described as crushing chest pain/chest tightness; pain that moves to arms, neck, back; vomiting.
  • Shared/overlapping: palpitations (rapid, slow or irregular heartbeat), sweating, shortness of breath, tingling/numbness, nausea, faint/dizzy.
  • Panic attack symptoms only: often described as discomfort or sharp pain; pain often in the chest area; abdominal distress; feelings of choking; fear of losing control/“going crazy”.

Other defining features:

  • Acute cardiac symptoms (heart attack): typical age ≥45 years for males, ≥55 years for females; symptoms tend to persist and exacerbate over time.
  • Panic attack symptoms: peak onset of panic disorder is in the late 20s; short-lived and improves over time; managed with de-escalation strategies.

Despite these distinguishing features, the line between cardiac and non-cardiac presentations is not always definitive.

The blurred line between cardiac and non-cardiac

  • A 2017 UK multi-centre study of 8762 patients found 72% were NCCP.
  • At 1-3 year follow-up, 32% of deaths from cardiac causes had initially been diagnosed as NCCP.
  • This difficulty arises because the relationship between anxiety/panic attack and cardiac conditions is bidirectional: anxiety/panic attack may accelerate underlying cardiac disease, and cardiac conditions may increase risk of anxiety, making it a “chicken and egg” problem of circular/uncertain causality.

Anxiety as a risk factor for heart disease

  • Panic disorder increases risk of chronic cardiac disease by 2-fold.
  • Vicious cycle of panic disorder: a trigger (feeling chest pain or noticing heart rate elevation) leads to perception of threat to health (“there is something wrong with my heart”), which produces catastrophising thoughts (“this is serious”/“I’m going to have a heart attack”/“I might die”) and increasing anxiety (emotion); these feed into physiology, activation of the stress response system (HPA axis) causing increased breathing rate, sweating, elevated heart rate, and dizziness/lightheadedness; this physiological response loops back to reinforce the catastrophic thoughts, perpetuating the cycle.
  • Excess activation of the HPA axis (“alarm”) triggers release of stress hormones, producing body-wide changes, via three main mechanisms:
    1. Increased catecholamines: dopamine (regulates movement, emotions, memory), adrenaline (increases blood flow), noradrenaline (increases heart rate and blood pressure). Nerve impulses travel from the hypothalamus down the spinal cord to the adrenal gland, which releases catecholamines into the bloodstream; these act on the heart (increased heart rate), liver, intestines, blood vessels (high blood pressure) and lungs.
    2. Heightened physiological reactivity to stress: for a given stress level, the body’s reactivity response is steeper/greater.
    3. Poor health behaviours: excess HPA-axis activation is associated with behaviours such as stress eating.
  • Overall pathway: anxiety disorders lead to cardiac conditions via two routes, behavioural changes and physiological changes, both of which feed into cardiac conditions.

Cardiac conditions increase risk of anxiety

Evidence cited:

  • Coronary artery disease: 5-8% of patients have panic disorder.
  • Cardiac disease: 26% of patients have generalised anxiety disorder (GAD).
  • Acute coronary syndrome: 20-30% of patients have elevated anxiety levels.

Communication strategies for NCCP

Case scenario: a patient presents to ED in panic, with shortness of breath, racing heartbeat, dizziness, and fear that it is a heart attack; assessment concludes it is a panic attack. Recommended communication approach:

  • Acknowledge the reality of the symptoms.
  • Understand and empathise with the patient’s and whānau’s beliefs and worries.
  • Provide other possible explanations while validating the person’s experience.
  • Reassure through normalising and discussing prognosis.
  • Collaboratively develop a treatment plan.
  • Follow-up.

Example patient information approach (NHS “Safe & Rapid Chest Pain Management”, for low-risk chest pain patients):

  • Explains chest pain is common and often not serious.
  • Reports results of tests done: a troponin blood test (checks for heart muscle damage) and an ECG (heart trace, checks heart activity and oxygenation) — reassures the patient when both are normal/negative.
  • States it is safe to go home, with advice to return or call emergency services if pain recurs or worsens, and to improve long-term health (stop smoking, reduce alcohol, exercise, eat healthily, involve GP).
  • Communicates personal risk in concrete terms: for every 100 people presenting like the patient with a normal troponin and ECG, 99 will not have had a heart attack (i.e. risk of a missed heart attack is less than 1%), while noting future heart complications cannot be entirely ruled out.

Take-home messages

  1. NCCP is a common presentation in ED/cardiology.
  2. Anxiety/panic disorder is something to consider and rule out in clinical assessment.
  3. It is not always easy to distinguish between cardiac and non-cardiac issues.
  4. Anxiety and cardiac conditions have a bidirectional relationship, so assessment and intervention around both are important.
  5. Where anxiety alone is the issue, mental health professionals will provide treatment, but GPs will likely assess and screen for this first and refer on.

Self-test

  1. What proportion of ED/cardiology chest-pain presentations have panic disorder, and what behaviour do panic attack patients typically show regarding seeking treatment?
  2. List the causes that fall under the umbrella term “non-cardiac chest pain (NCCP)”.
  3. Distinguish anxiety from a panic attack in terms of onset, intensity and duration.
  4. Describe the symptoms that overlap between acute cardiac events and panic attacks, and the symptoms that are distinctive to each.
  5. What age thresholds are used as a defining feature for heart attack risk, and at what age does panic disorder typically peak in onset?
  6. What did the 2017 UK study of 8762 patients find about NCCP prevalence and about deaths from cardiac causes among patients initially diagnosed with NCCP?
  7. Describe the steps of the vicious cycle of panic disorder, from trigger to physiological response.
  8. By what factor does panic disorder increase the risk of chronic cardiac disease, and via what two general pathways do anxiety disorders lead to cardiac conditions?
  9. Describe the three main downstream effects of excess HPA-axis activation, including the roles of dopamine, adrenaline and noradrenaline.
  10. List the evidence rates given for anxiety/panic disorder among patients with coronary artery disease, cardiac disease, and acute coronary syndrome.
  11. A patient presents to ED in panic with shortness of breath, racing heart and fear of a heart attack, and is assessed as having a panic attack. Describe the communication strategies that should be used to address this.
  12. How is personal risk of a missed heart attack communicated to a low-risk chest pain patient with normal troponin and ECG results, according to the NHS handout?

Answers