CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 2, May/June 2023 AFRICA 125 (RHC): (1) fall in mean PA pressure of 10 mmHg, (2) to a value of < 40 mmHg, and (3) no change of increase in cardiac output. Inhaled nitric oxide, adenosine and epoprostenol are commonly used to evaluated for vasodilator response. Treatment of PAH involves pulmonary vasodilators, which are not indicated and may cause harm in patients with WHO group II PH due to left heart disease. Calcium channel blockers are indicated for patients with a positive vasodilator response. Three classes of pulmonary vasodilators are indicated for PAH: (1) prostacyclins, (2) oral endothelin receptor antagonists, and (3) mediators of the nitric oxide system such as phosphodiesterase inhibitors and soluble guanylate cyclase inhibitors. The treatment for group II PH involves treating the underlying left heart disease. A key take-away message from this section is the distinction between WHO groups of PH and the role of RHC in diagnosis, recognising the limited cardiac catheterisation capacity in most of SSA. Advanced heart failure, cardiogenic shock and LVAD The presentation started by defining advanced HF as a clinical syndrome characterised by persistent or progressive symptoms of HF and ventricular dysfunction despite GDMT. Data remain sparse but the INTER-CHF showed about 20.9% of African patients were NYHA class IV HF.8 Advanced HF can have a highly unpredictable clinical course and can challenge even the most experienced clinician to correctly identify the optimal timing of referral to an advanced cardiomyopathy/ HF specialist.41 Patients with advanced HF are typically ACC/ AHA stage D HF, NYHA class IV or INTERMACS profile 1–4 (critical cardiogenic shock and inotrope dependence). A useful pneumonic is ‘I NEED HELP’ where I = inotropes, previous or current need for inotropes; N = NYHA III/IV/ natriuretic peptides, persisting NYHA III–IV symptoms or increased NT-proBNP; E = end-organ dysfunction, deteriorating kidney and/or liver function; E = ejection fraction, severely depressed left ventricular function (EF < 20%); D = defibrillator shocks, repeated ICD shocks; H = hospitalisations, more than one admission for HF in the last 12 months; E = oedema/escalating diuretics, persisting congestion or increasing diuretic dose; L = low blood pressure, consistent low systolic blood pressure (< 90–100 mmHg); P = prognostic medication, cannot up-titrate, inability to titrate evidence-based medication (ACE inhibitor/ ARB/BB/MRA or ARNI). Many patients with advanced HF may progress to acute decompensated HF cardiogenic shock (CS).42 The ‘shock pyramid’ system describes stages of CS from A–E based on physical examination, biochemical markers and haemodynamics.43 The stage A ‘at risk’ patient may have non-ST-segment myocardial infarction (STEMI), prior MI or decompensated HFrEF or HFpEF with normal laboratory results and physical examination. The stage B ‘beginning CS’ patient has clinical evidence of relative hypotension [systolic blood pressure (SBP) < 90 mmHg or mean arterial pressure (MAP) < 60 mmHg or > 30 mmHg drop from baseline) or tachycardia without hypoperfusion. Stage C is the ‘classic’ CS, a patient with hypoperfusion that requires initial interventions (inotropes, pressor, mechanical support) beyond volume resuscitation to restore perfusion. Laboratory findings may include impaired kidney function, elevated lactate, brain natriuretic peptide, and/or liver enzymes. Invasive haemodynamics (if available) demonstrate the classic depressed cardiac index that is associated with CS. Stage D, ‘deteriorating or doom’ CS, describes a patient who has failed to stabilise despite initial efforts, further escalation is required and 30 minutes have elapsed, but the patient has not responded with resolution of hypotension or end-organ hypoperfusion. Stage E: ‘extremis’ CS is the patient with circulatory collapse, frequently (but not always) in refractory cardiac arrest with ongoing cardiopulmonary resuscitation or is being supported by multiple simultaneous acute interventions, including extracorporeal membrane oxygenation. LVADs represent a therapeutic option for patients with Stage D HFrEF who may not be candidates for HT and provide improved survival rates, functional capacity and quality of life. General cardiologists and internists may encounter LVAD patients in routine practice. With the withdrawal of the Medtronic Heartware, the Abbott Heartmate 3 (HM3) is the only US Food and Drug Administration approved LVAD that is commercially available. The basic LVAD design, regardless of manufacturer, consists of internal components such as the inflow cannula, implantable pump and outflow graft, and external components such as the driveline exiting the abdominal wall, the controller: a smartphone-sized ‘computer’ that gives the patients and clinician basic diagnostics and triggers alarms in certain dangerous scenarios, and an energy source connected to a controller that comes from batteries or an AC power source. Warfarin and aspirin therapy are required by all patients because of the interaction of blood along the surface of the LVAD, and the subsequent development of thrombus. The recommended international normalised ratio (INR) goal is 2.0–3.0 and the recommended dose of aspirin is 325 mg for patients with an HMII or HeartWare device, and 81 mg for an HM3. Blood pressure measurement for LVAD patients is best achieved with a Doppler device by evaluating the pressure at which the Doppler sound returns during cuff deflation (which corresponds to the MAP). Most patients with LVAD have a narrow arterial pulse pressure and their pulses may be absent or intermittent on palpation. In case of arrest for the LVAD patient, the first step is to listen over the chest to see if there is an LVAD hum, then an assessment of end-organ perfusion must be done. In patients without an LVAD hum, or with signs of impaired end-organ perfusion, LVAD connections should be assessed to ensure adequate connection between the driveline and controller and that flows are maintained. In patients with constant low-flow alarms as well as evidence of end-organ dysfunction, such as marked hypotension (MAP < 50 mmHg), or an end-tidal carbon dioxide tension (PetCO2) value of < 20 mmHg, routine advanced CV life support and basic life support protocols should be followed as recommended by current guidelines.44,45 Atrial and ventricular arrhythmias are common in LVAD patients, due to pre-existing cardiomyopathy, alterations in electrical conduction system post-LVAD, scar tissue with previous myocardial ischaemia, scar around the LVAD inflow cannula, suction events (because of LV underfilling or high pump speed), or changes in the QT interval secondary to LV unloading.46 Treatment includes anti-arrhythmic agents (BB, especially propranolol), ventricular tachycardia ablation and stellate ganglion block in refractory cases.
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