Cardiovascular conditions Flashcards
Conditions and emergencies
Left Sided Heart failure Pathophysiology
Increase in left ventricle size due to increased work load and end diastolic volume.
Increase in size occurs with stretched rather than functional tissue.
Contractility of left ventricle decreases.
Blood pools and backs up in left atrium, pulmonary vein.
Back up in pulmonary circulation leads to pulmonary oedema.
Cardiac output decreases as less ventricular contraction.
Right sided Heart Failure Pathophysiology
Increase in right ventricle with stretched tissue normally due to overcompensation from LVHF.
Blood pools in right atrium and vena cava.
Blood backs up in systemic veins causing peripheral oedema and JVD.
LVHF signs and symptoms
Signs
Crackles
Increased Resp Rate
Increased Heart rate
Decreased O2
Cyanosis
Orthopnoea
Dec tissue perfusion
Symptoms
PE symptoms
SOB
pleuritic chest pain
Dyspnoea
RVHF Signs and Symptoms
Peripheral Oedema
Inc Heart rate
Decreased tissue perfusion
Cyanosis
Ascites
Anorexia
Jugular vein distension
Risk Factors HF
Coronary artery disease
hypertension
Cardiomyopathies
Obesity
Vascular disease
COPD
Pericardial disease
arrythmias
Treatment and Management HF
RVHF suspected - referral to GP
LVHF suspected - GTN if blood pressure is over 110
- CPAP to aid breathing
- administer O2
- IV furosemide to decrease oedma and blood pressure.
Cardiogenic Shock!!! (BP less than 90 and Heart rate less than 40 or over 110)
- administer O2
- urgent transfer to ED/CCU with pre-alert.
GTN
Vasodilator used to increase size of vessels to aid blood flow around the heart and body.
Administered sublingually in sprays of 400-800mcg every 5-10 minutes.
Classifications of Heart Failure
Acute/Chronic
Left/Right sided
High/Low output
3 Acute Coronary syndromes
ST elevation Myocardial infarction STEMI
Non ST elevation Myocardial Infarction NSTEMI
Unstable Angina
ACS Pathophysiology
- blockage in coronary arteries (most common cause is atherosclerosis)
- plaque build-up blocks artery or plaque breaks and triggers thrombosis.
- Blockage means less blood flows to myocardium and cardio myocytes do not receive sufficient oxygen (Ischaemia), leading to decreased functioning and weaker contraction.
- Less blood flow means toxic waste is not carried away from cells and so membranes breakdown.
- troponin is one of the proteins contained in the myocytes which leaks when the cells breakdown.
- Due to decreased contraction function, blood backs up in lungs and impedes on gas exchange.
ACS signs and symptoms
Chest, epigastric and retrosternal pain
dull aching pain, crushing pain, tightness, burning.
Radiating pain to neck/jaw/left arm
Pallor
Diaphoresis
Nausea
Anxiety
SOB
Fatigue
ACS: risk Factors
Valve disease
Atherosclerosis
High cholesterol
Physical inactivity
Cardiomyopathy
Smoking
drug misuse
Hypertension
Diabetes
Age/gender/ethnicity/genetics
Difference between unstable angina and STEMI and NSTEMI
Unstable angina patients do not have raised troponin levels but have ACS presentation.
ACS: treatment and management
Analgesia: IV paracetamol or morphine ideally left arm
Oxygen therapy if below 94/88, avoid over oxygenation as can lead to vasoconstriction and occlusion
Aspirin: anti-platelet drug (300mg chewed)
Anti- sickness: to combat pre-existing or morphine induced sickness, especially if lying flat … aspiration !
Nitrates: GTN is a vasoconstrictor which improves blood flow around heart and body. Can cause hypotension and wooziness
sublingual sprays of 400-800mcg every 5-10minutes.
Pathway 1 ACS
RED!
ST segment elevation
ST depression in v2-v3 with ST elevation in V8-v9
Left coronary artery main STEM
New or suspected onset LBBB with clear history of AMI
Pathway 2
No ST elevation but other ST changes or T wave changes
LBBB without clear AMI history
NO ECG changes but current cardiac chest pain
ST segment elevation and symptoms resolve with use of GTN spray.
Pathway 3 ACS
No ECG changes and currently pain free but with chest pain in last 12 hours.
Hospital care for ACS
Cath lab for stents or bypass graph
CCCU = coronary critical care unit
PPCU - primary percutaneous coronary intervention
3 types of acute heart failure
Acute pulmonary oedema
Peripheral oedema
Cardiogenic shock
DVT: presentation
Discolouration on one calf (purple/blue/black)
Unilateral calf swelling
Pain and tenderness
Difficulty weight bearing
Increased discomfort with flexion
DVT: risk factors (Virchows triad of thrombosis)
Blood:
- hypercoagulability
-trauma
-malignancy
-pregnancy
-thrombophilia
-Dehydration
Vessels
-thrombophlebitis
-cellulitis
-atherosclerosis
-venepuncture
-trauma
Circulation
-immobility
-venous obstruction
varicose veins
-AF or left heart failure/dysfunction
DVT: pathophysiology
In a normal vein, blood moves towards the heart.
Due to stagnation of blood and/or hypercoagulable states, thrombus occurs in the veins of the lower legs forming thrombi which get stuck in venous circulation.
PE: pathophysiology
Thrombi which form in venous circulation, specifically DVT travel in the venous circulation until they get stuck in the small vessels of the lungs causing occlusion. Blockage can also come from embolus (not blood) but thrombi is more common. This blockage impedes of pulmonary perfusion as well as gas exchange.
